Introduction. Exercise Physiology: An Overview
EXERCISE PHYSIOLOGY: AN OVERVIEW What is Exercise Physiology?
Exercise Physiology is the study of the effects of exercise on the body . Specifically, Exercise Physiology is concerned with the body’s responses & adaptations to the stress of exercise , ranging from the system level (e.g., cardiovascular system) to the subcellular level (e.g., production of ATP for energy). These modifications can be short term – that is lasting only for the duration of the activity/exercise – or long term – present as long as the activity is continued on a regular basis. Exercise physiologists are interested in both the acute (immediate) & chronic (long-term) effects & adaptations of exercise on all aspects of body functioning. Acute adaptations – the changes in human physiology that occur during exercise. Chronic adaptations – the alterations in the structure & functions of the body that occur in response to the regular completion of exercise or physical activity.
Exercise training – the repeated use of exercise to improve physical fitness.
Exercise Physiology
The study of how body structure & function is altered by exposure to physical activity and exercise.
Sport Physiology
The application of the concepts of exercise physiology to training athletes & enhancing sports performance. (Sport Physiology is is derived or evolved from Exercise Physiology)
The Importance of exercise physiology to the practitioner
Knowledge from exercise physiology is used to design effective fitness programs for people of all ages, to guide the development & implementations of cardiac rehabilitation programs, to plan programs to help children & youths to incorporate physical activity into their life, and to structure rehabilitation programs for injured athletes.
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Chapter 1. Basic Energy Systems
BASIC ENERGY SYSTEMS A. Energy
All plants & animals depend on energy to sustain life. Humans derive this energy from food. Many forms: chemical, electrical, electromagnetic, thermal, mechanical & nuclear. All energy forms are interchangeable; e.g. chemical energy used to create electrical energy stored in battery. Never lost or newly created – it undergoes steady degradation from one form to another, ultimately becoming heat. 60%-70% of the total energy in humans is degraded to heat.
1. Energy for Cellular Activity All energy originates from the sun as light energy. Chemical reactions in plants convert light into stored chemical energy. Humans obtain energy by eating plants, or animals that feed on plants. Energy is stored in food in the form of carbohydrate, fats & proteins. Human cells can break down these 3 basic food components to release the stored energy.
Energy Sources Foods are composed of carbon, hydrogen, oxygen, & nitrogen (protein). Molecular bonds in foods are weak & provide little energy when broken. Food is NOT used directly for cellular activity. Energy in food molecules’ bonds chemically released within cells, then stored in the form of a high-energy compound called adenosine triphosphate (ATP). At rest, energy that body needs is derived almost equally from the breakdown of CHO & fats. Proteins provide little energy for cellular function/activity. During mild to severe exercise, more CHO is used. In maximal, short-duration exercise, CHO is used exclusively to produce ATP.
Carbohydrate (CHO) CHO – to be useful must be converted into glucose (monosaccharide) that is transported to all body tissue via blood. During rest, ingested CHO taken up by muscle & liver, then converted into glycogen (a more complex glucose molecule). Glycogen is stored in cytoplasm until cells use it to form ATP. Liver & muscle glycogen reserves are limited & can be depleted unless CHO is increase. CHO stores in liver & skeletal muscle are limited to < 2,000 kcal of energy.
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Chapter 1. Basic Energy Systems
Fats Fat provides 2 times more energy than CHO but less accessible for cellular metabolism because it must first be reduced from its complex form (triglyceride) to its basic components: glycerol & free fatty acids (FFA). Only FFA are used to form ATP. Fat is a good source of energy, can be stored exceeding 70,000 kcal of energy.
Protein Protein can be used as energy source if convert into glucose. Protein converted into glucose through gluconeogenesis. In severe energy depletion (starvation), protein can be converted to FFA for cellular energy through lipogenesis. Protein can supply up to 5-10% of the energy needed to sustain prolonged exercise. Protein can be used as energy source in basic form of amino acids.
Energy Yield 1 g of CHO (C6H12O6) yields 4 kcal of energy. 1 g of fat (C16H18O2) yields 9 kcal of energy. 1 g of protein (NH2 + CO2H) yields 4.1 kcal of energy. (Though 1 g of fat can generate 2.25 times as much as a similar amount of CHO, it also takes substantially more oxygen to metabolize fat than CHO)
B. Bioenergetics
The chemical processes involved with the production of cellular ATP by converting foodstuffs (i.e., carbohydrates, fats, proteins) into a biologically usable form of energy.
ATP Production An ATP molecule consists of adenosine (adenine joined to ribose) combined with 3 inorganic phosphate (P i) groups. When acted on by enzyme ATPase (adenosine triphosphatase), the last phosphate group splits away from the ATP molecule, rapidly releasing a large amount of energy (7.6 kcal per mole of ATP). This reduces the ATP to ADP & Pi.
ATPase ATP
ADP + Pi
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Chapter 1. Basic Energy Systems
The process of storing energy by forming ATP from other chemical sources is called phosphorylation. Through various chemical reactions, a phosphate (P i) groups is added to a relatively low-energy compound, ADP, converting it to ATP. ADP + Pi
ATP
When these reactions occur without oxygen, the process is called anaerobic metabolism. With the aid of O2, the overall process is called aerobic metabolism & the aerobic conversion of ADP to ATP is oxidative phosphorylation. Cells generate ATP by 3 methods: 1. ATP-PC system 2. Glycolytic system 3. Oxidative system
1. ATP-PC system: (Anaerobic ATP Production)
Formation of ATP by PC breakdown. The simplest of the energy system. Phosphocreatine (PC) is a high-energy phosphate molecule that store in the muscle cells. Energy is released when PC is breakdown / separate to Pi and creatine by enzyme creatine kinase (CK). This energy is not used directly to accomplish cellular work. Energy released from the breakdown of PC is used to combine Pi with ADP to form ATP. This system is anaerobic that functions to maintain the ATP levels. 1 mole of PC will yield 1 mole of ATP. Provides energy for short-term and high-intensity exercise that lasting about 315 seconds.
creatine kinase PC
Pi + C + energy
ADP + Pi + energy
ATP
Figure: ATP-PC system
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Chapter 1. Basic Energy Systems
2. Glycolytic system
Occurs in the sarcoplasm of the muscle cells. Use only carbohydrate as the main source of fuel. Involves glycolysis the breakdown (lysis) of glucose or liver glycogen to pyruvic acid via glycolytic enzymes. Glycogen is synthesized from glucose by a process called glycogenesis & stored in the liver or in muscle until needed. Before either glucose 0r glycogen can be used to generate energy, they must be converted to a compound called glucose-6-phosphate. Conversion of a molecule of glucose requires 1 mole of ATP. 1 mole of glucose produces 2 ATPs or 1 mole of glycogen produces 3 ATPs. Provides energy for high-intensity exercise (80-90% max) up to 2 minutes. If O2 is not available to accept the hydrogen ions in the mitochondria, pyruvic acid can accept the hydrogen ions to form the lactic acid. This accumulation of lactic acid is a major limitation of anaerobic glycolysis. This acidification of muscle fibers inhibits further glycogen breakdown because it impairs glycolytic enzymes functions. In addition, the acid decreases the fibers’ calcium-binding capacity & thus may impede muscle contraction.
Glucose (Need 1 ATP)
or
Glycogen
Glucose-6-phosphate ATP
Pyruric acid
Lactic acid Figure: Glycolytic system
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Chapter 1. Basic Energy Systems
(Lactic acid is an acid with the chemical formula C 3H6O8. Lactate is any salt of lactic acid. When lactic acid releases H+, the remaining compound joins Na+ or K+ to form a salt. Anaerobic glycolysis produces lactic acid, but it quickly dissociates & the salt (lactate) is form.) 3. Oxidative system The body’s most complex energy system, which generates energy by breakdown of fuels with the aid of O 2 (cellular respiration). Because O2 is used, this is an aerobic process. Has a very high-energy yield and yields more energy than the ATP-PC or glycolytic system. Oxidative production of ATP occurs within the mitochondria. Main energy production during endurance activities.
Oxidative production of ATP involves: i. Oxidation of CHO ii. Oxidation of Fat
i Oxidation of Carbohydrate Involves 3 processes: a. Aerobic glycolysis b. The Krebs cycle c. The electron transport chain
Aerobic glycolysis In CHO metabolism, glucose or glycogen is broken down to pyruvic acid via glycolytic enzymes. Hydrogen is released as glucose is metabolized to pyruvic acid. In the presence of O 2, the pyruvic acid is converted into acetyl coenzyme A (acetyl CoA). 1 mole of glucose produces 2 moles of ATP or 1 mole of glycogen produces 3 moles of ATP.
The Krebs cycle Once the acetyl CoA is formed, it enters the Krebs cycle (citric acid cycle), a complex series of chemical reactions that permits the complete oxidation of acetyl CoA. At the end of the Krebs cycle, 2 moles of ATP have been formed. The substrate (CHO) has been broken down into carbon (C) & hydrogen (H). Remaining C then combine with O 2 to form CO2. H+ released combines with 2 coenzymes: NAD (nicotinamide adenine dinucleotide) & FAD (flavin adenine dinucleotide) to enter electron transport chain (Supplies electrons to be passed through the electron transport chain).
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Chapter 1. Basic Energy Systems
The Electron Transport Chain (Respiratory chain or cytochrome chain) The coenzymes carry the H atom (NADH & FADH) to the electron transport chain, split into protons & electrons. At the end of the chain, H + combines with O2 to form H20 (O2–accepting electrons), thus preventing acidification. The electrons that were split from the H pass through a series of reactions (ETC) & ultimately provide energy for the phosphorylation of ADP, thus forming ATP. This process relies on O 2, referred to as oxidative phosphorylation .
Energy yield from Carbohydrate - 1 mole of glycogen generates up to 39 moles of ATP. - If 1 mole of glucose, the net gain is 38 ATP (1 mole of ATP is used for conversion to glucose-6-phosphate before glycolysis).
ii Oxidation of Fat Muscle & liver glycogen stores provide only 1,200 – 2,000 kcal of energy. Fat stored inside the muscle fibers (fat cells) can supply about 70,000 – 75,000 kcal. Triglycerides (major energy sources) stored in fat cells in the skeletal muscle fibers. Triglycerides break down to its basic units to be used for energy: 1 mol of glycerol to 3 moles of free fatty acids/FFA (= process lipolysis with lipases enzymes). FFA can enter blood & be transported throughout the body, entering muscle fibers by diffusion.
ß Oxidation - Upon entering the muscle fibers, FFA are enzymatically activated with energy from ATP, preparing FFA for catabolism (breakdown) within the mitochondria. - This enzymatically catabolism of fat (FFA) by the mitochondria = beta oxidation (ß oxidation). - The carbon chain of FFA is cleaved into separate 2-carbon units of acetic acid. eg. FFA with 16-carbon chain, ß oxidation yields 8 moles of acetic acid. Each acetic acid converted to acetyl CoA.
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Chapter 1. Basic Energy Systems
The Krebs Cycle & the Electron Transport Chain - Fat metabolism follows the same path as CHO metabolism. - Acetyl CoA formed by ß oxidation enters the Krebs cycle, - Krebs cycle generates H + that is transported to the electron transport chain, along with H+ generated during ß oxidation, to undergo oxidative phosphorylation – produce ATP, H 2O & CO2. - The complete combustion of FFA molecule requires more O 2 because FFA contains more carbon (C) than a glucose molecule.
More carbon in FFA, more acetyl CoA is formed from the metabolism of fat, so more enters the Krebs cycle & more electrons are sent to the e. t. chain. (Fat metabolism generate more energy than glucose metabolism) Eg. Palmitic acid, 16-carbon FFA. The combine reaction of oxidation, Krebs cycle, & e. t. chain produce 129 molecules of ATP from 1 mole of palmitic acid. (1 mol of glucose/glycogen = 38/39 moles of ATP) 40% of the energy released by metabolism is captured to form ATP, 60% is given off as heat.
4. Protein Metabolism Proteins (amino acids) are also used as body fuels. Some amino acids can be converted into glucose (gluconeogenesis) Some can be converted into various intermediates of oxidative metabolism (such as pyruvate or acetyl CoA) to enter the oxidative process. Protein’s energy yield is not easy because it contains nitrogen (N). When amino acids are catabolized, some of the released N is used to form new amino acids, but remaining N cannot be oxidized by body. N is converted into urea & then excreted in the urine. This conversion use ATP, so some energy is spent in this process. In laboratory, 1 gram of protein = 5.65 kcal of energy. When metabolized in the body, energy used to convert N to urea, energy yield is only about 5.20 kcal per gram (8% less than the lab. Value). Healthy body utilizes little protein during rest & exercise (< 5-10% of total energy expended). Estimates of energy expenditure generally ignore protein metabolism.
5. The Oxidative Capacity of Muscle Oxidative metabolism has the highest energy yields. Oxidative capacity (QO2) – A measure of the muscle’s maximal capacity to use oxygen. Oxidative capacity depends on: a. Enzyme Activity b. Fiber-type Composition c. Oxygen Needs
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Chapter 1. Basic Energy Systems
Enzyme Activity Many enzymes are required for oxidation. The enzyme activity of the muscle fibers provides an indication of the oxidative potential. The enzymes most frequently measured are SDH (succinate dehydrogenase), CS (citrate synthase) & mitochondria enzymes in the Krebs cycle. Endurance athletes’ muscles have oxidative enzyme activities 2-4 times greater than those untrained men & women.
Fiber-type Composition Muscle’s fiber-type composition determines its oxidative capacity. Slow-twitch (ST) fibers have a greater capacity for aerobic activity than the Fasttwitch (FT) fibers because ST fibers have more mitochondria & higher concentrations of oxidative enzymes. More ST fibers, the greater oxidative capacity in the muscle. FT fibers are better suited for glycolytic energy production. Elite distance runners have reported to process more ST fibers, more mitochondria & higher muscle oxidative enzyme activity than untrained individuals. Endurance training enhances the oxidative capacity of fibers, especially FT fibers. Training that places demands on oxidative phosphorylation stimulates the muscle fibers to develop more mitochondria that are also larger & contain more oxidative enzymes. By increasing the fiber’s enzymes for ß oxidation, this training also enables the muscle to rely more heavily on fat for ATP production. With endurance training, even people with large % of FT fibers can increase their muscles’ aerobic capacities. Endurance-trained FT fiber will not develop the same high-endurance capacity as a similarly trained ST fiber.
Oxygen Needs Oxidative metabolism depends on an adequate supply of O 2. When at rest, body’s need for ATP is small, requiring minimal O 2 delivery. As exercise intensity increases, to meet the energy demands, the rate of oxidative ATP production also increases. In an effort to satisfy the muscle need for O 2, the rate & depth of the respiration increase, improving gas exchange in the lungs, & heart beats faster, pumping more oxygenated blood to the muscle.
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Chapter 1. Basic Energy Systems
C. Causes of Fatigue 1. Depletion of PC or glycogen. The depletion of PC or glycogen will impairs ATP production, thus fatigue is caused by inadequate energy supply. 2. Accumulation of metabolic by-products. Accumulation of hydrogen (H+) decreases muscle pH, causes muscle acidification (acidosis), which impairs the cellular processes that produce energy (inhibits the action of glycolytic enzyme, slowing the rate of glycolysis & ATP production) & muscle contraction. 3. Failure of neural transmission in the muscle fiber. Fatigue may occur at the motor end plate, preventing nerves impulse transmission to the muscle fiber membrane, thus cause the neuromuscular block and leads to neuromuscular fatigue. 4. CNS may cause fatigue. Perceived fatigue usually leads to psychologically exhausted/fatigue and the exhausted feeling can often be psychologically trauma and may inhibit the athlete’s willingness to tolerate further pain or to continue exercise.
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Chapter 1. Basic Energy Systems
SUMMARY 1.
About 60% to 70% of the energy in human body is degraded to heat. The remainder is used for mechanical work & cellular activities.
2.
Humans derive energy from food sources – CHO, fats, & proteins.
3.
The energy humans derive from food is stored in a high-energy compound – ATP.
4.
CHO provides about 4 kcal of energy per gram, compared to about 9 kcal of energy per gram for fat; but CHO is more accessible. Protein can also provide energy.
5.
ATP is generated through 3 energy systems: The ATP-PC system The glycolytic system The oxidative system
6.
7.
In the ATP-PC system, Pi is separated from phosphocreatine through the action of creatine kinase. The P i can then combine with ADP to form ATP. This system is anaerobic, and its main function is to maintain ATP levels. The energy yield is 1 mole of ATP per 1 mole of PC. The glycolytic system involves the process of glycolysis, through which glucose or glycogen is broken down to pyruvic acid via glycolytic enzymes. When conducted without oxygen, the pyruvic acid is converted to lactic acid. 1 mole of glucose yields 2 moles of ATP, but 1 mole of glycogen yields 3 moles of ATP.
8.
The ATP-PC and glycolytic systems are major contributors of energy during the early minutes of high-intensity exercise.
9.
The oxidative system involves breakdown of fuels with aid of oxygen. This system yields more energy than the ATP-PC or glycolytic system.
10.
Oxidation of carbohydrate involves glycolysis, the Krebs cycle, and the electron transport chain. The end result is H 2O, CO2, and 38 or39 ATP molecules per carbohydrate molecule.
11.
Fat oxidation begins with ß oxidation of free fatty acids, then follows the same path as carbohydrate oxidation: the Krebs cycle and the electron transport chain. The energy yield for fat oxidation and it varies with the free fatty acid being oxidized.
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Chapter 1. Basic Energy Systems
12.
Protein oxidation is more complex because protein (amino acids) contains nitrogen, which cannot be oxidized. Protein contributes relatively little to energy production, so its metabolism is often overlooked.
13.
Your muscles’ oxidative capacity depends on their oxidative enzyme levels, their fiber-type composition, and oxygen availability.
14.
Fatigue may result from depletion of PC or glycogen. Either of these situations impairs ATP production.
15.
Lactic acid has often been blamed for fatigue, but it is actually the H+ generated by lactic acid that leads to fatigue. The accumulation of H+ decreases muscle pH, which impair the cellular processes that produce energy & muscle contraction.
16.
Failure of neural transmission may be a cause of some fatigue. Many mechanisms can lead to such failure, & all need further research.
17.
The CNS may also cause fatigue, perhaps as a protective mechanism. Perceived fatigue usually leads to physiological fatigue, and athletes who feel psychologically exhausted can often inhibit their willingness to continue exercise or to tolerate further pain.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Basic Energy System) Name : _____________________________________
Group : _______________________
1. What is bioenergetics? ________________________________________________________________________________ ________________________________________________________________________________
2. Draw the chemical pathway of ATP breakdown during muscular contraction.
3. Name the three (3) methods that cells generate ATP. i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________
4. What is the role of PC in the process of anaerobic metabolism? i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________ iv. _____________________________________________________________________________ v. _____________________________________________________________________________
5. Draw the chemical pathway of PC in maintaining the levels of ATP.
Basic Energy System
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
6. Draw the chemical pathways of the glycolytic system in energy production.
7. Define oxidative system. i.
____________________________________________________________________________
ii.
____________________________________________________________________________
iii. ____________________________________________________________________________ iv. ____________________________________________________________________________
8. Name the three (3) processes that involve the oxidative of carbohydrate in production of ATP. i.
____________________________________________________________________________
ii.
____________________________________________________________________________
iii. ____________________________________________________________________________
9. Name the three (3) processes that involve the oxidative of fat in production of ATP. i.
____________________________________________________________________________
ii.
____________________________________________________________________________
iii. ____________________________________________________________________________ 10. List two (2) roles of oxygen in the process of aerobic metabolism. i.
____________________________________________________________________________
ii.
____________________________________________________________________________
11. List the causes of fatigue. i.
____________________________________________________________________________
ii.
____________________________________________________________________________
iii. ____________________________________________________________________________ iv. ____________________________________________________________________________
Basic Energy System
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
13. Define the term aerobic metabolism. ________________________________________________________________________________ ________________________________________________________________________________
14. Define the term anaerobic metabolism. ________________________________________________________________________________ ________________________________________________________________________________
15. Briefly discuss the function of glycolysis in bioenergetics. i.
_____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________
16. Briefly explain the operation of the Krebs cycle. i.
____________________________________________________________________________ ____________________________________________________________________________
ii.
____________________________________________________________________________
iii. ____________________________________________________________________________ ____________________________________________________________________________
17. What is the role of NAD and FAD in the Krebs cycle? ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
Basic Energy System
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
18. What is electron transport chain? ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
19. Explain briefly the possible causes of fatigue during exercise. i.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
iv. ________________________________________________________________ ________________________________________________________________ ________________________________________________________________ ________________________________________________________________
Basic Energy System
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Chapter 2. Metabolic Adaptations To Training
METABOLIC ADAPTATIONS TO TRAINNING A. Adaptations to Aerobic Training
Aerobic training or cardiorespiratory endurance training, will leads to improved central & peripheral blood flow & enhanced capacity of muscle fibers to generate greater amounts of ATP. The most observable changes with aerobic training are an increased ability to performed prolonged submaximal exercise & an increased in one’s maximal aerobic capacity (VO2max) or aerobic power.
1. Adaptations in Muscle Repeated use of muscle fibers stimulates changes in their structure & function. Endurance training & the changes it produces in Muscle fiber type, Capillary supply, Myoglobin content, Mitochondrial function, & Oxidative enzymes. Muscle fiber type Endurance training stresses ST muscle fibers more than FT fibers. Consequently, ST muscle fibers enlarge. FT b fibers may adopt FT a characteristics with endurance training, but percentages of ST & FT fibers do not appear to change.
Capillary supply Aerobic training increases both the number of capillaries supplying each muscle fiber and the number of capillaries for a given cross-section area of muscle. Therefore, both changes improve/increases blood perfusion in the muscles, thus enhancing the exchange of gases, wastes, & nutrients between the blood and muscle fibers.
Myoglobin content Muscle myoglobin content increases by 75%-80% with endurance training. Myoglobin stores O 2.
Mitochondrial function Endurance training increases both in number and size of the skeletal muscle mitochondria, proving the muscle with much more efficient oxidative metabolism. Ability to use O2 & ATP production via oxidation depends on the number, size & efficiency of mitochondria.
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Chapter 2. Metabolic Adaptations To Training
Study of 27 weeks of training had increased number of mitochondria by 15% and the average size also increased, by about 35%.
Oxidative enzymes Aerobic training also increases the activities of many oxidative enzymes. E.g. succinic dehydrogenase (SDH) & citrate synthase. Increase in enzymatic activities shows the increases in number & size of mitochondria and capacity of ATP production.
2. Adaptations to source of energy
Aerobic training increases the storage of carbohydrate (glycogen) & f ats (triglycerides). Endurance-trained muscle stores more glycogen than untrained muscle. Endurance-trained muscle also stores more fat (triglyceride) than untrained muscle. Enzymatic activities involved in ß-oxidation of fat increases with training, therefore increase FFA release, hence increase the use of fat as energy source, so sparing muscle glycogen, postponing exhaustion. With aerobic training, the body increases the efficiency in using fat as an energy source for exercise, allows muscle & liver glycogen to be used at a slower rate. Improvements in muscles’ aerobic capacity result in a greater capacity to produce energy, with a shift toward greater reliance on fat for ATP production. Endurance-trained muscles’ improved capacity to use fat is caused by the enhance ability to mobilize FFA & the improved capacity to oxidize fat. In activities lasting several hours, these adaptations prevent early glycogen depletion & thus ensure a continued supply of ATP. Thus, endurance performance is enhanced.
B. Training the Aerobic System 1. Volume of Training (Frequency) Depends on optimal amount of work in each training session and over a given period of time. The ideal training regimen should have a caloric expenditure of about 5000-6000 kcal per week (715 – 860 kcal per day). Seems to be little benefit if more than this level.
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Chapter 2. Metabolic Adaptations To Training
2. Intensity of Training Intensity is a critical factor in improving performance. Adaptations are specific to the speed & duration of training bouts, so those who perform at higher intensities must train at higher intensities.
Aerobic interval training Involves repeated bouts of high-intensity performance separated by brief rest periods. Based on ‘work: rest’ ratio. This training, although traditionally considered only anaerobic, generates aerobic benefits because the rest period is so brief that full recovery cannot occur, thus the aerobic system is stressed.
Continuous training Prolonged bout of exercise, therefore athletes find it boring. However, aerobic benefits of both training interval & continuous are about the same.
C. Adaptations to Anaerobic Training
Anaerobic training leads to increase muscular strength and a greater tolerance for acid-base imbalances during highly intense exercise.
1. Adaptations in the ATP-PC System
Activities that emphasize maximal muscle force production (sprinting & weight lifting) rely most on the ATP-PC system for energy.
Maximal efforts lasting less than 6-s demands on the breakdown & resynthesis of ATP-PC.
Costill et al. (1979): Maximal knee extensions for training. - One leg was trained using 6-s maximal work bouts that are repeated 10 times. (ATP-PC system) - The other leg was trained with repeated 30-s maximal bouts. (Glycolytic system) - Both forms of training produced the same muscular strength gains (about 14%) & the same resistance to fatigue. - Activities of muscle enzymes creatine phosphokinase (CPK) & myokinase (MK) increased as a result of the 30-s training, but were unchanged in the 6-s training. - These findings concluded that maximal sprint bouts (6-s) would improve muscular strength, but contribute little to mechanisms responsible for ATP breakdown. 3
Chapter 2. Metabolic Adaptations To Training
2. Adaptations in the Glycolytic System
Anaerobic training (30-s bouts) increased the activities of several glycolytic enzymes. (phosphorylase, phosphofructokinase & lactate dehydrogenase) The activities of these enzymes increase 10% - 25% with repeated 30-s training bouts, but change little with the short bouts (6-s). These enzymes are essential to the anaerobic yield of ATP; such training might enhance glycolytic capacity & allow the muscle to develop greater tension for a longer period of time. This conclusion is not supported by results of the 60-s sprint performance test. The power output & the rate of fatigue (decrease in power production) were affected to the same degree after sprint training with both 6-s & 30-s training bouts. Performance gains with these forms of training result from improvement in strength rather than yield of ATP.
# Anaerobic training increases the ATP-PC & glycolytic enzymes but has no effect on the oxidative enzymes. Conversely, aerobic training leads to increases in oxidative enzymes, but has no effect on the ATP-PC or glycolytic enzymes. # This fact reinforces a recurring theme – physiological alterations resulting from training are highly specific to the type of training pursued.
3. Other Adaptations to Anaerobic Training
In addition to strength gains, the changes are improvements in Efficiency of movement, Aerobic energetics, Buffering capacity. Efficiency of Movement Training at high speeds improves skill & coordination for performing at higher intensities. Training at fast speeds & with heavy loads improves efficiency, economizing use of the muscles’ energy supply. Aerobic Energetics Anaerobic training does not stress only the anaerobic energy systems. Part of the energy needed for sprints that last at least 30-s is derived from oxidative metabolism. Consequently, repeated bouts of sprint-type exercise (30-s maximal bouts) also increase the muscles’ aerobic capacity. 4
Chapter 2. Metabolic Adaptations To Training
This changes is small, this enhancement of the muscles’ oxidative potential will assist the anaerobic energy systems’ efforts to meet muscle energy needs during highly anaerobic effort.
Buffering Capacity Anaerobic training improves the muscles’ capacity to tolerate the acid that accumulates within them during anaerobic glycolysis. Lactic acid accumulation is a major cause of fatigue during sprint-type exercise because the H+ that dissociates from it is to interfere with both metabolism & the contractile process. Buffer (such as bicarbonate & muscle phosphates) combine with hydrogen to reduce the fibers’ acidity; thus they can delay the onset of fatigue during exercise. 8 weeks of anaerobic training has been shown to increased muscle buffering capacity by 12% - 25% (Sharp et al., 1986). Aerobic training has no effect on buffer potential. With the increased buffering capacity, sprint-trained athletes can accumulate more lactate in their blood & muscle during & following an all-out sprint to exhaustion than untrained individuals. This is because the H+ that dissociates from the lactic acid, not the lactate that accumulates, leads to fatigue. With enhanced buffering capacity, muscle can generate energy for longer periods before a critically high concentration of H+ inhibits the contractile process.
D. Monitoring Training Changes
VO2max is considered to be the best means for evaluating training adaptations. But the test is too impractical for widespread use, & it cannot measure muscle adaptations to training. Multiple measurements of blood lactate levels during an exercise bout of increasing intensity have been proposed as a good means for monitoring progress of training, but these tests are also impractical. Various methods for monitoring training adaptations have been tried, but the easiest seems to be comparing single blood lactate values taken at various times during a training period, after a fixed-pace activity is performed. Even with his method, many questions remain unanswered about what actually happens within the body in response to the training stimulus.
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Chapter 2. Metabolic Adaptations To Training
SUMMARY 1.
Aerobic training stresses ST muscle fibers more than FT fibers. Consequently, the ST muscle fibers tend to enlarge with training. Although the percentages of ST & FT fibers do not appear to change, aerobic training may cause FT b fibers to take on more FT a fiber characteristics.
2.
The number of capillaries supplying each muscle fiber increases with training.
3.
Aerobic training increases muscle myoglobin content by about 75% to 80%. Myoglobin stores oxygen.
4.
Aerobic training increases both the number and the size of mitochondria.
5.
Activities of many oxidative enzymes are increased with aerobic training.
6.
All the changes that occur in the muscles, combined with adaptations in the O 2 transport system, lead to enhanced functioning of the oxidative system & improve endurance.
7.
Endurance-trained muscle stores more glycogen than untrained muscle.
8.
Endurance-trained muscle also stores more fat (triglyceride) than untrained muscle.
9.
Enzymatic activities involved in ß-oxidation of fat increases with training, therefore increase FFA release, hence increase the use of fat as energy source, so sparing glycogen.
10.
The ideal training regimen should have a caloric expenditure of about 5000-6000 kcal per week (715 – 860 kcal per day). There seems to be little benefit in the aerobic system beyond this level.
11.
Intensity is also a critical factor in improving performance. Adaptations are specific to the speed & duration of training bouts, so those who perform at higher intensities must train at higher intensities.
12.
Aerobic interval training involves repeated bouts of high-intensity performance separated by brief rest periods. This training, although traditionally considered only anaerobic, generates aerobic benefits because the rest period is so brief that full recovery cannot occur, thus the aerobic system is stressed.
13.
Continuous training is done as one prolonged bout of exercise, but many athletes find it boring. 6
Chapter 2. Metabolic Adaptations To Training
14.
The aerobic benefits from both interval training & continuous high-intensity training seem to be about the same.
15.
Anaerobic training bouts improve anaerobic performance, but the improvement appears to result more from strength gains than from improvements in the functioning of the anaerobic energy system.
16.
Anaerobic training also improves the efficiency of movement, and more efficient movement requires less energy expenditure.
17.
Although sprint-type exercise is anaerobic by nature, part of the energy used during longer sprint bouts comes from oxidation, so muscle aerobic capacity can also be increased with this type of training.
18.
Anaerobic training, allowing the achievement of higher muscle & blood lactate levels, increases muscle-buffering capacity. This allows the H + that dissociates from lactic acid to be neutralized (the bicarbonate & muscle phosphates combine with H+, decreasing the acidity), thus delaying fatigue.
19.
Changes in muscle enzyme activity are highly specific to the type of training.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE 6 (Metabolic Adaptations to Training) Name : _______________________________________
Group : _________ Date : _______________
Answer ALL questions.
1. Define aerobic training . ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ 2. Define anaerobic training. ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
3. Explain briefly the adaptations that occur in the muscle as the result of aerobic training. a. ____________________________________________________________________________ ____________________________________________________________________________
b. ____________________________________________________________________________ ____________________________________________________________________________
c. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________
d. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________
e. ____________________________________________________________________________ ____________________________________________________________________________
f. ____________________________________________________________________________ ____________________________________________________________________________ Metabolic Adaptations to Training
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
4. What effect does aerobic training have on the energy sources used during exercise? a. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________
b. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ 5. Describe the changes in muscle buffering capacity resulting from anaerobic training. How might this improve performance? a. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
Metabolic Adaptations to Training
2
Chapter 3. Muscular Control of Movement
MUSCULAR CONTROL OF MOVEMENT A. The Structure & Function of Skeletal Muscle 1. The Muscle Fiber
A single muscle cell is known as a muscle fiber.
Number of muscle fibers depends on the muscle’s size and function.
A muscle fiber is enclosed by a plasma membrane called the sarcolemma.
The cytoplasm of a muscle fiber is called the sarcoplasm.
Sarcoplasm contains proteins, minerals, glycogen, fats & other organells. It differs from other cytoplasm because it contains high glucose and myoglobin ( O 2- binding compound found in the muscle).
The extensive tubule network found in the sarcoplasm includes T tubules (transverse tubules), which allow communication & transport of substances throughout the muscle fiber.
Sarcoplasmic reticulum (SR) are extensive network that runs longitudinally through the muscle fiber. Its main function is to store calcium (Ca++) ions essential for muscle contraction.
2. The Myofibril
Each muscle fiber contains hundreds to thousands of myofibrils - the contractile elements of skeletal muscles.
Myofibrils are composed of sarcomeres, the smallest functional units of a muscle.
A sarcomere is composed of filaments of 2 protiens (myosin & actin), which are responsible for muscle contraction.
There are striation consisting of the A-band (dark region/zone) and the I-band (light region/zone).
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Chapter 3. Muscular Control of Movement
Myosin A thick filament, folded into a globular head at one end. Composed of 2 protein strands twisted together. Each myosin head protrudes from the filaments to form cross-bridges, which also contains binding sites for ATP & ATPase. Actin Consists of 3 different protein molecules: Actin – contains active sites to which myosin heads can bind. Tropomyosin – during rest lie on top of active sites. Troponin – work together with ca++ ions to maintain relaxation or initiate action of the myofibril. One end of each actin filament is attached to a Z disk.
3. Muscle Fiber Action
Each muscle fiber is innervated by a single motor nerve, ending near the middle of the muscle fiber.
A single motor nerve & all the muscle fibers it supplies/innervates are collectively termed a motor unit.
The synapse between a motor nerve & a muscle fiber is referred to a neuromuscular junction. This is where communication between the nervous & muscular system occurs.
Muscle action is initiated by a motor nerve impulse. The motor nerve releases Ach (acetylcholine), which opens up ion gates in the muscle cell membrane, allowing sodium to enter the muscle cell (depolarization). If the cell is sufficiently depolarized, an action potential is fired and muscle action occurs.
The action potential travels along the sarcolemma, then through the tubule system, & eventually causes stored calcium to be released from sarcoplasmic reticulum.
Calcium binds with troponin , & then troponin lifts the tropomyosin molecules off of the active sites on the actin filament, opening these sites for binding with the myosin head.
Once it binds with the actin active site, the myosin head tilts, pulling the actin filaments so that the two slide across each other. The tilting of myosin head is the power stroke (The sliding filament theory). 2
Chapter 3. Muscular Control of Movement
Energy is required before muscle action can occur. The myosin head binds to ATP, & ATPase found on the head splits ATP into ADP & P i, releasing energy to fuel the contraction.
Muscle action ends when calcium is actively pumped out of the sarcoplasm back into the sarcoplasmic reticulum for storage. This process, leading to relaxation, also requires energy supplied by ATP.
B. Skeletal Muscle and Exercise Endurance & speed during exercise depend on the muscle’s ability to produce energy and force. 1. Slow-Twitch & Fast-Twitch Muscle Fibers
Most skeletal contain both ST and FT fibers.
Muscle Fiber Classification
Slow-Twitch (ST) fibers / Type I / SO (Slow Oxidative) fibers.
Fast-Twitch (FT a) fibers / Type II a / FOG ( Fast Oxidative Glycolytic) fibers.
Fast- Twitch (FT b) fibers / Type II b / FG (Fast Glycolytic) fibers. * (System 3 classifies the fibers based on the fibers’ contraction speed & primary mode of energy production.)
On average most muscles are composed of roughly 50% ST fibers, & 25% FT a. Remaining 25% are mostly FT b.
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Chapter 3. Muscular Control of Movement
Classification of Muscle Fiber Types
System 1 System 2 System 3 Characteristic: Oxidative capacity Glycolytic capacity Contractile speed Fatigue resistance Motor unit strength
ST Type I SO High Low Slow High Low
Fiber classification FTa Type IIa FOG Moderately high High Fast Moderate High
FTb Type IIb FG Low Highest Fast Low High
Structural & Functional Characteristics of Muscle Fiber Types
Characteristic: Aerobic capacity Anaerobic capacity Motor unit force Sarcoplasmic reticulum development Type of myosin ATPase Nerve conduction velocity Motor neuron size Fiber per motor neuron Contractile speed
High Low Low Low
Fiber type FTa Moderate High High High
Low High High High
Slow Slow Small 10-180 50
Fast Fast Large 300-800 110
Fast Fast Large 300-800 110
ST
FTb
Characteristics of ST & FT Fibers
The different fiber types have different ATPases. (ATPase is the enzyme that located on the myosin head, splits the ATP to yield energy that used to bind myosin head to the actin filament)
The ATPase in the FT fibers acts faster, providing energy for muscle action more quickly than the ATPase in ST fibers.
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Chapter 3. Muscular Control of Movement
FT fibers have a more highly developed sarcoplasmic reticulum, enhancing the delivery of calcium needed for muscle action than ST fibers.
Motor neurons supplying FT motor units are larger and supply more fibers than do neurons for ST motor units. Thus FT motor units have more fibers to contract and can produce more force than ST motor units.
The proportions of ST and FT fibers in an individual’s arm and leg muscles usually quite similar.
ST fibers have high aerobic endurance and are well suited to low-intensity endurance activities.
FT fibers are better for anaerobic activity. FT a fibers are well utilized in explosive bouts of exercise. FT b fibers are not well understood, but it is known that they are not easily recruited into activity.
Fiber Type & Exercise
ST Fibers High level of aerobic endurance, therefore ST fibers are very efficient at producing ATP from the oxidation of carbohydrates & fats. Recruited at low-intensity and long duration exercise. Therefore, mostly used during high muscular endurance exercise such as marathon running or channel swimming.
FT Fibers Anaerobic FT a - > force that ST but fatigue easily, therefore recruited mostly during high intensity exercise that last for short period of time e.g. 1-mile run, 400m swim FT b – not easily recruited. Therefore only during very high intensity and explosive events e.g. 100m dash/sprint & 50m sprint swim.
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Chapter 3. Muscular Control of Movement
2. Muscle Fiber Recruitment
Motor units give all-or-none responses. For a unit to be recruited into activity, the motor nerve impulse must meet or exceed the threshold. When this occurs, all muscle fibers in the motor unit act maximally. If the threshold is not met, no fibers in that unit act.
More force is produced by activating more motor units, and thus more muscle fibers.
In low intensity activity, most muscle force is generated by ST fibers. As the resistance increases, FT a fibers are recruited, and if maximal strength is needed the FT b are activated. The same pattern of recruitment is followed during events of long duration.
3. Fiber Type & Athletic Success
World champions in marathon have been reported to posses 93% to 99% ST fibers in their gastrocnemius muscles. World-class sprinters, however, have about 25% ST fibers in this muscle.
4. Use of Muscle
Muscles involved in a movement can be classed as: Agonists (prime movers), muscles primarily responsible for the movement. Antagonists (opponents), muscles that oppose the prime movers. Synergists (assistants), muscles that assist the prime movers.
Flexion of elbow requires shortening of brachialis & biceps brachii muscles (agonists) and relaxation of the triceps brachii (antagonist). The brachioradialis muscle (synergist) assists the brachialis & biceps brachii in their flexion of the joint. Agonists produce most of the force needed for any particular movement. Synergists assist the agonists & sometimes are involved in fine-tuning the direction of movement. The antagonists play a protective role.
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Chapter 3. Muscular Control of Movement
Types of muscle Action
The 3 main types of muscle action are: Concentric action, in which the muscle shortens Static action, in which the muscle acts but the joint angle is unchanged. Eccentric action, in which the muscle lengthens.
Generation of force
Force production can be increased by recruiting more motor units.
Force production can be maximized if the muscle is stretched 20% prior to action. At this point, the amount of energy stored & the number of linked actin-myosin cross-bridges are optimum.
All joints have an optimal angle at which the muscle crossing the joint function to produce maximum force. This angle varies with the relative position of the muscle’s insertion on the bone & the load placed on the muscle.
Speed of action also affects the amount of force produced. For concentric action, maximum force can be achieved with slower contractions. The closer to get to zero velocity (static) the more force can be generated. With eccentric actions, however, faster movement allows more force production.
Generation of force depends on:
Number of motor units activated Types of motor units activated Size of muscle Muscle’s initial length when activated Angle of joint (angle of force application – AFA) Muscle’s speed of action
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Chapter 3. Muscular Control of Movement
SUMMARY 1.
An individual muscle cell is called a muscle fiber.
2.
A muscle fiber is enclosed by a plasma membrane called the sarcolemma.
3. 4.
The cytoplasm of a muscle fiber is called the sarcoplasm. The extensive tubule network found in the sarcoplasm includes T tubules , which allow communication & transport of substances throughout the muscle fiber and sarcoplasmic reticulum , which stores calcium.
5.
Myofibrils are composed of sarcomeres, the smallest functional units of a muscle.
6.
A sarcomere is composed of filaments of 2 protiens (myosin & actin), which are responsible for muscle contraction.
7.
Myosin is a thick filament, folded into a globular head at one end.
8.
An actin filament is composed of actin, tropomyosin, and troponin. One end of each actin filament is attached to a Z disk.
9.
Muscle action is initiated by a motor nerve impulse. The motor nerve releases Ach, which opens up ion gates in the muscle cell membrane, allowing sodium to enter the muscle cell (depolarization). If the cell is sufficiently depolarized, an action potential is fired and muscle action occurs.
10.
The action potential travels along the sarcolemma, then through the tubule system, & eventually causes stored calcium ions to be released from sarcoplasmic reticulum.
11.
Calcium ions bind with troponin, & then troponin lifts the tropomyosin molecules off of the active sites on the actin filament, opening these sites for binding with the myosin heads to bind strongly with them.
12.
Once a strong binding state is established with the actin, the myosin head tilts, pulling the actin filament so that the two slide across each other. The tilting of myosin head is the power stroke.
13.
Energy is required before muscle action can occur. The myosin head binds to ATP, & ATPase found on the head splits ATP into ADP & P i, releasing energy to fuel the contraction.
8
Chapter 3. Muscular Control of Movement
14.
Muscle action ends when calcium is actively pumped out of the sarcoplasm back into the sarcoplasmic reticulum for storage. This process, leading to relaxation, also requires energy supplied by ATP.
15.
Most skeletal muscles contain both ST & FT fibers.
16.
The different fiber types have different ATPases. The ATPase in the FT fibers acts faster, providing energy for muscle action more quickly than the ATPase in ST fibers.
17.
FT fibers have a more highly developed sarcoplasmic reticulum, enhancing the delivery of calcium needed for muscle action than ST fibers.
18.
Motor neurons supplying FT motor units are larger and supply more fibers than do neurons for ST motor units. Thus FT motor units have more fibers to contract and can produce more force than ST motor units.
19.
The proportions of ST and FT fibers in an individual’s arm and leg muscles usually quite similar.
20.
ST fibers have high aerobic endurance and are well suited to low-intensity endurance activities.
21.
FT fibers are better for anaerobic activity. FT a fibers are well utilized in explosive bouts of exercise. FT b fibers are not well understood, but it is known that they are not easily recruited into activity.
22.
Muscles involved in a movement can be classed as agonists (prime mover), antagonists (opponents), or synergists (assistants).
23.
The 3 main types of muscle action are concentric, in which the muscle shortens; static, in which the muscle acts but the joint angle is unchanged; & eccentric, in which the muscle lengthens.
24.
Recruiting more motor units can increase force production.
25.
Force production can be maximized if the muscle is stretched 20% prior to action. At this point, the amount of energy stored & the number of linked actin-myosin cross-bridges are optimum.
26.
All joints have an optimal angle at which the muscle crossing the joint function to produce maximum force. This angle varies with the relative position of the muscle’s insertion on the bone & the load placed on the muscle. 9
Chapter 3. Muscular Control of Movement
27.
Speed of action also affects the amount of force produced. For concentric action, maximum force can be achieved with slower contractions. The closer to get to zero velocity (static) the more force can be generated. With eccentric actions, however, faster movement allows more force production.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Muscular Control of Movement) Name : _____________________________________________
Group : _____________________
1. List the principal functions of skeletal muscles. i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________
2. Outline the steps leading to the muscle contraction. i.
_____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ iv. _____________________________________________________________________________ _____________________________________________________________________________ 3. List five (5) characteristics of a slow-twitch muscle fiber. i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________ iv. _____________________________________________________________________________ v.
_____________________________________________________________________________
4. Why slow-twitch muscle fibers better suited to perform low-intensity and long duration events such as long distance swimming and cross-country running? i.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
Muscular Control of Movement
1
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
5. List five (5) characteristics of a fast-twitch muscle fiber. i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________ iv. _____________________________________________________________________________ v.
_____________________________________________________________________________
6. Why fast-twitch muscle fibers better suited to perform short and explosive events such as the 100-m dash and 50-m sprint swim? i.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 7. List two (2) functional differences between the fast twitch and the slow twitch fibers. i.
_____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________
8. Describe the roles of the following classes of muscles. a) Agonists. _____________________________________________________________________________ b) Synergists. _____________________________________________________________________________ b) Antagonists. _____________________________________________________________________________
Muscular Control of Movement
2
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
9. Distinguish the following types of muscle contraction. a) Isometric. _____________________________________________________________________________ b) Concentric. _____________________________________________________________________________ c) Eccentric. _____________________________________________________________________________ 10. Describe the function of Golgi tendon organs in monitoring muscle tension. i.
____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________
ii.
____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________
11. Discuss the role of the muscle spindles in controlling muscle action. i.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
12. Discuss the primary factors thought to be responsible for generating force during muscular contractions. i.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
Muscular Control of Movement
3
Chapter 4. Neurological Control of Movement
NEUROLOGICAL CONTROL OF MOVEMENT A. The structure & Function of the Nervous System 1. The Neuron
Individual nerve fibers or nerve cells are called neurons Neuron is composed of three regions:1. The cell body or soma
2. The dendrites
3. The axon
Most neurons contain many dendrites (neuron’s receivers) – receive impulses then carry toward the cell body. Most neurons have only one axon (neuron’s transmitter) – conducts impulses away from the cell body. Axon splits near its end into branches called axon terminals (terminal fibrils). The tips of the axon terminals are called the synaptic knobs containing vesicle (sacs) filled with chemicals, known as neurotransmitter – used for communication between neuron and another cell.
2. The Nerve Impulse
Nerve impulse is an electrical charge – is the signal that passes from one neuron to the next and finally to an end organ.
Resting Membrane Potential (RMP) The cell membrane of a neuron at rest has a negative electrical potential of about -70 mV. (mV=milivolt) That means, the electrical charges found inside and outside the cell were differ by 70 mV, and the inside was negative relative to the outside. This potential difference (-70 mV) is called the resting membrane potential or RMP. It is caused by a separation of charges across the membrane. When the charges across the membrane differ, the membrane is said to be polarized. The neuron (axon) has a high concentration of potassium ions (K+) on the inside and a high concentration of sodium ions (Na+) on the outside because the sodiumpotassium pump actively moves sodium out of the cell and potassium into the cell. The “Na-K Pump” moves three (3) Na+ ions out of the cell for each two (2) K+ ions it brings into the cell. The cell membrane is much more permeable to K+ ions, so some of the K+ ions may also move to the outside. The Na+ cannot move in this manner. Therefore, the inside of the cell is more negative than outside, creating the potential difference across the membrane.
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Chapter 4. Neurological Control of Movement
Maintenance of a constant RMP of -70mV is primarily a function of the “Na-K pump”.
Depolarization & Hyperpolarization If the inside of the cell becomes less negative relative to the outside, the potential difference across the membrane will decrease. The membrane will be less polarized. When this happen, the membrane is said to be depolarized. Thus, depolarization happens any time when the charge difference is less than the RMP of -70 mV, moving closer to zero. This is result from a change in the membrane’s Na+ permeability. The opposite can also occur. If the charge difference across the membrane increases, moving from the RMP to an even more negative number, then the membrane becomes more polarized. This is known as hyperpolarization.
Changes in the membrane potential are signals used to receive, transmit and integrate information within & between cells. These signals are of two (2) types – graded potentials & action potentials. Both are electrical currents created by the movement of ions Graded Potentials These are localized changes in the membrane potential – can be either depolarizations or hyperpolarizations. These are triggered by local changes in the neuron’s local environment. Action Potentials An action potential is a rapid and substantial depolarization of the neuron’s membrane. Typically, membrane potential changes from the RMP -70 mV to a value of +30 mV, and then rapidly returns to its resting value. All action potentials begin as graded potentials. Action potentials are generated when enough stimulation occurs to cause a depolarization (at least 15 – 20 mV). That means if the membrane depolarizes from the RMP of -70 mV to a value of -50 mV to -55 mV, the cell will experience an action potential. The minimum depolarization required to produce an action potential is called the “threshold”. Any depolarization less than the threshold value of 15 – 20 mV will not result in an action potential. This is the “All-or-None Principle”.
Sequence of Events in an Action Potential 1. Increased sodium (Na+) permeability through opening of sodium gates, 2. Decreased sodium (Na+) permeability as sodium gates close, & 3. Opening of potassium gates and repolarization. 2
Chapter 4. Neurological Control of Movement
Propagation of the Action Potential The myelin sheath – a fatty sheath that insulates the cell membrane of axons. The gaps between sheaths which are not insulated are called nodes of Ranvier. The action potential appears to jump from one node to the next as it t raverses a myelinated fibers. This is referred to as “saltatory conduction”, a much faster rate (5-50 times faster) of conduction than in unmyelinated fibers of the same size.
Diameter of the neuron – the velocity of nerve impulses transmission is also determined by the neuron’s size. The larger diameter neurons conduct nerve impulses faster because larger neurons present less resistance to local current flow.
3. The Synapse
A synapse is the site of impulse transmission from one neuron to another. A synapse between two neurons includes: 1. Axon terminals of the presynaptic neuron (neuron carrying impul se), 2. Postsynaptic receptors on the dendrite or cell body of the next neuron, & 3. Space (synaptic cleft) between the two neurons. Impulses are transmitted in 1 direction only. The presynaptic terminals of the axon contain a large number of sac-like structure, called synaptic vesicles. Synaptic vesicles contain neurotransmitters chemicals. When the impulse reaches the presynaptic terminals, the synaptic vesicles respond by dumping their chemicals into the synaptic cleft. These neurotransmitters then diffuse across the synaptic cleft to the postsynaptic neuron’s receptors. Once the postsynaptic receptors bind with the neurotransmitters, the impulse has been transmitted successfully to the next neuron and can be transmitted onward.
4. The Neuromuscular Junction
The neuromuscular junction is where motor neuron communicates with the muscle fiber. It involves:1. Presynaptic axon terminals (motor endplates), 2. The synaptic cleft, & 3. Receptors on the sarcolemma of the muscle fiber. The neuromuscular junction functions much like a neural synapse. 3
Chapter 4. Neurological Control of Movement
5. Neurotransmitters
There are more than 40 identified neurotransmitters. Acetylcholine and Norepinephrine are the two major neurotransmitters involved in regulating our physiology responses to exercise. A nerve impulse causes the release of neurotransmitters from presynaptic axon terminals into the synaptic cleft which then diffuse across the cleft and bound to postsynaptic receptors. Once the neurotransmitter binds to the postsynaptic receptors, the nerve impulse has been successfully transmitted. Neurotransmitters are then either destroyed by enzymes or return into presynaptic neuron for reuse when the next impulse arrives. Neurotransmitter binding at the postsynaptic receptors can cause either depolarization ( excitation) or hyperpolarization (inhibition).
6. The Postsynaptic Response
The incoming impulse may be excitatory or inhibitory. An excitatory impulse causes depolarization, known as an Excitatory Postsynaptic Potential (ESSP). An inhibitory impulse causes hyperpolarization, known as an Inhibitory Postsynaptic Potential (IPSP). A single presynaptic terminal is not sufficient to generate enough depolarization to fire an action potential. Multiple signals are needed which may come from numerous axon terminals that release neurotransmitters repeatedly and rapidly. Summation is the process of accumulation of the incoming signals. The summation must reach the threshold for an action potential to be released.
SUMMARY 1.
Nerve impulses typically pass from the dendrites to the cell body and from the cell body along the length of the axon to its terminal fibrils.
2.
A neuron’s RMP of -70 mV results from the separation of sodium & potassium ions maintained primarily by the sodium-potassium pump, coupled with low sodium permeability & high potassium permeability of the neuron membrane
3.
Any change making the membrane potential more positive is a depolarization. Any change making this potential more negative is a hyperpolarization. These changes occur when ion gates in the membrane open, permitting ions to move from one side to the other. 4
Chapter 4. Neurological Control of Movement
4.
If the membrane is depolarized by 15 -10 mV, threshold is reached & an action potential results. Action potentials are not generated if threshold is not met.
5.
The chain of events for action potential are: increased sodium permeability through opening of sodium gates, decreased sodium permeability as sodium gates close, and opening of potassium gates and repolarization.
6.
In myelinated neurons, the impulse travels through the axon by jumping between nodes of Ranvier (gaps between the cells that form the myelin sheath). This process, salutatory conduction, is 5 to 50 times faster than in unmylinated fibers of the same size.
7.
Impulses also travel faster in neurons of larger diameters.
8.
Neurons communicate with each other across synapses.
9.
A synapse involves: the axon terminals of the presynaptic neuron, the postsynaptic receptors on the dendrite or cell body of the next neuron, & the space (synaptic cleft) between the two neurons.
10.
A nerve impulse causes chemicals called neurotransmitters to be released from the presynaptic axon terminals into the synaptic cleft.
11.
Neurotransmitters diffuse across the cleft and are bound to the postsynaptic receptors.
12.
Once neurotransmitters are bound, the impulse has been successfully transmitted and the neurotransmitter is then either destroyed by enzymes or actively returned to the presynaptic neuron for future use.
13.
Neurotransmitter binding at the postsynaptic receptors opens the ion gates in that membrane and can cause depolarization (excitation) or hyperpolarization (inhibition), depending on the specific neurotransmitter and the receptors to which it binds.
14.
Neurons communicate with muscle cells at the neuromuscular junctions.
15.
The neurotransmitters most important to regulation of exercise are acetycholine and norepinephrine.
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Chapter 4. Neurological Control of Movement
B. The Central Nervous System (CNS)
The functional organization of the nervous system
Central Nervous System (CNS) Brain Spinal Cord
Peripheral Nervous System (PNS) Cranial Nerves Spinal Nerves
Sensory Division (Afferent)
Motor Division (Efferent)
Autonomic Nervous System (Involuntary)
Somatic Nervous System (Voluntary)
CNS CNS is composed of the brain and the spinal cord. CNS houses more than 100 billion neurons.
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Chapter 4. Neurological Control of Movement
1. The Brain
Subdivide into 4 regions:- cerebrum, diencephalon, cerebellum & brain stem.
Cerebrum Composed of the right & left cerebral hemispheres. These are connected to each other by fiber bundles (tracts) referred to as the corpus callosum, allowing the 2 hemispheres to communicate with each other. The cerebral cortex (gray matter) forms the outer portion has been referred to as the site of the mind & intellect. Cerebral cortex is the conscious brain. It allows us to think, to be aware of sensory stimuli, & to voluntary control of movements.
Cerebrum consists of 5 lobes: - 4 outer lobes & the central insula (not discuss) 1. Frontal lobe – general intellect & motor control, 2. Temporal lobe – auditory input & its interpretation, 3. Parietal lobe – general sensory & its interpretation, 4. Occipital lobe - visual input & its interpretation.
Diencephalon Composed of the thalamus & the hypothalamus. Thalamus is an important sensory integration center. All sensory input (except smell) enters the thalamus & is relayed to the appropriate area of the cortex. Thalamus regulates what sensory input reaches the conscious brain, & thus is very important for motor control.
Hypothalamus, directly below the thalamus, is responsible for maintaining homeostasis by regulating almost all processes that affect the body’s internal environment. Hypothalamus regulate:1. the autonomic nervous system (BP, HR, respiration, digestion, etc.), 2. body temperature, 3. fluid balance, 4. neuroendocrine control, 5. emotions, 6. thirst, 7. food intake, & 8. sleep-wake cycle.
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Chapter 4. Neurological Control of Movement
Cerebellum Located behind the brain stem. Connected to numerous parts of the brain & has a crucial role in controlling movement.
Brain stem Composed of the midbrain, the pons, & the medulla oblongata. Is the stalk of the brain, connecting the brain & the spinal cord. All sensory & motor nerves pass through the brain stem as they relay information between the brain & the spinal cord. Also contains the major autonomic regulatory centers that exert control over the respiratory & cardiovascular systems.
A specialized collection of neurons running the entire length of the brain stem, known as the reticular formation, are influenced by & have an influence on nearly all areas of the CNS. These neurons help:1. coordinate skeletal muscle function, 2. maintain muscle tone, 3. control cardiovascular & respiratory functions, & 4. determine our state of consciousness (both arousal & sleep).
The brain has a pain control system, called an analgesia system. The enkephalins & ß-enorphin are important opiate substances that act on the opiate receptors in the analgesia system to help reduce pain. Exercise of long duration has been postulated to increase the natural levels of these opiate substances.
2. The Spinal Cord
Composed of tracts of nerves fibers that allow two-way conduction of nerves impulses. The sensory (afferent) fibers carry neural signals from sensory receptors, such those in the muscle & joints, to the upper levels of the CNS. Motor (efferent) fibers from the brain & upper spinal cord travel down to end organs (muscle, glands).
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Chapter 4. Neurological Control of Movement
C. The Peripheral Nervous System (PNS)
PNS contains 43 pairs of nerves: 12 pairs of cranial nerves that connect with the brain, & 31 pairs of spinal nerves that connect with the spinal cord. Functionally, the PNS has 2 major divisions: sensory division & motor division.
1. The Sensory Division
The sensory division of PNS carries sensory information from sensory receptors toward the CNS. Sensory (afferent) neurons originate in such areas: blood & lymph vessels, internal organs, special sense organs (taste, touch, smell, hearing, vision), the skin, and muscles & tendons. Sensory neurons in the PNS end either in the spinal cord or in the brain. The sensory division receives information from 5 primary types of receptors:o Mechanoreceptors that respond to mechanical forces such as pressure, touch, vibration, or stretch. o Thermoreceprtors that respond to changes in temperature. o Nociceptors that respond to painful stimuli. o Photoreceptors that respond to electromagnetic radiation (light) to allow vision. o Chemoreceptors that respond to chemical stimuli, such as from foods, odors, or changes in blood concentrations of substances such as O 2, CO2, glucose, electrolytes, & so on. The nerve endings of mechanoreceptors, thermoreceprtors & nociceptors are important for the prevention of injury during athletic performance. Special muscle & joint nerve endings are of many types & functions, and each type is sensitive to a specific stimulus: Joint kinesthetic receptors located in the joint capsules are sensitive to joint o angles & rates of change in these angles. Thus, they sense the position & any movement of the joints. Muscles spindles sense how much a muscle is stretched. o Golgi tendon organs detect the tension applied by a muscle to its tendon, o providing information about the strength of muscle contraction.
2. The Motor Division
The motor division of PNS carries motor impulses out from the CNS to various part of the body (target areas – muscles) through the motor (efferent) neurons. 9
Chapter 4. Neurological Control of Movement
The motor division is divided into 2 components: the autonomic nervous system (involuntary) & the somatic nervous system (voluntary).
3. The Autonomic Nervous System (ANS)
The ANS controls the body’s involuntary internal functions. Some of these functions that are important to sport & activity include heart rate, blood pressure, blood distribution, & respiration. ANS has 2 major divisions: the sympathetic NS & the parasympathetic NS. The effects of the two systems are often antagonistic, but both systems are always functioning together. The Sympathetic Nervous System
Sympathetic NS is the “fight-or-flight system” : It prepares the body to face a crisis (acute stress or physical activity). When we are excited, our sympathetic NS produces a massive discharge throughout the body, preparing us for action. The effects of sympathetic stimulation are important to the athlete: Heart rate & strength of cardiac contraction increase (Heart muscle). Coronary vessels dilate, increasing the blood supply to the heart muscle to meet its increased demands (Coronary blood vessels). Peripheral vasodilation allows more blood to enter the active skeletal muscles (Blood vessels). Vasoconstriction in most other tissues diverts blood away from them & to the active muscles (Blood vessels). Blood pressure increases, allow better perfusion of the muscles & improving the return of venous blood to the heart (Blood vessels). Bronchodilation improves gas exchange (Lungs). Metabolic rate increases, reflecting the body’s effort to meet the increased demands of physical activity (Cellular metabolism). Mental activity increases, allowing better perception of sensory stimuli & more concentration on performance (Brain). Glucose is released from the liver into the blood as an energy source (Liver). Stimulates lipolysis (Adipose tissue). Increases sweating (Sweat glands). Stimulates secretion of epinephrine & norepinephrine (Adrenal glands). Functions not directly needed are slowed (e.g., renal function, digestion), conserving energy so that it can be used for action. Causes vasoconstriction; decreases urine formation (Kidney). Decreases activity of glands & muscles; constricts sphincters (Digestive System). 10
Chapter 4. Neurological Control of Movement
The Parasympathetic Nervous System
Parasympathetic NS is the body’s “housekeeping system” : It has a major role in carrying out such processes as digestion, urination, glandular secretion, & conservation of energy. This system is more active when we are calm & at rest. Its effects tend to oppose those of the sympathetic system. The parasympathetic division causes: Decreased HR & the force of the heart muscle contraction (Heart muscle), constriction of coronary vessels (Coronary blood vessels), bronchoconstriction (Lungs), & Increases peristalsis & glandular secretion; relaxes sphincters (Digestive System).
D. The Sensory-Motor Integration
Sensory-motor integration is the process by which the periphery NS relays sensory input to the CNS & the CNS interprets this information then sends out the appropriate motor signal to elicit the desired motor response.
1. Sensory Input Sensory input can terminate in sensory areas of the brain stem, the cerebellum, the thalamus, or the cerebral cortex. An area in which the sensory impulses terminate is referred to as an integration center. This is where the sensory input is interpreted & linked to the motor system.
2. Motor Control Skeletal muscles are controlled by impulses conducted by motor (efferent) neurons that originate from any of 3 levels: the spinal cord, the lower regions of the brain, & the motor area of the cerebral cortex. The degree of movement complexity increases from simple reflex control to complicated movements requiring thought processes. Motor responses for more complex movement patterns typically originate in the motor cortex of the brain.
3. Reflex Activity A motor reflex is a preprogrammed response; any time the sensory nerves transmit certain impulses, the body responds instantly & identically Reflexes are the simplest form of motor control. They are preprogrammed responses, therefore not the conscious response.
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Chapter 4. Neurological Control of Movement
All neural activity occurs extremely rapidly, but the reflex is the fastest mode of response because the body does not need time to make a conscious decision. Two reflexes that help control muscle function: 1. Muscle spindles trigger reflexive muscle action when the muscle spindle is stretched. 2. Golgi tendon organs trigger a reflex that inhibits contraction muscles if the tendon fibers are overstretched. Muscle Spindles MS are sensory receptors located in the muscle that senses how much the muscle is stretched. A muscle spindle comprises specialized muscle fibers called intrafusal fibers (inside the spindle) & these fibers are controlled by specialized motor neurons, called gamma motor neurons. Golgi Tendon Organs GTO are encapsulated sensory receptors located in muscle tendon fibers that monitor tension. GTO are sensitive to tension in the muscle tendon & operate like a strain gauge, a device that senses changes in tension. GTO are inhibitory in nature, performing a protective function by reducing the potential for injury.
4. The Higher Brain Centers
Most movements used in sport activities involve control & coordination through the higher brain centers specially: The primary motoe cortex, The basal ganglia, & The cerebellum. The Primary Motor Cortex PMC which located in the frontal lobe. Neurons here, known as pyramidal cells, allow us consciously control movement of the skeletal muscles. PMC is responsible for the control of fine discrete muscle movements. The Basal Ganglia Basal ganglia (nuclei) located in the cerebral white matter, deep to the cortex. BG are known to be important in the initiation of movements of a sustained & repetitive nature (such as arm swinging while walking), & thus they control complex semivoluntary movements such as walking & running. 12
Chapter 4. Neurological Control of Movement
BG also involved in maintaining posture & muscle tone. The Cerebellum Cerebellum is crucial to control of all rapid & complex muscular activities. It helps coordinate the timing of motor activities & the rapid progression from one movement to the next by monitoring & making corrective adjustments in the motor activities that are elicited by other parts of the brain. It assists the functions of both the primary motor cortex & the basal ganglia. It facilitates movement patterns by smoothing out the movement, which would otherwise be jerky & uncontrolled.
5. Engrams
Specific learned motor patterns appear to be stored in the brain, to be replayed on request. These memorized motor patterns are referred to as motor programs, or engrams.
E. The Motor Response 1. The Motor Unit
The motor nerve (neuron) and the group of muscle fibers it innervates form a single motor unit. Each muscle fiber is innervated by only one motor neuron, but each motor neuron can innervates up to several thousand muscle fibers. All muscle fibers within a single specific motor unit are homogeneous with respect to fiber type. Thus we do not find a motor unit has both FT & ST fibers.
2. The Orderly Recruitment of Muscle Fibers & the Size Principle
Motor units are generally activated on the basis of a fixed order of recruitment. This is known as the principle of orderly recruitment. Motor unit are recruited in an orderly manner, therefore specific ones are called on each time a specific activity is performed. The size principle explained that the order of recruitment of motor units is directly related to their motor neuron size. Motor units with smaller neurons (ST fibers) will be recruited first before larger neurons (FT fibers).
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Chapter 4. Neurological Control of Movement
SUMMARY 1.
The central nervous system is composed of the brain and the spinal cord.
2.
The 4 major divisions of the brain are the cerebrum, the diencephalon, the cerebellum & the brain stem.
3.
The cerebral cortex is the conscious brain.
4.
The diencephalon includes the thalamus, which reveices all sensory input entering the brain & the hypothalamus, which is a major control center for homeostasis.
5.
The cerebellum, which is connected to numerous parts of the brain, is critical for coordinating movement.
6.
The brain stem is composed of the midbrain, the pons, & the medulla oblongata.
7.
The spinal cord carries both sensory & motor fibers between the brain and the periphery.
8.
The PNS contains 43 pairs of nerves: 12 pairs of cranial nerves & 31 pairs of spinal nerves.
9.
The PNS subdivided into sensory division & motor division. The motor division also includes the autonomic nervous system.
10.
The sensory division carries information from sensory receptors to the CNS so that the CNS is constantly aware of the current status & environment.
11.
The motor division carries motor impulses out from the CNS to the muscles.
12.
The autonomic nervous system includes the sympathetic NS, which is the fight-orflight system, & the parasympathetic NS, which is the housekeeping system. Though these systems often oppose each other, they always function together.
13.
Sensory-motor integration is the process by which the PNS relays sensory input to the CNS and the CNS interprets this information then sends out the appropriate motor signal to elicit the desired motor response.
14.
Sensory input can terminate at various levels of the CNS. Not all information reaches the brain.
14
Chapter 4. Neurological Control of Movement
15.
Reflexes are the simplest form of motor control. They are not the conscious response. For a given sensory stimulus, the motor response is always identical and instantaneous.
16.
The level of nervous system control varies in response to sensory input according to the complexity of movement necessary. Simple reflexes are handled by the spinal cord, whereas complex reactions require involvement of the brain.
17.
Muscle spindles trigger reflexive muscle action when the muscle spindle is stretched.
18.
Golgi tendon organs trigger a reflex that inhibits contraction if the tendon fibers are overstretched.
19.
The primary motor cortex, located in the frontal lobe, is the center of conscious motor control.
20.
The basal ganglia, in the cerebral white matter, help initiate some movements (sustained & repetitive ones) & help control posture & muscle tone.
21.
The cerebellum is involved in all rapid & complex movement processes & assists the primary motor cortex & the basal ganglia in coordinating the response. It is an integration center that decides how to best execute the desired movement, given the body’s current position & the muscle’s current status.
22.
Though not well understood, engrams are memorized motor patterns, stored in both the sensory & motor areas of the brain, that are called upon as needed.
23.
Each muscle fiber is innervated by only one motor neuron, but each neuron can innervates up to several thousand muscle fibers.
24.
All muscle fibers within a single motor unit are of the same fiber typ e.
25.
Motor units are recruited in an orderly manner, so that specific ones are called on each time a specific activity is performed.
26.
Motor units with smaller neurons (ST fibers) are called on before those with larger neurons (FT fibers).
15
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Neurological Control of Movement) Name : _______________________________________
Group : _________
Date: ______________
1. Nerve impulse is an electrical signals that ______________________________________________ _______________________________________________. 2. An action potential is _______________________________________________________________. 3. A synapse is _____________________________________________________________________. 4. Neuromuscular junction is ___________________________________________________________. 5. The neurotransmitters involved in regulation of exercise are _____________________________ and ______________________________. 6. The CNS is composed of ____________________ and ___________________________________. 7. ______________________ is the conscious brain. 8. ______________________ is the sensory integration center and _______________________ is a major control center for homeostasis. 9. ______________________ has a critical role in controlling and coordinating movement. 10. The spinal cord composed of ________________________________________________________. 11. PNS contains of _______ pairs of cranial nerves and _______ pairs of spinal nerves. 12. The sensory division carries _________________________________________________________. 13. The motor division carries __________________________________________________________. 14. ____________________ division is the fight-or-flight system, which is more active when we are involved in physical activity. 15. _____________________ division is the body’s housekeeping system, which is more active when we are at rest. 16. _____________________ division causes the decreased of heart rate and the force of the heart muscle contraction. 17. _____________________ division causes peripheral vasodilation and bronchodilation. 18. Reflexes are _____________________________________________________________________. 19. ________________________ are sensory receptors located in the muscle that senses how much the muscle is stretched. 20. ________________________ are encapsulated sensory receptors located in muscle tendon fibers that monitor tension.
Neurological Control of Movement
1
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
21. Describe briefly the significance of the sympathetic stimulation to perform physical activity. i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________ iv. _____________________________________________________________________________ _____________________________________________________________________________
22. What is the significance of the parasympathetic division during rest? i.
_____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________
iii. _____________________________________________________________________________ _____________________________________________________________________________ iv. _____________________________________________________________________________ _____________________________________________________________________________
23. Identity the major functions of the nervous system. i.
_____________________________________________________________________________
ii.
_____________________________________________________________________________
iii. _____________________________________________________________________________ iv. _____________________________________________________________________________
24. Discuss the general organization of the nervous system. i.
_____________________________________________________________________________ _____________________________________________________________________________
ii.
_____________________________________________________________________________ _____________________________________________________________________________
Neurological Control of Movement
2
Chapter 5. Cardiovascular Control During Exercise
CARDIOVASCULAR CONTROL DURING EXERCISE A. Structure & Function the Cardiovascular System (CVS) Major functions: 1. 2. 3. 4. 5.
– CV S delivers O2 & nutrients to cells. – CV S removes CO2 & metabolic waste products from every cell. - CVS transports hormones from endocrine glands to their target receptors. Maintenance - CVS maintains body temperature & the blood’s buffering capabilities help control the body’s pH. Prevention – CV S maintains appropriate fluid levels to prevent dehydration & helps to prevent infection by invading organisms. Delivery Removal Transport
1. The Heart (A Pump)
2 atria acting as receiving chambers. 2 ventricles acting as sending units (discharging chambers). As a pump that circulates blood through the entire vascular system.
Blood Flow Through the Heart
Blood delivering O2 & nutrients & picking up waste products, returns through the great veins – superior vena cava & inferior vena cava to the right atrium (RA). The (RA) chamber receives all the body’s deoxygenated blood. From the (RA), blood passes through the tricuspid valve into the right ventricle (RV). The (RV) chamber pumps the blood through the pulmonary semilunar valve into pulmonary artery, which carries the blood to the lungs. Thus, the right side of the heart is known as the pulmonary side, sending the blood that has circulated throughout the body into the lungs for reoxygenation. After receiving a fresh supply of O 2, the blood exits the lungs through the pulmonary veins, which carry it back to the heart & into the left atrium (LA). The (LA) chamber receives all the freshly oxygenated blood. From (LA), blood passes through the bicuspid (mitral) valve into the left ventricle (LV). Blood leaves the left ventricle by passing through the aortic semilunar valve into the aorta, which sends it out to all body parts & systems. The left side of the heart is known as the systemic side – receives the oxygenated blood from the lungs then sends it out to supply all body tissues. 1
Chapter 5. Cardiovascular Control During Exercise
The Myocardium (Cardiac muscle)
Cardiac muscle is collectively called the myocardium. Left ventricle (LV) is the most powerful of the 4 chambers – pump oxygenated blood out through the entire systemic route. When the body is standing or sitting, the (LV) must contract with enough force to overcome the effect of gravity, which tends to pool blood in the lower extremities. (LV) has the greater size ( hypertrophy) of its muscular wall – this hypertrophy is the result of demands placed on it. With more vigorous exercise – intense aerobic activity, which working muscles’ need for blood, increases the demands on the (LV) are high. Over time it responds by increasing it size (hypertrophy). * The atria receive blood into the heart; the ventricles eject blood from the heart. Left ventricle must produce more power than other chambers because has to pump blood to all parts of the body; therefore its myocardium is thicker, due to hypertrophy.
The Cardiac Conduction System (Intrinsic Control of The Heart)
Cardiac muscle has the unique ability to generate its own electrical signal, called autoconduction, which allows it contract rhythmically without neural stimulation. The intrinsic heart rate (HR) averages 70 -80- beats per minute (contractions). HR can drop below this rate in endurance-trained people.
Four (4) components of the cardiac conduction system: 1. Sinoatral (SA) node 2. Atrioventricular (AV) node 3. Atrioventricular (AV) bundle (Bundle of His) 4. Purkinje fibers
The impulse for heart contraction is initiated in the sinoatrial (SA) node , a group of specialized cardiac muscle fibers located in the posterior wall of the right atrium. This tissue (SA node) generates the impulse at about 60 -80 beats per minutes. SA node is known as the heart’s pacemaker, & the beating rate is establishes is called the sinus rhythm. The electrical impulse generated by the SA node spreads through both atria & reaches the atrioventricular (AV) node , located in the right atrial wall near the center of the heart. As the impulse spreads through the atria, both atria are signaled to contract immediately & simultaneously. AV node conducts the impulse from the atria into the ventricles. 2
Chapter 5. Cardiovascular Control During Exercise
The impulse is delayed by about 0.13s as it passes through the AV node, then it enters the AV bundle. The delay allows the atria to fully contract before the ventricle, maximizing ventricular filling. AV bundle travels along the ventricular septum & then sends right & left bundle branches into 2 ventricles. These branches send the impulse toward the apex of the heart, then outward. These terminal branches of the AV bundles are the Purkinje fibers (Pf). Pf transmit the impulse through the ventricles 6 times faster than the rest of the cardiac conduction system. * Cardiac tissue is capable of autoconduction. Cardiac conduction system has own conduction system initiates own pulse without neural control. * SA node is the heart’s pacemaker, establishing the pulse and coordinate activity throughout the heart.
Extrinsic Control of Heart Activity
The heart initiates its own electrical impulse (intrinsic control), their timing & effects can be altered through 3 extrinsic system: 1. The parasympathethic nervous system (Autonomic nervous system)
Acts on the heart through the vagus nerve (cranial nerve X). Parasympathetic stimulation = vagal tone Vagus nerves has a depressant effect, it slows impulse conduction & thus decrease the HR. Maximal vagal stimulation can lower the HR to 20 -30 beats per minute. Vagus nerve also decreases the force of cardiac contraction.
2. The sympathetic nervous system (Autonomic nervous system)
Sympathetic stimulation increases the impulse conduction speed thus increase the HR Maximal sympathetic stimulation will allows the HR to soar up to 250 beats per minute. Sympathetic input also increases the contraction force . Predominates during times of physical or emotional stress. After the stress subsides the parasympathetic system again predominates. 3
Chapter 5. Cardiovascular Control During Exercise
3.
The endocrine system (hormones)
Hormones released by the adrenal medulla: norepinephrine & epinephrine (catecholamines). Stimulates the heart & increase its HR. Released of these hormone triggered the sympathetic stimulation during stress & their actions prolong the sympathetic response.
Normal resting HR = 60 – 85 beats per minute (bpm). With extended periods of endurance training (months to years), the resting HR can decrease to 35 beats per minute or less. A world-class long-distance runner = 28 beats per minute. Lower RHR are postulated to result from increased parasympathetic stimulation (vagal tone), with a reduced sympathetic activity probably playing a lesser role. * Heart rate and contraction strength of the heart can be altered by the autonomic nervous system or the endocrine system.
Cardiac Arrhythmias
Disturbances in the normal sequence of cardiac events can lead to an irregular heart rhythm, called an arrhythmia. Can affect blood circulation. Bradycardia (slow heart) = resting HR lower than 60 beats per minute. Tachycardia (fast heart) = resting HR higher than 100 beats per minute.
Symptoms of both arrhythmias include fatigue, dizziness, lightheadedness, & fainting. Other arrhythmias: Premature Ventricular Contractions (PVC), which result in the feeling of skipped or extra beats, result from impulses originating outside the SA node. Atrial Flutter, in which atria contract at rates of 200-400 bpm. Atrial Fibrillation – atria contract in a rapid & uncoordinated manner – is more serious arrhythmias, which cause the atria to pump little blood or no blood. Ventricular fibrillation – uncoordinated ventricular contraction – cause heart cannot pump blood & leads to fatal. Use of a defibrillator to shock the heart to get back normal sinus rhythm. * Endurance training cause low resting HR (bradycardia)
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Chapter 5. Cardiovascular Control During Exercise
The Electrocardiogram (ECG)
Electrical activity of heart can be recorded to diagnose potential cardiac problems or to monitor cardiac changes.
The principle involved is simple – Body fluids are good electrical conductors. Electrical impulses generated in the heart are conducted through body fluids to the skin, where they can be detected & printed out by a sensitive machine called an electrocardiograph. This printout is called an electrocardiogram (ECG).
Three components of ECG represent aspects of cardiac function: 1. The P wave 2. The QRS complex 3. The T wave
The P wave represents atrial depolarization & occurs when the electrical impulse travels from the SA node through the atria to the AV node. * “Depolarization” = a decrease in the electrical potential across a membrane, such as when the inside of a neuron becomes less negative relative to the outside.
The QRS complex represents ventricular depolarization & occurs as the impulse spreads from the AV bundle to the Purkinje fibers & through the ventricles.
The T wave represents ventricular repolarization. Atrial repolarization cannot be seen as it occurs during ventricular depolarization (QRS complex).
Often ECGs are obtained during exercise. ECGs are valuable diagnostic tests. As exercise intensity increases, the heart must beat faster and work harder to deliver more blood to active muscle. If the heart is diseased, an indication may show up on the ECG as the heart increases its rate of work. Exercise ECGs have also been invaluable tools for research in exercise physiology because they provide a convenient method for tracking cardiac changes during acute & chronic exercise.
* ECG is a recording of the heart’s electrical functioning. An exercise ECG may reveals underlying cardiac disorders.
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Chapter 5. Cardiovascular Control During Exercise
Terminology of Cardiac Function Cardiac Cycle
Includes all events occurring between 2 consecutive heartbeats: a relaxation phase (Diastole) & a contraction phase (Systole). During diastole, the chambers fill with blood. During systole, the chambers contract & expel blood. Diastolic phase is longer than systolic phase. Eg: An individual with HR = 74 bpm, the entire cardiac cycle takes 0.81s to complete (60s/74 bpm); diastole accounts for 0.50s (62%) of the cycle & systole accounts for 0.31s (38%). As HR increases, these absolute time intervals shorten proportionately. * (Refer to Normal ECG) One cardiac cycle spans the time between one systole & the next. Ventricular contraction (systole) begins during the QRS complex & the ends in the T wave. Ventricular relaxation (diastole) occurs during the T wave & continues until the next contraction.
Stroke Volume (SV)
The volume of blood pumped per stroke (contraction). A certain amount of blood is ejected from the left ventricle during systole. At the end of diastole, just before systole, the ventricle has completed filling with blood. This volume of blood is called ‘end-diastole volume’ (EDV). At the end of systole, just after contraction, the ventricle has completed its ejection phase. This volume of blood left in the ventricle is called ‘end-systole volume’ (ESV). SV is the volume of blood that was ejected, & is the difference between the amounts originally there & the amount remaining in the ventricle after contraction. SV = EDV - SDV
EDV = 100 ml End of ventricle filling
-
ESV = 40 ml End of ventricle contraction
=
SV = 60 ml Blood vessels
6
Chapter 5. Cardiovascular Control During Exercise
Ejection Fraction (EF)
The proportion of blood pumped out of the left ventricle at each beat.
EF =
SV x 100 EDV
=
60 x 100 100
=
60%
Expressed as a percentage, average 60% at rest. Thus 60% of the blood in the ventricle is ejected & 40% remains.
Cardiac Output (Q)
The total volume of blood pumped by ventricle per minute.
Q = HR x SV
(The product of HR & SV)
SV at rest in the standing position averages between 60-80 ml of blood foe most adults. Thus RHR = 80 bpm, the resting Q = 4.8 –6.4 L/min. Average adult body contains 5 L of blood, so this means all our blood is pumped through our heart about once every minute.
2. The Vascular System (The Blood Vessel/ A system of channels)
Composed of a series of vessels that transport blood from the heart to the tissue and back. Arteries are typically the largest, most muscular, & most elastic vessels, & carry blood away from the heart to the arterioles. From the arterioles, blood enters the capillaries, the narrowest vessels. All exchange between the blood and the tissues occurs at the capillaries. Blood leaves the capillaries to begin the return trip to the heart in the venules, & the venules form larger vessels – the veins - that complete the circuit. *Heart has also own vascular system – coronary arteries & veins
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Chapter 5. Cardiovascular Control During Exercise
Return of Blood to the Heart
CV system requires assistance to overcome the force of gravity (upright position) when returning blood from the lower extremities back to the heart. Three basic mechanisms assist in this process: a. Breathing – pressure changes in the abdominal & thoracic cavities. b. Muscle pump – During skeletal muscle contraction, veins are compressed & blood is pushed upwards toward the heart c. Valves within veins - allow blood flow in one direction only. Blood returns to the heart through the veins, assisted by breathing, the muscle pump, and valves within the vessels.
Distribution of Blood
Varies depending on the needs of specific tissue & of the whole body. At rest – Most metabolically active tissue receive the greatest blood supply: 27% to liver; 22% to kidneys & only 15% to skeletal muscles. During exercise – blood is redirected to the needed areas. Heavy endurance exercise, skeletal muscles receive up to 80% or more of the available blood. After meal – digestive system receives more blood. During heat stress – the skin’s blood supply increases as the body attempts to maintain normal temperature. *Blood is redistributed throughout the body based on the tissues’ needs. The most active tissues receive the most blood. (The more active the muscle is, the more blood goes to it.)
Distribution of blood to various areas is controlled primarily by the arterioles. These vessels have strong muscular wall & respond to the mechanisms that control blood flow: autoregulation & extrinsic neural control. Autoregulation (intrinsic control). Causes vasodilation in response to local chemical changes, thus increases blood flow or supply to the areas where more O 2 demand. Chemical changes also increases in clearing the by-products (CO 2, K+, H+ & lactic acid) Extrinsic Neural Control of distribution is accomplished by the SNS stimulation causing constriction of blood vessels (decrease blood flow into that area). But SNS can also cause vasodilation e.g. during fight – or – flight response or exercising (increase blood flow to the skeletal muscle & in the heart).
8
Chapter 5. Cardiovascular Control During Exercise
Redistribution of Venous Blood – At rest 64% blood in the veins, but during exercise SNS causes vasoconstriction of these veins, therefore more blood flow to areas in need.
Blood Pressure
The pressure exerted by the blood on the vessel walls, & the term usually refers to the arterial blood pressure. Expressed by 2 numbers: the systolic pressure & the diastolic pressure. BP =
Systolic BP Diastolic BP
The higher number is the systolic blood pressure. Represent the highest pressure in the artery & corresponds to ventricular systole of the heart. Ventricular contraction pushes the blood through the arteries with tremendous force, which exerts high pressure on the arterial wall. The lower number is the diastolic blood pressure. Represent the lowest pressure in the artery & corresponds to ventricular diastole when the heart is at rest. Blood moving through the arteries during that phase is not pushed along by a forceful contraction. *Systolic blood pressure is the highest pressure within the vascular system. Diastolic blood pressure is the lowest pressure. Mean arterial pressure is the average pressure on the vessel walls
Hypertension
Constriction of blood vessels increases blood pressure. Condition in which blood pressure is chronically elevated above normal, healthy values. The cause is generally unknown in approximately 90% of cases, but it can usually be controlled effectively by weight loss, proper diet, & exercise, although appropriate medication may also be required.
9
Chapter 5. Cardiovascular Control During Exercise
3. The Blood Basic 1. 2. 3.
Functions primary importance to exercise: Transportation Temperature regulation Acid-base (pH) balance
Blood & lymph are substances that transport materials to & from body tissues. Fluid from plasma enters the tissues, becoming interstitial fluid. Most interstitial fluid returns to the capillaries, but some enters the lymphatic system as lymph, eventually returning to the blood. Blood volume = 5-6 L in males & 4-5 L in females.
Blood Composition Plasma – 55% (90% water, 7% plasma proteins & 3% others) Formed elements - 45% (> 99% RBC & < 1% WBC & platelets)
RBC (Erythrocytes) % RBC volume in the blood is hematocrit (normal = 40-45%) O2 is primarily transported bound to the hemoglobin in RBC. RBC contains hemoglobin: Protein (globin) & Pigment (heme) that contains iron that binds O2. Each RBC contains approximately 250 million hemoglobin molecules, each able to binds 4 O2 molecules, so each RBC can bind up to a billion molecules of O 2. Average 15 g Hb per 100 ml of whole blood.
Blood Viscosity Viscosity refers to the thickness or stickiness of the blood. The more viscous, the more resistant it is to flow. Viscosity of blood is about twice than water. Increase viscosity of blood = Increase resistance of blood flow Increase hematocrit = Increase resistance of blood flow CV system’s normal adaptations to training – Increase hematocrit & normal or slightly increase RBC.
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Chapter 5. Cardiovascular Control During Exercise
SUMMARY 1.
The atria receive blood into the heart; the ventricles eject blood from the heart.
2.
Left ventricle must produce more power than other chambers because has to pump blood to all parts of the body; therefore its myocardium is thicker, due to hypertrophy.
3.
Cardiac
4.
SA node is the heart’s pacemaker, establishing the pulse and coordinate activity throughout the heart.
5.
Heart
6.
Endurance training cause low resting HR (bradycardia).
7.
ECG is a recording of the heart’s electrical functioning. An exercise ECG may reveals underlying cardiac disorders.
8.
Blood returns to the heart through the veins, assisted by breathing, the muscle pump, and valves within the vessels.
9.
Blood is redistributed throughout the body based on the tissues’ needs. The most active tissues receive the most blood.
10.
Redistribution of blood is controlled by autoregulation. Autoregulation causes vasodilation in response to local chemical changes, thus increasing blood flow or supply to the areas.
11.
Extrinsic neural control of distribution is accomplished by the SNS, primarily through vasoconstriction.
12.
Blood & lymph are substances that transport materials to and from body tissues.
13.
Blood is about 55% plasma and 45% formed elements,
14.
Oxygen is transported by binding to the hemoglobin in RBCs.
15.
As blood viscosity increases, so does resistance to flow.
tissue is capable of autoconduction. Cardiac conduction system has own conduction system initiates own pulse without neural control.
rate and contraction strength of the heart can be altered by the autonomic nervous system or the endocrine system.
11
Chapter 5. Cardiovascular Control During Exercise
B. Cardiovascular Response to Exercise 1. Heart Rate (HR)
HR is one of the simplest & most informative of the CV parameters. Measure pulse: Carotid pulse or radial pulse. HR reflects the amount of work the heart must do to meet the increased demands of the body when engaged in activity. HR increases with the increase rates of work.
Resting HR Averages 60-80 bpm. In middle-aged, unconditioned, sedentary individuals, RHR can exceed 100 bpm. High conditioned, endurance-trained athletes, RHR in the range of 28-40 bpm. RHR affected by environmental factors: RHR increases with extreme temperature and altitude.
HR During Exercise As exercise intensity increases, HR increases. The heart ejects blood more often, thus speeding up circulation. HR increases directly as increase in exercise intensity, until a point of exhaustion. As this point is approached, HR begins to level off. This indicates the maximum value is reached.
Maximum HR (HR max) HR max is the highest HR value achieve in an all-out effort to the point of exhaustion. Estimate of maximum HR can be made based on the age because maximum HR shows a slight but steady decrease of about 1 beat per year beginning at 10 to 15 years of age. Subtracting your age from 220 provides an approximation of your maximum HR.
To estimate maximum HR:
HR
max
= 220 – age in years
Eg: 40 years old individual:
HR
max
= 220 – 40 = 180 bpm
Steady State HR HR increase during submaximal exercise until reaches a plateau. This plateau is the steady state HR, & it is the optimal HR for meeting the circulatory demands at that specific rate of work. Lower rate of steady state HR shows a more efficient heart.
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Chapter 5. Cardiovascular Control During Exercise
2. Stroke Volume
SV increases with the increase rates of work , so the amount of blood ejected with each contraction increases. SV is determined by: 1. Volume of venous blood returned to the heart 2. Ventricular distensibility,(the capacity to enlarge the ventricle) 3. Ventricular contractility 4. Aortic or pulmonary artery pressure (the pressure against which the ventricles must contract)
3. Cardiac Output (Q)
Q increases with the increase rates of work. Increases in HR & SV increase Q. Thus more blood is forced out of the heart during exercise than when at rest, & circulation speed up. This ensures that adequate supplies of the needed materials (O 2 & nutrients) reach the tissues & the waste products, which build up much more rapidly during exercise, ere quickly cleared away. Exercise increases Q to match the need for O 2 supply to the working muscles.
4. Blood flow Redistribution of Blood During Exercise During rest, only 15-20% of the resting Q goes to muscle. During exercise, the muscles receive up to 80%- 85% of the Q. During exercise in heat, there is increase blood flow to the skin. More blood is redirected to the skin to conduct heat away from the core body to its periphery, promote heat loss to the environment.
The metabolic rate of the muscle tissues rises during exercise. As a result, metabolic waste products begin to accumulate. Increased metabolism causes an increase in acidity, CO 2 & temperature in the muscle tissue. These changes trigger vasodilation through autoregulation (effect of SNS), increasing blood flow through the local capillaries.
Cardiovascular Drift (CV drift) CV drift is an increase in HR during prolong exercise to compensate for a decrease in SV. This compensation helps to maintain a constant Q. Prolonged exercise in the heat causes decrease in blood volume due to water loss through sweating & a shifting of fluid out of the blood into the tissue, which results in decrease in SV. HR increases to compensate for the decreased SV, in an effort to maintain Q.
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Chapter 5. Cardiovascular Control During Exercise
CV drift allows the body to continue exercising at low to moderate intensities. At high intensities, the increase in HR cannot compensate the decreased in SV because the HR attains its maximal value (HR max) at much lower exercise intensity, HR begins to level off as this point is reached, thus limiting the maximal performances.
5. Blood Pressure (BP)
BP is pressure exerted by blood against the blood vessels. Systolic Pressure = highest Pressure in the artery Diastolic Pressure = lowest Pressure in the artery With endurance exercise, systolic blood pressure increase in direct proportion to increased exercise intensity. Increase systolic BP results from the increased Q that accompanies increasing rates of work. Diastolic BP changes little if any during endurance exercise, regardless of the intensity. Remember that diastolic pressure reflects the pressure in the arteries when the heart is at rest.
6. Blood
The changes that occur in the blood during exercise demonstrate that the blood is carrying out its necessary tasks. The major changes are: 1. The arterial-venous oxygen difference (a-vO2 diff) increases. This happens because the venous O 2 concentration decreases during exercise, reflecting increased extraction of O 2 from the blood for use by the active tissues. 2. Plasma volume decreases during exercise. The fluid (water) is pushed out of the capillaries by increases in hydrostatic pressure as BP increase & is drawn into the muscle by the increased osmotic pressure that results from waste accumulation. However, with prolonged exercise or exercise in hot environment, increasingly more plasma fluid is lost through sweating in an attempt to maintain body temperature, placing the person at risk of dehydration. 3. Hemoconcentration occurs as plasma fluid is lost. Although the actual number of RBC might not increase, the net effect of this process is to increase the number of RBC per unit of blood, which increases oxygen –carrying capacity. 4. Blood pH can change significantly during exercise, becoming more acidic as it move from the slightly alkaline resting value of 7.4 down to 7.0 or lower. The muscle pH decreases even further. The decrease in pH primarily results from increased blood lactate accumulation during increased exercise intensity.
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Chapter 5. Cardiovascular Control During Exercise
SUMMARY 1.
As exercise intensity increases, Heart rate increases. The heart ejects blood more often, thus speeding up circulation.
2.
Stroke volume also increases with the increase rates of work, so the amount of blood ejected with each contraction increases.
3.
Increases in HR & SV increase cardiac output (Q). Thus more blood is forced out of the heart during exercise than when at rest, and circulation speed up.
4.
During exercise, cardiac output increases primarily to match the need for increased O2 supply to the working muscles.
5.
During exercise, the muscles receive up to 80%- 85% of the cardiac output.
6.
Cardiovascular drift is increases in HR during prolong exercise to compensate for a decrease in SV. This compensation helps to maintain a constant Q.
7.
With endurance exercise, systolic blood pressure increase in direct proportion to increased exercise intensity.
8.
With increasing rates of exercise, the arterial-venous oxygen difference (a-vO2 diff) increases progressively.
9.
Plasma volume decreases during exercise.
10.
When plasma volume reduces, hemoconcentration occurs as plasma fluid is reduced and increasing the concentration of the substances that remain in the blood.
11.
Blood pH can change significantly during exercise, becoming more acidic due to increases in blood lactate.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Cardiovascular Control During Exercise) Name : _______________________________________
Group : _________ Date : _______________
Answer ALL questions.
1. Define cardiac cycle. ________________________________________________________________________________ ________________________________________________________________________________ 2. Define stroke volume. ________________________________________________________________________________
3. Define cardiac output. ________________________________________________________________________________
4. Name the three principal mechanisms for increasing venous return during exercise. a_______________________________________________________________________________ b_______________________________________________________________________________ c________________________________________________________________________________
5. Discuss the two (2) mechanisms for returning blood back to the heart when the athlete exercising in an upright position. a_______________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ b_______________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ 6. What is arterial blood pressure? ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
1
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
7. Define systolic blood pressure and diastolic blood pressure. a_______________________________________________________________________________ ________________________________________________________________________________ b_______________________________________________________________________________ ________________________________________________________________________________
8. Identify four (4) responses that occur in the cardiovascular during exercise. a________________________________________________________________________________ _________________________________________________________________________________ b________________________________________________________________________________ _________________________________________________________________________________ c________________________________________________________________________________ _________________________________________________________________________________ d________________________________________________________________________________ _________________________________________________________________________________
9. Estimate the maximum heart rate (HRmax) of a person who aged 32 years old.
10. Calculate the stroke volume in milliliters if heart rate equals 75 bpm and cardiac output equals 4.5 L. -1 min .
11. Calculate the cardiac output in liter per minute when stoke volume equals 75 ml and heart rate equals 80 bpm.
12. Calculate the Body Mass Index (BMI) of an athlete weighing 80 kg and 172 cm tall.
13. Calculate the Body Mass Index (BMI) of an athlete weighing 75 kg and 180 cm tall.
2
Chapter 6. Respiratory Regulation During Exercise
RESPIRATORY REGULATION DURING EXERCISE A. Pulmonary Ventilation
Pulmonary Ventilation (breathing) is the process by which air is moved into and out of the lungs. It has two phases: inspiration & expiration.
1. Inspiration Inspiration is an active process in which the diaphragm and the external intercostals muscles increase the dimension, and thus the volume, of the thoracic cage. This decreases the pressure in the lungs and draws air in.
During forced or labored breathing (such as during heavy exercise), inspiration is further assisted by the action of other muscles (neck & pectoral muscles). These muscles help raise the ribs even more than during regular breathing.
2. Expiration Expiration is usually a passive process. The inspiratory muscles relax and the elastics tissue of the lung recoils, returning the thoracic cage to its smaller, normal dimensions. This increases the pressure in the lungs and forces air out.
During forced breathing, expiration becomes a more active process. The internal intercostals muscles can actively pull the ribs down. This action assisted by the latissimus dorsi & lumborum muscles. These muscles also pull the rib cage down.
B. Pulmonary Diffusion
Pulmonary diffusion is the process by which gases are exchanged across the respiratory membrane (alveolar-capillary membrane) in the alveoli (lungs). The amount of gas exchange that occurs across the membrane depends primarily on the partial pressure of each gas, though gas solubility and temperature are also important. Gases diffuse along a pressure gradient, moving from an area of higher pressure to one of lower pressure. Thus, oxygen enters the blood and carbon dioxide leaves it. The greater the pressure gradient across the respiratory membrane, the more rapidly oxygen diffuses across it. Oxygen diffusion capacity increases as the body move from rest to exercise. When the body needs more oxygen, oxygen exchange is facilitated. The pressure gradient for carbon dioxide exchange is less than for oxygen exchange, but carbon dioxide’s membrane solubility is 20 times greater than of oxygen, so carbon dioxide crosses the membrane easily, even without a large pressure gradient. 1
Chapter 6. Respiratory Regulation During Exercise
C. Transport of Oxygen and Carbon Dioxide 1. Oxygen Transport Oxygen is transported in the blood primarily bound to hemoglobin (oxyhemoglobin), though a small part of it is dissolved in blood plasma.
Hemoglobin oxygen saturation decreases when : a) Partial pressure of oxygen (PO2) decreases, b) pH decreases, or c) temperature increases. Each of these conditions can reflect increased local oxygen demand. They increase oxygen unloading in the needy area. Hemoglobin is usually about 98% saturated with oxygen. This is a much higher oxygen content than our bodies require, so the blood’s oxygen-carrying capacity seldom limits performance.
2. Carbon Dioxide Transport Carbon dioxide is transported in the blood primarily as bicarbonate ion. This prevents the formation of carbonic acid, which can cause H + to accumulate, decreasing the pH. Smaller amounts of carbon dioxide are carried either dissolved in the plasma or bound to hemoglobin (carbaminohemoglobin).
D. Gas Exchange at the Muscle 1. The Arterial-Venous Oxygen Difference The a-vO2 diff is the difference in the oxygen content of arterial and venous blood. This measure reflects the amount of oxygen taken up by the tissues.
2. Factors Influencing Oxygen Delivery and Uptake Oxygen delivery to the tissues depends on: a) the oxygen content of the blood, b) the amount of blood flow to the tissues, and c) local conditions (e.g., tissue temperature & PO 2)
3. Carbon Dioxide Removal Carbon dioxide exchange at the tissues is similar to oxygen exchange, except that CO2 leaves the muscles, where it is formed, and enters the blood to be transported to the lungs for clearance.
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Chapter 6. Respiratory Regulation During Exercise
E. The Regulation of Pulmonary Ventilation 1. The Mechanisms of Regulation The respiratory centers in the brain stem set the rate and depth of breathing.
Central chemoreceptors in the brain respond to changes in concentrations of CO 2 and H+. When either of these rises, the inspiratory center increases respiration. Peripheral receptors in the arch of the aorta and the bifurcation of the common carotid artery respond primarily to changes in blood O 2 levels, but also to changes in CO2 and H+ levels. If O2 levels drop too low, or if the other levels rise, these chemoreceptors relay their information to the inspiratory center, which in turn increases respiration. Stretch receptors in the air passages and lungs can cause the expiratory center to shorten respirations to prevent overinflation of the lungs. In addition, the body can exert some voluntary control over respiration.
2. Pulmonary Ventilation During Exercise During exercise, ventilation shows an almost immediate increase, resulting from increased inspiratory center stimulation caused by the muscle activity itself. This is followed by a more gradual increase that results from the rise in temperature and chemical changes in the arterial blood that are caused by the muscular activity.
3. Problems Associated With Breathing During Exercise Breathing problems associated with exercise include dyspnea (shortness of breath), hyperventilation (overbreathing), and performance of the Valsalva maneuver. Valsalva maneuver is referred to a respiratory procedure that is frequently performed in certain types of exercise and that can be potentially dangerous. This occurs when the individual: a) Closes the glottis (the opening between the vocal cords), b) Increases the intra-abdominal pressure by forcibly contracting the diaphragm and the abdominal muscles, and c) Increases the intrathoracic pressure by forcibly contracting the respiratory muscles.
F. Ventilation and Energy Metabolism 1. The Ventilatory Equivalent for Oxygen During mild, steady-state exercise, ventilation accurately reflects the rate of energy metabolism. Ventilation parallels oxygen uptake. The ratio of air ventilated to O2 consumed is the ventilatory equivalent of oxygen (VE/VO2).
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Chapter 6. Respiratory Regulation During Exercise
2. The Ventilatory Breakpoint The Ventilatory Breakpoint is the point at which ventilation abruptly increases, even though O2 consumption does not. This increase reflects the need to remove excess CO2.
3. Anaerobic Threshold The anaerobic threshold can be determined by identifying the point at which VE/VO 2 shows a sudden increase while VE/VO2 stays relatively stable. Anaerobic threshold has been used as a noninvasive estimate of lactate threshold.
G. Respiratory Limitations to Performance
More than 15% of the body’s total O 2 consumption during heavy exercise can occur in the respiratory muscles. Pulmonary ventilation is usually not a limiting factor for performance, even during maximal effort, though it can limit performance in highly trained people. The respiratory muscles seem to be better designed for avoiding fatigue during longterm activity than muscles of the extremities. Airway resistance and gas diffusion usually do not limit performance in normal, healthy individuals. The respiratory system can limit performance in people with restrictive or obstructive respiratory disorders.
H. Respiratory Regulation of Acid-Base Balance
Excess H+ (decreased pH) impairs muscle contractility and ATP formation. The respiratory system plays an integral role in maintaining acid-base balance. Whenever H+ levels start to rise, the inspiratory center responds by increasing respiration. Removing CO2 is an essential means for reducing the H+ concentrations. CO2 is transported primarily bound to bicarbonate. Once it reaches the lungs, CO 2 is formed again and exhaled. Whenever H+ levels begin to rise, whether from CO 2 or lactate accumulation, bicarbonate ion can buffer the H+ to prevent acidosis.
4
Chapter 6. Respiratory Regulation During Exercise
SUMMARY 1.
Pulmonary Ventilation (breathing) is the process by which air is moved into and out of the lungs. It has two phases: inspiration & expiration.
2.
Inspiration is an active process in which the diaphragm and the external intercostals muscles increase the dimension, and thus the volume, of the thoracic cage. This decreases the pressure in the lungs and draws air in.
3.
Expiration is usually a passive process. The inspiratory muscles relax and the elastics tissue of the lung recoils, returning the thoracic cage to its smaller, normal dimensions. This increases the pressure in the lungs and forces air out.
4.
Forced inspiration and expiration are active processes, dependent on muscles actions.
5.
Pulmonary diffusion is the process by which gases are exchanged across the respiratory membrane in the lungs.
6.
The amount of gas exchange that occurs across the membrane depends primarily on the partial pressure of each gas.
7.
The greater the pressure gradient across the respiratory membrane, the more rapidly oxygen diffuses across it.
8.
Oxygen diffusion capacity increases as the body move from rest to exercise. When the body needs more oxygen, oxygen exchange is facilitated.
9.
The pressure gradient for carbon dioxide exchange is less than for oxygen exchange, but carbon dioxide’s membrane solubility is 20 times greater than of oxygen, so carbon dioxide crosses the membrane easily, even without a large pressure gradient.
5
Chapter 7. Cardiorespiratory Adaptations to Training
CARDIORESPIRATORY CARDIORESPIRATORY ADAPTATIONS TO TRAINING A. Endurance
Muscular endurance The ability of a muscle or muscle group to exert force repeatedly to sustain a contractive state over a period of time.
For sprinters, muscular endurance is the ability to sustain a high speed over the full distance of a 100m 0r 200m race.
In weight lifting, boxing and wrestling, muscular endurance is the ability of a single muscle or muscle group to sustain high-intensity, repetitive, or static exercise.
Muscular endurance is highly related to muscular strength and anaerobic development.
Cardiorespiratory endurance The ability of the body to deliver oxygen effectively to the working muscle to sustain prolonged, rhythmical exercise.
Cardiorespirarory Cardiorespirarory endurance is the ability of the body to sustain prolonged, rhythmical exercise. (e.g., : cycling, distance running & long distance swimming)
Cardiorespiratory Cardiorespiratory endurance is highly related to the development of the CV & respiratory system, thus the aerobic development.
B. Evaluating Endurance Capacity
VO2 max: maximal O2 uptake The highest rate of O 2 consumption obtainable during maximal or exhaustive exercise.
VO2 max representing aerobic power, as the best laboratory measure of CR endurance capacity & is the best indicator of CR endurance.
VO2 max is measured in ml · kg -1 · min-1. 1
Chapter 7. Cardiorespiratory Adaptations to Training
O2 Transport System Refer to all components of the CV & respiratory systems that are related to the transportation & delivery of O 2.
The functioning of O2 transport system is defined by the interaction of the cardiac output & the arterial-venous oxygen difference ( a-vO2 diff).
Arterial-venous oxygen difference (a-vO2 diff), which is the difference between the O2 content of the arterial blood & the O2 content of the venous blood.
Q (SV x HR) tells how much O2-carrying blood leaves the heart in 1 min. a-vO2 diff tells how much O 2 is extracted from the blood by the tissues.
The product tells us the rate of O2 consumption: VO2 = SV x HR x a-vO2 diff
The active tissues’ O 2 demand increases during exercise. Body endurance depends on the O 2 transport system’s ability to deliver sufficient O 2 to these active tissues to meet the high demands.
C. Cardiovascular Adaptations to Training 1. Heart size
‘Cardiac hypertrophy’ – the left ventricle undergoes the most change in response to endurance training. The internal dimensions of the left ventricle increase, mostly in response to an increase in ventricular filling. Left ventricle wall thickness also increase, increasing the strength potential of the chamber’s contraction. (increases contractility)
2. Stroke Volume
Following endurance training, SV increases during rest, submaximal levels of exercise, and maximal exercise. A major factor leading to the SV increase is an increased end-diastolic volume (EDV), probably caused by an increased in blood plasma . Another major factor is increased left ventricle contractility. This is caused by hypertrophy of the cardiac muscle and increased elastic recoil, which results f rom increased stretching of the chamber with more diastolic filling. 2
Chapter 7. Cardiorespiratory Adaptations to Training
3. Heart Rate (HR)
Resting heart rate (RHR)- the HR at rest, averaging 60-80 bpm. RHR decreased as a result of endurance training. In a sedentary person the decrease is typically about 1 bpm per week during initial training. Highly trained endurance athletes often have resting rates of 40 bpm or less. Submaximal HR also decreases, often by about 20 to 40 bpm following 6 months of moderate training. Maximum heart rate (HR max) – the highest HR value attainable during an all out effort to the point of exhaustion. HR max either remains unchanged or decreases slightly with training. When decrease occurs, it is probably to allow optimum SV to maximize cardiac output. ‘HR recovery period’ – the time it take for HR to return to the resting rate after exercise. ‘HR recovery period’ decreases with increased endurance, making this value well suited to tracking an individual’s progress in training. However, this is not useful for comparing fitness of different people because of the potential influence of other factor like exercise in hot environment or high altitudes can prolong HR elevation. Resistance training can also lead to reduced HR; however, these decreases are not reliable or as large as those seen with endurance training. (Resistance training is designed to increase strength, power, & muscular endurance)
4. Cardiac Output (Q)
Q at rest or during submaximal levels of exercise remains unchanged or decreases slightly after training. Q at maximal levels of exercise increases considerably. This is largely the result of the substantial increases in SV.
5. Blood Flow
Endurance training increases blood flow to muscle because: i. Increased capillarization ii. Greater opening of existing capillaries iii. More effective blood redistribution.
6. Blood Pressure
Resting BP is decreases with endurance training in those with borderline or moderate hypertension. Endurance training has little or no effect on BP during submaximal or maximal exercise. 3
Chapter 7. Cardiorespiratory Adaptations to Training
7. Blood Volume
Endurance training causes increased in blood volume, due to increased in plasma volume which is one of the most significant effects of training. Increased in RBC count, but the gain in plasma is much higher, resulting in a relatively greater fluid portion of the blood. (Increased in plasma volume is >, therefore > fluid, hence decreased in blood viscosity, therefore increased in blood circulation) Plasma volume increases because increased in SV and VO 2max.
D. Respiratory Adaptations to Training 1. Lung Volumes Effects of endurance training In general, lung volumes change little with training. Vital capacity (VC) increases slightly. Residual volume (RV) slightly decreases. Overall, total lung capacity remains unchanged. Tidal volume is unchanged at rest & during submaximal exercise, but increases during maximal exercise .
Vital capacity (VC) = the maximum volume/amount of air expelled from the lungs after maximum inspiration/inhalation. Residual volume (RV) = the amount of air that cannot be exhaled from the lungs or remains in the lungs. Tidal volume = the amount of air breathed in and out (inspired or expired) during normal respiration.
2. Respiratory Rate
After training, respiratory rate remains steady at rest, decrease slightly with submaximal exercise, but increases with maximal exercises .
3. Pulmonary Ventilation
After training, pulmonary ventilation is unchanged or slightly decreases at rest & at submaximal exercise, but increases at maximal exercise due to increased in tidal volume and respiration rate. Pulmonary ventilation = the movement of gases into & out of the lungs. 4
Chapter 7. Cardiorespiratory Adaptations to Training
4. Pulmonary Diffusion
After training, pulmonary diffusion is unaltered/ unchanged at rest and during submaximal exercise, because of increased in ventilation and increased in lung perfusion. (More blood is brought into lungs for gas exchange, & at the same time ventilation is increased, so more air is brought into the lungs) however increases at maximal exercise Pulmonary diffusion = the exchange of gases between the lungs & the blood.
5. Arterial-Venous Oxygen Difference ( a-vO2 diff)
Training increases a-vO2 diff, especially at maximal exercise because the increased in O 2 extraction by tissues and increased in blood distribution.
* Respiratory system is quite adept at bringing adequate amounts of O 2 into the body, thus it usually does not limit endurance performance.
E. Metabolic Adaptations 1. Lactate Threshold (LT)
Endurance training increases LT, therefore can perform at a higher rates of work and at a higher rate of O 2 consumption without increasing the blood lactate above resting levels. The increase in LT is because a greater ability to clear lactate produced in the muscle, and an increase in skeletal enzymes coupled with a shift in metabolic substrate. Maximal blood lactate concentration is increased slightly. Lactate threshold (LT) = the point during exercise of increasing intensity at which blood lactate begins to accumulate above resting levels.
2. Respiratory Exchange Ratio (RER)
RER reflects the types of substrates being used as an energy source. After training, RER is decrease at submaximal work rate, indicating a greater utilization of FFA instead of CHO. At maximal work, RER increases due to the ability to perform at max levels for longer periods of time. 5
Chapter 7. Cardiorespiratory Adaptations to Training
Respiratory exchange ratio (RER) = the ratio of CO2 expired to the O2 consumed at the level of the lungs.
3. Resting & Submaximal O2 Consumption
O2 consumption can be increase slightly at rest & decreased slightly or unaltered during submaximal exercise.
4. Maximal O2 Consumption
VO2max increases with training, but the amount of increase is limited in each individual. The major limiting factor is O 2 delivery to the active muscles.
F. Long–term Improvement in Endurance
VO2max has an upper limit. The highest attainable VO 2max is usually reached within 18 months of intense endurance conditioning. Endurance performance can continue to improve for years with continued training.
G. Factors Affecting the Response to Aerobic Training 1. Heredity
VO2max depends on genetic limits which predetermines the range for VO 2max. (25%-50% of the variance in VO 2max values) Heredity also explains for individual variations in response to identical training program.
2. Age
Age-related decreases in aerobic capacity is partly due to the decreased in activity.
3. Gender
VO2max of highly conditioned female endurance athletes is only about 10% lower than highly conditioned male endurance athletes.
4. Responders and Non-responders
Response to a training program is also genetically determined. 6
Chapter 7. Cardiorespiratory Adaptations to Training
5. Specificity of training
The more specific the training program to the sports involved, the more improvement there will be. To maximize CR gains from training, the training should be specific to the type of activity that an athlete usually performs.
6. Cross–training
Resistance training combines with endurance training does not appear to improve the aerobic capacity, but may increase short term endurance.
H. Cardiorespiratory Endurance and Performance
Cardiorespiratory endurance is regarded as the most important component of physical fitness & is an athlete’s major defense against fatigue. Even minor fatigue can have a detrimental effect on the athlete’s total performance: Muscular strength is decreased. Reaction & movement times are prolonged. Agility & neuromuscular coordination are reduced. Whole –body movement speed is slowed. Concentration & alertness are reduced. Therefore, CV conditioning must be the foundation of general conditioning program. All athletes can benefit from maximizing their endurance.
7
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Cardiorespiratory Adaptations to Training) Name : _______________________________________
Group : _________ Date : _______________
Answer ALL questions. 1. Define muscular endurance and cardiorespiratory endurance. a._______________________________________________________________________________ _______________________________________________________________________________ b._______________________________________________________________________________ _______________________________________________________________________________
2. Define aerobic power (VO 2 max). What determines this maximal oxygen uptake rate? a.______________________________________________________________________________ ______________________________________________________________________________ b.______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________
3. Explain the cardiovascular adaptations that occur in response to endurance training. a._______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ b._______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ c._______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ 1
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
______________________________________________________________________________ d._______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ ______________________________________________________________________________ e._______________________________________________________________________________ _______________________________________________________________________________ f._______________________________________________________________________________ _______________________________________________________________________________ ______________________________________________________________________________ g._______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________
4. Describe the adaptations in the respiratory system that occur with endurance training. a._______________________________________________________________________________ _______________________________________________________________________________ _______________________________________________________________________________ ______________________________________________________________________________ b._______________________________________________________________________________ _______________________________________________________________________________ c._______________________________________________________________________________ ______________________________________________________________________________ d._______________________________________________________________________________ ______________________________________________________________________________ e._______________________________________________________________________________ _______________________________________________________________________________
5. Define lactate threshold. Explain briefly the effect of endurance training on lactate threshold. a._______________________________________________________________________________ _______________________________________________________________________________ ______________________________________________________________________________ b._______________________________________________________________________________ _______________________________________________________________________________ ______________________________________________________________________________
2
Chapter 8. Hormonal Regulation of Exercise
HORMONAL REGULATION OF EXERCISE The Endocrine System
This system includes all tissues or glands that secrete hormones. Endocrine glands secrete their hormones directly into the blood. Hormones act as chemical signals throughout the body. Specific hormone secreted by the specialized endocrine cells & transported via the blood to specific target cells. Upon reaching their destinations, they can control the activity of the target tissue. Some hormones affect many body tissues, whereas others target specific cells of the body.
A. The Nature of Hormones
Hormones are involved in most physiological processes, so their actions are relevant to many aspects of exercise & sport performance.
1. Chemical Classification of Hormones Steroid Hormones
Chemical structure similar to cholesterol & most are derived from it. Lipid soluble & diffuse easily through cell membranes. E.g. hormones secreted by adrenal cortex (cortisol & aldosterone), ovaries (estrogen & progesterone), testes (testosterone), & placenta (estrogen & progesterone). Nonsteroid Hormones
Not lipid soluble, so they cannot easily cross cell membranes. Subdivided into 2 groups: protein or peptide hormones & amino acid-derivative hormones. Hormones from thyroid gland (thyroxine & triiodothyronine) & adrenal medulla (epinephrine & norepinephrine) are amino acid hormones. All other nonsteroid hormones are protein or peptide hormones.
1
Chapter 8. Hormonal Regulation of Exercise
2. Hormone Action
The interaction between the hormone & its specific receptor has been compared to a lock (receptor) & key (hormone) arrangement, in which only the correct key can unlock a given action within the cells. The combination of hormone bond to its receptor is referred to as a hormone-receptor complex. Receptors for nonsteroid hormones are located on the cell membrane, whereas receptors for steroid hormones are found either in the cell’s cytoplasm or in its nucleus. Each hormone is usually specific for a single type of receptor & binds only with its specific receptors, thus affecting only tissues that contain those specific receptors. The Mechanism of Action of a Steroid Hormones, Leading to direct gene activation Steroid hormones pass easily through the cell membrane. Once inside the cell, a steroid hormone binds to its specific receptors. The hormone-receptor complex then enters the nucleus, binds to part of the cell’s DNA, & activates certain genes. This process is referred to as direct gene activation. In response to this activation, mRNA is synthesized within the nucleus. The mRNA then enters the cytoplasm & promotes protein synthesis. These proteins may be: enzymes that can have numerous effects on cellular processes, structural proteins to be used for tissue growth & repair, or regulatory proteins that can alter enzymes function. The Mechanism of Action of a Nonsteroid Hormones, Using a second messenger within the cell Nonsteroid hormones cannot cross the cell membrane; they react with specific receptors outside the cell, on the cell membrane. A nonsteroid hormone molecule binds to its receptor and triggers a series of enzymatic reactions that lead to the formation of an intracellular second messenger : cyclic adenosine monophosphate (cyclic AMP, or cAMP). Attachment of the hormone to membrane receptor activates an enzyme, adenylate cyclase, situated within the cell membrane. This enzyme catalyzes the formation of cAMP from cellular ATP. cAMP can then produce specific physiological responses, which may include: activation of cellular enzymes, change in membrane permeability, promotion of protein synthesis, or stimulation of cellular secretions. Thus, nonsteroid hormones typically activate the cAMP system of the cell, which then leads to changes in intracellular functions. 2
Chapter 8. Hormonal Regulation of Exercise
3. Control of Hormone Release
Hormone released can be fluctuating over short periods (an hour or less) or over longer periods of time (daily or even monthly cycle: monthly menstrual cycle). Most hormone secretion is regulated by a negative feedback system. Secretion of a hormone causes some change in the body, and this change in turn inhibits further hormone secretion. Negative feedback is the primary mechanism through which the endocrine system maintains homeostasis. The number of receptors on a cell can be altered to increase or decrease that cell’s sensitivity to a certain hormone. Up-regulation (sensitization) refers to an increase in receptors, thus the cell becomes more sensitive to that hormone because more can be bound at one time. Down-regulation (desensitization) refers to a decrease in receptors, thus the cell becomes less sensitive to that hormone because with fewer receptors, less hormone can bind.
SUMMARY 1.
Hormones can be classified as either steroid or nonsteroid.
2.
Steroid hormones are lipid soluble, and most are formed from cholesterol. Nonsteroid hormones are formed from proteins, or amino acids.
3.
Hormones are generally secreted into the blood and then through the body to exert an effect only on their target cells. They act by binding in a lock-and-key manner with specific receptors found only in the target tissues.
4.
Steroid hormones pass through cell membranes and bind to receptors inside the cell. They use a mechanism called direct gene activation to cause protein synthesis.
5.
Nonsteroid hormones cannot enter the cells easily, so they bind to receptors on the cell membrane. This activates a second messenger within the cell, which in turn can trigger numerous cellular processes.
6.
A negative feedback system regulates secretion of most hormones.
7.
The number of receptors for a specific hormone can be altered to meet the body’s demands. Up-regulation refers to an increase in receptors, and down-regulation is a decrease. These two processes change cell sensitivity to hormones. 3
Chapter 8. Hormonal Regulation of Exercise
B. The Endocrine Glands & Their Hormones 1. The Pituitary Gland (or the Hypophysis)
Anterior lobe: Hormone 1 : Growth hormone (GH). Target organ: All cells in the body. Major functions: Promotes development & enlargement of all body tissues up through maturation (growth of bone & muscle); increases rate of protein synthesis; increases mobilization of fats and use fat as an energy source; decreases rate of carbohydrate use (sparing glucose). Hormone 2 : Prolactin (PRL). Target organ: Breasts. Major functions: Stimulates breast development & milk secretion (promotes lactation). Hormone 3 : Thyrotropin or Thyroid-stimulating hormone (TSH). Target organ: Thyroid gland. Major functions: Controls the amount of thyroxin & triiodothyronine produced & released by the thyroid gland (promotes release of thyroid hormones). Hormone 4 : Adrenocorticotropin (ACTH). Target organ: Adrenal cortex. Major functions: Controls the secretion of hormones from the adrenal cortex. Hormone 5 : Follicle-stimulating hormone (FSH). Target organ: Ovaries, testes. Major functions: Females - initiates growth & maturation of follicles in the ovaries & promotes secretion of estrogen from the ovaries. Males – promotes development or production of sperm in testes. Hormone 6 : Luteinizing hormone (LH). Target organ: Ovaries, testes. Major functions: Females – promotes secretion of estrogen & progesterone and cause the follicle to rupture, releasing the ovum. Males – causes testes to secrete testosterone.
Posterior lobe: Hormone 1 : Antidiuretic hormone (ADH or vasopressin). Target organ: Kidneys. Major functions: Assists in controlling water excretion by the kidneys; elevates blood pressure by constricting blood vessels. 4
Chapter 8. Hormonal Regulation of Exercise
Hormone 2 : Oxytocin. Target organ: Uterus, breasts. Major functions: Stimulates contraction of uterine muscles & milk secretion.
2. Thyroid Gland Hormone 1 : Triiodothyronine (T 3) & Thyroxine (T 4). Target organ: All cells in the body. Major functions: Increases the rate of cellular metabolism; increases rate & contractility of the heart. Hormone 2 : Calcitonin. Target organ: Bones. Major functions: Control calcium ion concentration in the blood.
3. The parathyroid Gland Hormone: Parathyroid hormone (PTH/parathormone). Target organ: Bones, intestines, & kidneys. Major functions: Control calcium ion concentration in extracellular fluid through its influence on bones, intestines, and kidneys.
4. The Adrenal Gland
Medulla Hormone 1 : Catecholamine (Epinephrine 0r Adrenaline). Target organ: Most cells in the body. Major functions: Mobilizes glycogen; increases skeletal muscle blood flow; increases heart rate & contractility; oxygen consumption. Hormone 2 : Catecholamine (Norepinephrine or Noradrenaline). Target organ: Most cells in the body. Major functions: Constricts arterioles & venules, thereby elevating blood pressure.
Cortex Hormone 1 : Mineralocorticoids (aldosterone). Target organ: Kidneys. Major functions: Increase sodium (NA+) retention & potassium (K +) excretion through the kidneys. 5
Chapter 8. Hormonal Regulation of Exercise
Hormone 2 : Glucocorticoids (cortisol). Target organ: Most cells in the body. Major functions: Controls metabolism of carbohydrates, fats, & proteins; antiinflammatory action. Hormone 3 : Gonadocorticoids (androgens & estrogens). Target organ: Ovaries, breasts, & testes. Major functions: Assists in the development of female & male sex characteristics.
5. The Pancreas Hormone 1 : Insulin. Target organ: All cells in the body. Major functions: Controls blood glucose levels by lowering glucose levels; increases use of glucose & synthesis of fat. Hormone 2 : Glucagon. Target organ: All cells in the body. Major functions: Increases blood glucose; stimulates the breakdown of fats & proteins. Hormone 3 : Somatostatin. Target organ: Islets of Langerhans & gastrointestinal tracts. Major functions: Depresses the secretion of both insulin & glucagons.
6. The Gonads
Testes Hormone : Testosterone. Target organ: Sex organs, muscle. Major functions: Promotes development of male sex characteristics, including growth of testes, scrotum, & penis, facial hair, & change in voice; promotes muscle growth. Ovaries Hormone : Estrogen & progesterone. Target organ: Sex organs, adipose tissue Major functions: Promotes development of female sex organs & characteristics; provides increased storage of fat, assists in regulating the menstrual cycle.
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Chapter 8. Hormonal Regulation of Exercise
7. The Kidneys Hormone 1 : Renin. Target organ: Adrenal cortex. Major functions: Assists in blood pressure control. Hormone 2 : Erythropoietin. Target organ: Bone marrow. Major functions: Erythrocyte production.
C. Hormonal Effects on Metabolism & Energy
CHO & fat metabolism are responsible for maintaining muscle ATP levels during prolonged exercise. Various hormones work to ensure glucose & FFA availability for muscle energy metabolism.
1. Regulation of Glucose Metabolism During Exercise For the body to meet the energy demands of exercise, more glucose must be available to the muscle. Glucose is stored in the body as glycogen, primarily in the muscles & the liver. Glucose must be freed from storage, so glycogenolysis must increase. So glucose freed from the liver enters the blood to circulate throughout the body. (Glycogenolysis = the conversion of glycogen to glucose) Plasma glucose levels can also be increased through gluconeogenesis. (Gluconeogenesis = the conversion of protein or fat into glucose)
Plasma Glucose Level 4 hormones work to increase the amount of plasma glucose (involved in both glycogenolysis & gluconeogenesis) are: glucagon, epinephrine, norepinephrine, & cortisol. At rest, glucose release from the liver is facilitated by glucagon, which promotes liver glycogen breakdown (glycogenolysis) and glucose formation from amino acids (gluconeogenesis). During exercise, glucagon secretion increases. Muscular activity also increases the rate of catecholamine release from adrenal medulla, & these hormones (epinephrine & norepinephrine ) work with glucagon to further increase glycogenolysis. Cortisol levels also increase during exercise. Cortisol increases protein catabolism, freeing amino acid to be used within the liver for gluconeogenesis. Thus, all 4 of these hormones can increase the amount of plasma glucose by enhancing the processes of glycogenolysis & gluconeogenesis. 7
Chapter 8. Hormonal Regulation of Exercise
Glucose Uptake by the muscles Releasing sufficient amounts of glucose into the blood does not ensure that the muscle cells will have enough glucose to meet their energy demands. The glucose must not only be delivered to these cells, it must also be taken up by the muscle cells. This job relies on insulin. Once glucose is delivered to the muscle, insulin facilitates its transport into the muscle fibers. Insulin helps the released glucose enter the muscle cells, where it can be used for energy production. But insulin levels decline during prolonged exercise, indicating that exercise facilitates the action of insulin so that less of the hormone is required during exercise than at rest.
2. Regulation of Fat Metabolism During Exercise During prolonged endurance exercise, CHO reserves become depleted, & the body must rely more heavily on the oxidation of fat for energy production. When CHO reserves are low (low plasma glucose & low muscle glycogen), the endocrine system can accelerate the oxidation of fats (lipolysis) to produce energy. Lipolysis is also enhanced through the elevation of epinephrine & norepinephrine.
FFA are stored as triglycerides in fat cells & inside muscle fiber. Adipose tissue triglycerides however must be broken down to release the FFA, which are then transported to the muscle fibers. Triglycerides are reduced to FFA & glycerol by a special enzyme called lipase, which is activated by at least 4 hormones: cortisol; growth hormone; epinephrine, & norepinephrine. Cortisol also accelerates the mobilization & use FFA for energy during exercise. Plasma cortisol levels peak after 30-45 min of exercise then decrease to normal levels. Growth hormone & catecholamine (epinephrine & norepinephrine) continue to activate the mobilization & metabolism of FFA.
D. Hormonal Effects on Fluid & Electrolyte Balance During Exercise
The two primary hormones involved in the regulation of fluid balance are aldosterone & antidiuretic hormone (ADH).
1. Aldosterone & the Renin-Angiotensin Mechanism When plasma volume or blood pressure decreases, the kidneys form an enzyme called renin that converts angiotensinogen into angiotensin I, which later becomes angiotensin II. Angiotensin II increases peripheral arterial resistance, raising the blood pressure.
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Chapter 8. Hormonal Regulation of Exercise
Angiotensin II also triggers the release of aldosterone from the adrenal cortex. Aldosterone promotes sodium reabsorption in the kidneys, which in turn causes water retention, thus increasing the plasma volume.
** The influence of water loss from plasma during exercise leads to a sequence of events that promotes sodium (Na +) & water reabsorption from renal tubules, thereby reducing urine production. In the hours after exercise when fluids are consumed, the elevated aldosterone levels cause an increase in the extracellular volume and an expansion of plasma volume.
1. Muscular activity promotes sweating and increases blood pressure. 2. Sweating reduces plasma volume and blood flow to the kidneys. 3. Reduced renal blood flow stimulates rennin release from the kidneys. Renin leads to the formation of angiotensin I, which is converted to angiotensin II. 4. Angiotensin II stimulates the release of aldosterone from the adrenal cortex. 5. Aldosterone increases Na+ and H2O reabsorption from the renal tubules. 6. Plasma volume increases & urine production decreases.
2. Antidiuretic Hormone (ADH) ADH is released in response to increased plasma osmolarity (= the ratio of solute to fluid). When osmoreceptors in the hypothalamus sense this increase, the hypothalamus triggers ADH release from the posterior pituitary.
ADH acts on the kidneys promoting water conservation. Through this mechanism, the plasma volume is increased, which results in dilution of the plasma solutes. Blood osmolarity decreases.
** The mechanism by which ADH conserves body water.
1. Muscular activity promotes sweating. 2. Sweating causes loss of blood plasma, resulting in hemoconcentration & increased blood osmolarity. 3. Increased blood osmolarity stimulates the hypothalamus. 4. The hypothalamus stimulates the posterior pituitary gland to secrete ADH. 5. ADH acts on the kidneys, increasing the water permeability of the renal tubules & collecting ducts, leading to increased reabsorption of water. 6. Plasma volume increases, so blood osmolarity decreases after exercise and water ingestion.
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Chapter 8. Hormonal Regulation of Exercise
SUMMARY 1.
Plasma glucose is increased by the combined actions of glucagon, epinephrine, norepinephrine, & cortisol. These hormones promote glycogenolysis & gluconeogenesis, thus increasing the amount of glucose available for use as a fuel source.
2.
Insulin helps the released glucose enter the muscle cells, where it can be used for energy production. But insulin levels decline during prolonged exercise, indicating that exercise facilitates the action of insulin so that less of the hormone is required during exercise than at rest.
3.
When carbohydrate reserves are low, the body turns more to fat oxidation for energy, and this process is facilitated by cortisol, epinephrine, norepinephrine & growth hormone.
4.
Cortisol accelerates lipolysis, releasing free fatty acids (FFA) into the blood so they can be taken up by the cells & used for energy production. But cortisol levels peak & than return to near normal levels during prolonged exercise. When this happens, the catecholamines & growth hormone (GH) taken over cortisol’s role.
5.
The two primary hormones involved in the regulation of fluid balance are aldosterone & antidiuretic hormone (ADH).
6.
When plasma volume or blood pressure decreases, the kidneys form an enzyme called rennin that converts angiotensinogen into angiotensin I, which later becomes angiotensin II. Angiotensin II increases peripheral arterial resistance, raising the blood pressure.
7.
Angiotensin II also triggers the release of aldosterone from the adrenal cortex. Aldosterone promotes sodium reabsorption in the kidneys, which in turn causes water retention, thus increasing the plasma volume.
8.
ADH is released in response to increased plasma osmolarity (= the ratio of solute to fluid). When osmoreceptors in the hypothalamus sense this increase, the hypothalamus triggers ADH release from the posterior pituitary.
9.
ADH acts on the kidneys promoting water conservation. Through this mechanism, the plasma volume is increased, which results in dilution of the plasma solutes. Blood osmolarity decreases.
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SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Hormonal Regulation of Exercise) Name : _______________________________________
Group : _________
Date: ______________
Answer ALL questions.
1. Endocrine glands secrete their _______________________________________________________. 2. Steroid hormones hormones use a mechanism mechanism called ________________________________ to to cause protein synthesis. 3. A ___________________________ activates a second messenger (cAMP) system system within the cell, which leads to changes in the intracellular functions. 4. Most hormone secretion is regulated by a _______________________________________ system. 5. ______________________ hormone increases mobilization of fats and use fat as an energy source. 6. ______________________ promotes lactation. 7. ______________________ hormone controls the secretion of hormones from from the adrenal cortex. 8. ______________________ hormone helps in controlling water excretion excretion by the kidneys. 9. ______________________ stimulates stimulates contraction contraction of uterine muscles muscles and initiates labor. 10. ______________________ control calcium ion concentration concentration in the blood when hypercalcemia. 11. ______________________ gland releases the hormone epinephrine when an athlete is exercising. +
+
12. ______________________ increases sodium (Na ) retention & potassium (K ) excretion through the kidneys. 13. The two primary hormones involved in the regulation of blood glucose are ____________________ and ____________________. 14. _______________________ stimulates the production of erythrocytes. 15. Plasma glucose is increased by the combined combined actions of ___________________________________ ________________________________________. 16. _______________________ helps the released glucose enter the muscle cells, where it can be used for energy production. 17. __________________ accelerates lipolysis and use free fatty acids (FFA) for energy during exercise. 18. The two primary hormones involved in the regulation of fluid balance are _________________ ____ and _________________________. +
19. ______________________ increases sodium (Na ) and water reabsorption from the renal tubules. 20. ______________________ acts on the kidneys promoting promoting water conservation. Hormonal Regulation of Exercise
1
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QUESTION 1 List and briefly explain the specific action of the two hormones produced and released by the adrenal medulla.
Two Hormones: 1) _____________________________ &
2) ________________________________
The combined effects include: 1) ________________________________________________________________________________ 2)
_______________________________________________________________________________
3)
_______________________________________________________________________________
4)
_______________________________________________________________________________
5)
_______________________________________________________________________________
6)
_______________________________________________________________________________
7)
_______________________________________________________________________________
8)
_______________________________________________________________________________
QUESTION 2 Describe briefly the hormones involved in the regulation of glucose metabolism during exercise.
1) ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ 2) ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
Hormonal Regulation of Exercise
2
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
QUESTION 3 Describe the mechanism by which antidiuretic hormone (ADH) conserves body water during exercise.
The ADH Mechanism: 1)
________________________________________________________________________________
2)
________________________________________________________________________________ ________________________________________________________________________________
3)
________________________________________________________________________________
4)
________________________________________________________________________________
5)
________________________________________________________________________________ ________________________________________________________________________________
6)
________________________________________________________________________________ ________________________________________________________________________________
QUESTION 4 Briefly discuss the aldosterone and renin-angiotensin mechanism that regulates fluid and electrolyte balance during exercise.
The aldosterone and renin-angiotensin mechanism: 1)
________________________________________________________________________________
2)
________________________________________________________________________________
3)
________________________________________________________________________________ ________________________________________________________________________________
4)
________________________________________________________________________________
5)
________________________________________________________________________________
6)
________________________________________________________________________________
Hormonal Regulation of Exercise
3
UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
QUESTION 5 Identify the four (4) mechanisms involved in maintaining the plasma glucose concentration.
1) ________________________________________________________________________________ ________________________________________________________________________________ 2) ________________________________________________________________________________ ________________________________________________________________________________ 3) ________________________________________________________________________________ ________________________________________________________________________________ 4) ________________________________________________________________________________
Hormonal Regulation of Exercise
4
Chapter 9. Thermal Regulation & Exercise
THERMAL REGULATION AND EXERCISE A. Mechanisms of Body Temperature Regulation
Humans are homeothermic, meaning that they maintain a constant internal body temperature, usually in the range of 36.1 oC to 37.8oC (97.0oF – 100.0oF).
Body temperature reflects the balance between heat production & heat loss. Whenever this balance is disturbed, the body temperature changes.
All metabolically active tissues produce heat that can be used to maintain the internal temperature of the body. But if the body’s heat production exceeds its heat loss, the internal temperature rises.
The ability to maintain a constant internal temperature depends on the body ability to balance the heat gain from metabolism & from the environment with the heat that the body loses
Metabolic heat + Environmental heat
HEAT GAIN
Conduction + Convection + Radiation + Evaporation
HEAT LOSS
The balance of body heat gain and loss (at temperatures below 92°F)
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Chapter 9. Thermal Regulation & Exercise
1. The Transfer of Body Heat
Heat gain from tissue metabolic & environment. The body heat from deep in the body (the core) is moved by the blood to the skin (the shell).
Heat can be transferred to the environment by any of 4 mechanisms or avenues:
Conduction – transfer of heat from one material to another through direct molecular contact.
Convection – transfer of heat from one place to another by the motion of a gas or a liquid across the heated surface.
Radiation – transfer of heat through electromagnetic waves; the primary method for discharging the body’s excess heat at rest.
Evaporation – transfer heat through the conversion of water (such as in sweat) to vapor; the primary avenue for heat dissipation during exercise.
Control of heat loss
Higher humidity decreases the capacity to lose heat by evaporation because the air already contains many water molecules.
2. Control of Heat Exchange
Internal body temperature when at rest is kept at approximately 37 oC (99oF), but during exercise can develop an internal temperature exceeding 40 oC (104oF).
The Hypothalamus : The Thermostat The hypothalamus houses the thermoregulatory center. It acts like a thermostat – monitoring the body temperature & accelerating heat loss or heat production as needed.
There are 2 sets of thermoreceptors provide & send temperature information to the thermoregulatory center in the brain: 1. The peripheral receptors in the skin relay information about temperature of the skin & the environment around it. 2. Central receptors in the hypothalamus transmit information about the internal body temperature. 2
Chapter 9. Thermal Regulation & Exercise
Hypothermia
Low body temperature
Stimulates thermoreceptors
Hyperthermia
High body temperature
Stimulates thermoreceptors
Impulses go to hypothalamus
Impulses go to hypothalamus
Vasoconstriction occurs in skin blood vessels
Vasodilation occurs in skin blood vessels
So less heat is lost across the skin
Skeletal muscle are activated
Causing Shivering & generates heat
Body temperature increases
So more heat is lost across the skin
Sweat glands become more active
Causing Evaporative heat loss
Body temperature decreases
An overview of the role of the hypothalamus in controlling body temperature
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Chapter 9. Thermal Regulation & Exercise
Effectors That Alter Body Temperature When body temperature fluctuates, the normal body temperature can usually be restored/alter by the actions of 4 effectors:
1. Increased sweat gland activity decreases body temperature by increasing evaporative heat loss. 2. Smooth muscle in the arterioles can dilate to direct blood to the skin for heat transfer, or constrict to retain heat deep in the body. 3. Increased skeletal muscle activity will increases body temperature by increasing metabolic heat production. 4. Metabolic heat production can be increased by the action of hormone (endocrine glands ) like thyroxine and catecholamines..
3. Assessing Mean Body Temperature
Mean Body Temperature (T body) is a weighted average of skin temperature and internal body temperature.
Body heat content is the total amount of heat in kilocalories that it contains.
Rate of Heat Exchange can be estimated form calculations of body heat content. If Heat Content remains constant during a long period of exercise therefore thermoregulatory system is efficient.
B. Physiological Responses to Exercise in the Heat 1. Cardiovascular Function
Exercising in the hot environments set up a competition between the active muscles & the skin for limited blood supply. The working muscles need blood & the O2 it delivers to sustain activity; the skin needs blood to facilitate heat loss to keep the body cool.
To maintain constant cardiac output in this condition where stroke volume has decreased, resulting in a gradual upward drift in HR. This is known as cardiovascular drift.
CV drift = An increased in HR during exercise to compensate for a decrease in SV. This compensation helps to maintain a constant cardiac output. 4
Chapter 9. Thermal Regulation & Exercise
2. Energy Production
Exercise in the heat also increases O2 uptake, therefore increase glycogen use by working muscle & produce more lactate. Thus exercise in the heat can cause glycogen depletion and increase muscle lactate, thus leads to fatigue & exhaustion.
Hot environment places greater stress on CV system, which raises the HR & also increased sweat production and respiration demand more energy, which requires a higher O2 uptake.
3. Body Fluid Balance: Sweating
Exercise in the heat increases sweating & this can quickly lead to dehydration and electrolyte loss. To compensate, the release of aldosterone & ADH increases, causing sodium & water retention, this can expand the plasma volume.
C. Health Risks During Exercise in the Heat
Heat stress involves more than just the air temperature. In observing the total physiological stress imposed on the body during exercising in a hot environment. At least 4 variables must be taken into account: 1. 2. 3. 4.
Air temperature Humidity Air velocity The amount of radiation.
1. Measuring Heat Stress
Wet Bulb Globe Temperature (WBGT) most accurate means to measure heat stress.
WBGT = A system that simultaneously accounts for conduction, convection, evaporation, & radiation, providing a single temperature reading to estimate the cooling capacity of surrounding environment. This apparatus consists of dry bulb, a wet bulb, & a black globe.
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Chapter 9. Thermal Regulation & Exercise
2. Heat-Related Disorders
a. Heat cramps Severe cramping of skeletal muscles that are most heavily used during exercise.
Probably caused by losses of fluids and minerals results from excessive sweating.
b. Heat exhaustion Rise of body temperature, extreme fatigue, breathlessness, hypotension, and a weak, rapid pulse results from the inability of the CV system to adequately meet the needs of the active muscles and skin.
Result from the inability of the CV system to adequately meet the needs of the active muscle & skin. It is brought on by a reduced blood volume, typically caused by excessive loss of fluids and minerals through prolonged heavy sweating. Though it is not in itself life-threatening, it can deteriorate to heat stroke if untreated.
c. Heat stroke Rise in internal body temperature to values exceeding 40 oC, rapid pulse & respiration, cessation of sweating, hot & dry skin, hypertension, and total confusion and unconsciousness caused by failure of the body’s thermoregulatory mechanisms.
If untreated it will progress and be fatal (death).
Prevention of Hyperthermia Several precautions must be taken when planning to exercise in the heat.
a. b. c. d.
Cancel training or event if WBGT > 28°C (82.4°F). Wear proper clothing. Be alert to the signs of hyperthermia. Ensure adequate fluid intake.
* When exercising in the heat, if the body suddenly fell chilled & goose bumps form on the skin, stop exercising, get into a cool environment, & drink plenty of cool fluids. The body’s thermoregulation system has become confused & thinks that body temperature needs to increase even more! If left untreated, this condition can lead to heat stroke & death. 6
Chapter 9. Thermal Regulation & Exercise
D. Acclimatization to Exercise in the Heat
Acclimatization – natural adaptation to an environmental stress. 1. How can we prepare for prolonged activity in the heat? 2. Does training in the heat make us more tolerant of thermal stress?
Repeated exercise in the heat causes a gradual adjustment that enables us to perform better in the hot conditions.
Heat acclimatization
Heat acclimatization is an adaptation of gradual improvement in ability to eliminate excess body heat during repeated exposure to heat stress (prolonged exercise bouts in the hot environment). Results in many adjustments in sweating & blood flow.
1. Effects of Heat Acclimatization
a. Increase sweat rate Therefore, increase heat loss through evaporation, hence reduces skin temperature, increasing the thermal gradient from the internal to the external body, promoting heat loss.
b. Sweat is more diluted Therefore, electrolytes are conserved and body is losing mainly water which can be easily replaced.
c. SV increases Therefore, increases blood flow and aids the delivery of more blood to the active or working muscles and skin when necessary.
d. Reduces the rate of muscle glycogen use for energy Therefore, more glycogen reserves and less lactate production, hence delaying the onset of fatigue.
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Chapter 9. Thermal Regulation & Exercise
2. Achieving Heat Acclimatization
Heat acclimatization requires exercise in a hot environment, not merely exposure to heat.
Amount of heat acclimatization depends on :a) Environmental conditions during each exercise session. b) Duration of heat exposure. c) Rate of internal heat production.
* You can adapt to heat by exercising in the heat for up to an hour or more each day for 5 – 10 days. Cardiovascular changes generally occur in the first 3 – 5 days, but changes in the sweating mechanisms generally take much longer, up to 10 days.
E. Exercise in the Cold
Cold stress = any environmental condition that causes a loss of body heat that threatens homeostasis.
Hypothalamus has a temperature set point of 37 oC.
A decrease in either skin or blood temperature provides feedback to the thermoregulatory center (hypothalamus) to activate the mechanisms that will conserve body heat & increase heat production.
This primary means by which the body to avoid excessive cooling: a) Shivering The involuntary muscle contractions increase metabolic heat production to help the body maintain or increase temperature. b) Nonshivering thermogenesis Involves stimulation of metabolism by the sympathetic nervous system & by the action of hormone thyroxine & catecholamines. Increasing the metabolic rate increases the amount of internal heat production. c) Peripheral vasoconstriction Occurs as a result of sympathetic stimulation to smooth muscle surrounding the arterioles, which constricts the arterioles & reduces the blood flow to the skin & prevents transfer of core heat to the skin, thus decreasing unnecessary heat loss to the environment. 8
Chapter 9. Thermal Regulation & Exercise
1. Factors Affecting Body Heat Loss a) Body size and composition Body size is an important consideration for heat loss. Both increased surface area & reduced subcutaneous fat facilitate the loss of body heat to the environment. So those who have a small surface-area-to-body-mass ratio & those with more fat are less susceptible to hypothermia. b) Windchill Wind increases heat loss by convection and conduction, so this effect, know as windchill, must be considered along with air temperature during cold exposure.
2. Heat Loss in Cold Water
Immersion in cold water tremendously increases heat loss through conduction. Exercise generates metabolic heat to offset some of this loss.
F. Physiological Responses to Exercise in the Cold 1. Muscle Function When muscle is cooled, it is weak, & fatigue occurs more rapidly. 2. Metabolic Responses During prolonged exercise in the cold, as energy supplies diminish & exercise intensity declines, a person become increasingly susceptible to hypothermia.
Exercise triggers release of catecholamines, which increase the mobilization & use of free fatty acids for fuel. But in the cold, vasoconstriction impairs circulation to the subcutaneous fat tissue, so this process is attenuated.
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Chapter 9. Thermal Regulation & Exercise
G. Health Risks During Exercise in the Cold
Hypothalamus begins to lose its ability to regulate body temperature if that temperature drops below 34.5oC (94.1oF)
1. Hypothermia The Heart’s SA node is primarily affected by hypothermia, causing HR to drop, which in turn reduces cardiac output.
Breathing cold air does not freeze the respiratory passages or the lungs.
Exposure to extreme cold does decreases respiratory rate and volume.
2. Frostbite Occurs as a consequence of the body’s attempts to prevent heat loss.
Vasoconstriction to the skin causes reduces blood flow, so the skin cools rapidly. This, combined with the lack of oxygen & nutrients, causes the skin tissues to die.
H. Cold acclimatization
Repeated exposure to cold alters peripheral blood flow and skin temperatures, allowing greater cold tolerance.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Thermal Regulation & Exercise) Name : _______________________________________
Group : _________ Date : _______________
Answer ALL questions.
1. What are the four major avenues for loss of body heat? a. __________________________
c. __________________________
b. __________________________
d. __________________________
2. What is cardiovascular drift? Why might this be a problem with prolonged exercise in high intensities? a.
________________________________________________________________________ ________________________________________________________________________ ________________________________________________________________________
b.
________________________________________________________________________ ________________________________________________________________________ ________________________________________________________________________ ________________________________________________________________________ ________________________________________________________________________ ________________________________________________________________________
3. Differentiate between heat cramps, heat exhaustion, and heat stroke. a. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ c.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 1
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4. Define heat acclimatization. ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
5. Discuss the physiological adaptations occur that allow a person to acclimatize to exercise in the hot environment. a. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ c.
_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
d. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
6. Identify and describe briefly the means by which the body avoids excessive cooling during exercise in the cold. a. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ b. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ c.
____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________
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Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
EXERCISE IN HYPOBARIC & HYPERBARIC ENVIRONMENTS Hypobaric environment Low atmospheric pressure. Barometric pressure is reduced at altitude. (e.g.: mountain) Lower atmospheric pressure also means lower partial pressure of oxygen (PO 2), which limits pulmonary diffusion and low O 2 transport to tissue. This reduces O2 delivery to the body tissue, resulting in hypoxia (O2 deficiency).
Hyperbaric environment High atmospheric pressure. (e.g.: underwater world) High partial pressure of certain gases can lead to life-threatening complication.
Microgravity Low gravitational force. (e.g.: environment in the outer space)
A. Hypobaric Environment: Exercising at Altitude
The term altitude refers to elevations above 1500 m (4,921 ft). Altitude presents a hypobaric environment which the atmospheric pressure is reduced. Altitudes of 1500 m or above have a physiological impact on the human body. Hypobaric Environment – an environment, such as that at high altitude, involving low atmospheric pressure.
1. Conditions at Altitude i. Atmospheric pressure
At Sea level, the barometric pressure (Pb) averages = 760 mmHg Summit of Mount Everest, barometric pressure (Pb) = 250 mmHg Therefore, barometric pressure is low at altitude. The % of gases in the air remain unchanged at altitude (O 2 = 20.93%, CO2 = 0.03%, & N2 = 79.04%). The partial pressures of each gas, is reduced in direct proportion to the increase in altitude. 1
Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
The reduced partial pressure of O 2 leads to decreased performance at altitude due to a reduced pressure gradient that hinder O 2 transport to the tissue. Differences in atmospheric conditions at sea level & at an altitude
Atmospheric Pressure Partial Pressure of O2 Ambient temperature
At sea level 760 mmHg 159.2 mmHg 15oC
At 8,900m 250 mmHg 48.4 mmHg -40oC
*Mount Everest (8,848m = 29,028 ft)
ii. Air Temperature
Air temperature decreases as altitude increases. Air temperature drops about 1 oC for every 150m (490 ft) of ascent (Mt. Everest = -40 oC). Cold air holds very little water, so the air at altitude is dry. humidity of the air is low The dry air increased evaporative water loss through sweating during exercise at altitude. The cold & dry air can lead to cold-related disorders & dehydration through increased insensible water loss.
iii. Solar Radiation
The intensity of solar radiation increases at high altitude because the atmosphere is thinner & drier.
2. Physiological Responses to Altitude
The hypoxic conditions (diminished O 2 supply) at altitude alter the body’s normal physiological responses.
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Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
i. Respiratory Responses
Pulmonary ventilation (breathing) increases at higher altitudes, when at rest & during exercise.
Because the number of O2 molecules in air is less, more air must be inspired to supply as much 02 during normal breathing at sea level.
Ventilation increases to bring in a larger volume of air.
People ventilate greater volumes of air at altitude because air is less dense.
Increased ventilation resulting in hyperventilation state in which too much CO 2 can be cleared & allows blood pH to increase, leading to respiratory alkalosis. In response, the kidneys excrete more bicarbonate ion, so less acid can be buffered. Pulmonary diffusion is not hinder by altitude, but O2 transport is slightly impaired because hemoglobin saturation at altitude is reduced, although by only a small amount.
The diffusion gradient that allows O2 exchange between the blood & active tissue is substantially reduced at elevation, thus O 2 uptake is impaired. This is partially compensated for by a decrease in plasma volume, concentrating the RBCs & allowing more O2 to be transported per unit of blood. Maximal O2 consumption decreases along atmospheric pressure. As the partial pressure of O2 decreases, VO2max (Maximal O2 uptake) decreases at a progressively greater rate.
Maximum O2 uptake decreases since PO 2 decreases. At sea level VO 2max = 50ml/kg/min but, at Mt. Everest peak, VO2max can be as low as 5ml/kg/min.
ii. Cardiovascular Responses
During submaximal work at altitude, the body increases its cardiac output, by increasing the heart rate, to compensate for the decrease in the pressure gradient that drives O2 exchange. During maximal work, stoke volume & heart rate are both lower, resulting in a reduced cardiac output. This combined with the decreased pressure gradient severely impairs O2 delivery & uptake. 3
Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
iii. Metabolic Responses
Because O2 delivery is restricted at altitude, oxidative capacity is decreased. More anaerobic energy production must occur, as evidenced by increased blood lactate levels for a given submaximal work rate. However, at maximal work rate, lactate levels are lower, perhaps because the body must work at a rate that cannot fully stress the energy systems. *lactate = A salt formed from lactic acid.
3. Performance at Altitude
Endurance activities are severely affected because oxidative energy production is limited. Anaerobic sprint activities (<1 min) are generally not impaired at moderate altitude. This is because thinner air imposes less resistance to movement. This explains the amazing performances of sprinters & long jumpers at the 1968 Olympics in Mexico City. Exhaustive activities – at altitude, less lactate is produced (actually should increase) due to decrease in muscle in muscle enzyme activities and total work.
4. Acclimatization: Prolonged Exposure to Altitude i. Blood adaptations
Hypoxic conditions stimulate the release of erythropoietin (EPO), which increases erythrocyte (RBC) production. More RBC means more hemoglobin. These adaptations improve the oxygen-carrying capacity of the blood. Although plasma volume decreases initially (within a few hours of arrival at altitude as a result of fluid shifts and respiratory water loss), which also concentrates the erythrocytes (RBC) - hemoglobin, this changes also increasing the blood’s oxygencarrying capacity.
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Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
ii. Muscle adaptations
Muscle fiber areas decrease when at altitude, thus decreasing total muscle area. Total muscle mass & total body weight decrease. Part of this is from dehydration and appetite suppression, which leads to protein breakdown in the muscles. Metabolic enzyme activities in the muscle also decreased. Capillary density in the muscle increased, which allow more blood & oxygen to be delivered to the muscle.
iii. Cardiorespiratory adaptations
Increased in pulmonary ventilation both at rest and during exercise. Ventilation is stimulated by the decreased O 2 content of the inspired air. Decreased in VO 2 max with initial exposure to altitude does not improve much (or improve very little) during several weeks of exposure.
5. Physical Training & Performance
Most studies show that training at altitude leads to no significant improvement of sea-level performance. The physiological changes that do occur, such as increased RBC production, are transient but could offer an advantage during the first few days after returning to sea level. This is still an area of debate. Athletes who must perform at altitude should do so within the first 24 hours of arrival while the detrimental changes that occur have not yet become too great. Alternatively, athletes who must perform at altitude could train at an altitude of 1500 m to 3000 m for at least 2 weeks prior to performing. This allows the body time to adapt to hypoxic & other environmental conditions at altitude.
6. Clinical Problems of Acute Exposure to Altitude
Acute altitude sickness typically causes symptoms such as headaches, nausea, vomiting, dyspnea, & insomnia. These usually appear in 6 to 96 hr after arrival at altitude. The exact cause of acute altitude sickness is not known, but many researchers suspect the symptoms may result from carbon dioxide accumulation in the tissues. 5
Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
Acute altitude sickness can usually be avoided by a gradual ascent to altitude; climbing not more than 300 m per day at elevations above 3000 m. Medications can also be used to reduce the symptoms. High-altitude pulmonary edema (HAPE) & high-altitude cerebral edema (HACE), which involve accumulation of fluid in the lungs & cranial cavity, respectively, are life-threatening conditions. Both are treated by O 2 administration & descent.
B. Hyperbaric Conditions: Exercising Underwater 1. Water Immersion & Gas Pressures
Submersion in water exposes the human body to a hyperbaric environment where external pressure is greater than at sea level. Because volume decreases when pressure increases. Therefore, air that is in the body before it goes underwater is compressed when the body is submerged. Conversely, the air taken in at depth expands during ascent. When the body is submerged, more molecules of gases are forced into solution, but with a rapid ascent, the molecule come out of solution and can form bubbles.
2. Cardiovascular Response to Water Immersion
Water reduces the stress on the CV system, reducing its work load. When the body is submerged, plasma volume also increases. Because of these factors, resting H R drops even when the body is only partially submerged. This effect is enhanced by cold water. Hyperventilation is often practiced before breath-hold diving to increase how long you can hold your breath. But this can lead to dangerously low O2 levels, which can cause you to lose consciousness underwater. During breath-hold diving, the gases in the body can become pressurized even when swimming at a depth of only 1 to 2 m below the surface. At greater depths, the volume of air in the lungs can be reduced to the residual volume, but not smaller. The depth limit to breath-hold diving is determined by the ratio of the total lung volume & the residual volume. Those with large TLV:RV ratios can safely dive deeper than those with smaller ratios. Scuba diving can alleviate many of the problems faced during breath-hold diving because you breathe pressurized air while submerged.
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Chapter 10. Exercise in Hypobaric & Hyperbaric Environments
3. Health Risks of Hyperbaric Hyperbaric Conditions
Breathing gases under pressure can cause the body to accumulate gases in toxic levels, so precautions must be taken when diving with pressurized gases. O2 poisoning occurs when PO2 values are above 318 mmHg. Less O 2 will be removed from hemoglobin for use by tissues. This impairs the biding of CO 2 to hemoglobin, so less CO2 is removed by this route. High PO 2 also causes vasoconstriction in the cerebral vessels, which decreases blood flow to the brain. Decompression sickness (the bends) results from ascending too rapidly. The nitrogen dissolved in the body cannot be removed by the lungs quickly enough, so it forms bubbles. The bubbles can form emboli, which can be fatal. To treat this, the diver must undergo recompression to force the nitrogen back to solution, then undergo gradual decompression at the rate that allows the nitrogen to be removed during normal breathing. Tables have been formulated that specify how much time must be allowed for ascension from various depths, 7 divers must adhere strictly to these. Nitrogen narcosis (rapture of the deep) results from the narcotic effects of nitrogen when its partial pressure is high, such as during depth diving. The symptoms are similar to alcohol intoxication. Judgment is impaired, which can lead to fatal mistakes. Spontaneous pneumothorax (rupture alveoli) & ruptured eardrum are other health risks associated with the changing pressure experienced when diving.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Exercise in Hypobaric Environment) Name : _______________________________________
Group : _________ __ Date : _____________
Answer ALL questions. 1. Define acclimatization, altitude, hypoxia and hypobaric environment. a. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ b. ____________________________________________________________________________ c.
____________________________________________________________________________
d. ____________________________________________________________________________
2. Discuss briefly the conditions at altitude that limit sport performance.
a. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ b. ____________________________________________________________________________ ____________________________________________________________________________ ____________________________________________________________________________ c.
____________________________________________________________________________ ____________________________________________________________________________
3. What types of activities are detrimentally influenced by exposure to high altitude? Why? ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
4. Explain briefly the adaptations that occur in the blood with prolonged altitude exposure. a. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
5. Explain briefly the adaptations that occur in the muscle with prolonged altitude exposure. a. _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________ c.
_____________________________________________________________________________ _____________________________________________________________________________
6. Explain briefly the adaptations that occur in the cardiorespiratory with prolonged altitude exposure. a. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
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Chapter 11. Ergogenic Aids
ERGOGENIC AIDS AND PERFORMANCE Ergogenic aid
Any substance or phenomenon that able to improve performance.
Ergolytic substance
Any substance that able to impair performance.
Placebo
An inactive substance usually provided in a manner identical to an active substance (real drug), typically to test for real versus imagined effects.
Placebo effect
An effect produced by the subject’s expectations after being administered an inactive substance (placebo).
Ergogenic Aids /Substances classified into : 1. Pharmacological agents Alcohol Amphetamines Beta Blockers Caffeine Cocaine Diuretics Marijuana Nicotine
2. Hormonal Agents Anabolic Steroid Human Growth Hormone Oral Contraceptives
3. Physiological Agents Blood Doping Erythropoietin Oxygen Supplementation Aspartic Acid Salts Bicarbonate Loading Phosphate Loading Warm-up & temperature variations
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Chapter 11. Ergogenic Aids
4. Nutrition Agents Carbohydrates Proteins Fats Vitamins & minerals Water & special beverages
5. Psychological Phenomena Hypnosis Mental practice or Covert rehearsal Stress management
6. Mechanical Factors Clothing Equipment Environment – structures & surfaces
A. Pharmacological agents: 1. Alcohol Classified as a drug because of its depressant effects on the CNS. Can elicit both stimulant and depressant effects (initial sensation of excitement and followed by depressive effects). Used by athletes because of its psychological effects. It is thought to increase self-confidence, calm nerves, reduce anxiety, increase mental alertness, and reduce pain & muscle tremor. Risks: No improvements in physiological functions. Decreases psychomotor functions. Can negatively affect health. Can cause physically addictive. Have ergolytic effects (decrease performance).
2. Amphetamines CNS stimulant. Increase concentration & mental alertness, elevate mood, decrease the sense of fatigue, and produce euphoria. Used as appetite suppressants in medically supervised weight-loss programs. Recent studies showed increase in strength, acceleration, and increase maximal lactate response during exhaustive exercise and increase time to exhaustion. Risks: – increase HR and BP that can trigger cardiac arrhythmias. Excessive use can cause deaths. Also cause psychological & physically addictive. 2
Chapter 11. Ergogenic Aids
3. Beta blockers Block beta–adrenergic receptors, therefore preventing neurotransmitters binding. This reduces the effects of stimulation by the sympathetic nervous system. Lowers HR, therefore advantage to shooters & archers. Impair endurance performance, reducing VO 2max because cardiac output is decreased due to decreased in HR. Risks: cause bradycardia that can lead to heart block, hypotension, bronchospasm, fatigue and decreased motivation.
4. Caffeine CNS stimulant. Increases mental alertness, increases concentration, elevates mood, enhances catecholamine release, increases free-fatty-acid mobilization, increases muscle use of triglycerides to spare glycogen, decreases fatigue & delays its onset. Risks: Can cause nervousness, restlessness, insomnia, tremors, and diuresis. Diuresis increases the risk of dehydration & heat-related illness when performing in hot environment. Disrupt normal sleep patterns, contributing to fatigue. Can cause physically addictive.
5. Cocaine CNS stimulant. Produce euphoria that is thought increase self confident & motivation. Masks fatigue & pain, increase alertness & cause energetic. No evidence that has any ergogenic properties. Risks: Extremely addictive. Trigger major psychological disorder and has numerous undesirable physiological effects, includes stress to heart function, which leads to death.
6. Diuretics Affect the kidneys, increasing urine formation and excretion. Often used by athletes for weight reduction or maintenance (weight category sports), and also by those trying to mask the use of other drugs during drug testing. Weight loss is proven the ergogenic effect of diuretics, but the weight loss is primarily from the extracellular fluid compartment, including blood plasma. Risks: Loss of body fluid leads to dehydration, which can impair thermoregulation & cause electrolyte imbalances, can cause fatigue & muscle cramping.
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Chapter 11. Ergogenic Aids
7. Marijuana Act on CNS & can elicit both stimulant and depressant effects (initial sensation of excitement and followed by depressive effects). No ergogenic qualities & in fact ergolytic. Impair performance that requires hand-eye coordination, fast reaction time, motor coordination, tracking ability & perceptual accuracy. Risks: can lead to personality changes, short-term memory impairment, hallucinations, & psychotic-like behavior.
8. Nicotine CNS stimulant. Ingest by smoking (cigarettes) or in smokeless forms - chewing (chewing tobacco), & snuff (powdered tobacco). Thought to increase alertness, better concentration & more calm. Detrimental to performance & cause several changes in CV, metabolic, respiratory & hormonal function. Risks: can lead to cancer & CV disease.
B. Hormonal Agents: 1. Anabolic Steroids Androgenic-anabolic steroids: – include androgenic (masculinizing) & anabolic (building) properties. Synthetic steroids have been designed to maximize the anabolic effects while minimizing androgenic effects. Proposed to increase muscle mass, strength, and endurance capacity, & to facilitate recovery from exhaustive training bouts. Proven can increase muscle mass, and strength. Do not increase endurance capacity & ability to facilitate recovery from exhaustive exercise has not been proven. Risks: personality changes, cardiovascular disease, liver damage, masculinization in women, breast regression in women, breast enlargement in men, prostate gland enlargement, testicular atrophy, & reduced sperm count.
2. Human Growth Hormone Stimulates protein synthesis & nucleic acid in skeletal muscle, increase bone growth, increase lipolysis (thus decreasing body fats), increase blood glucose levels, and enhances healing of musculoskeletal injuries. Limited research that supports its ability to increase fat-free mass & decrease fat mass, but GH might have little or no effect on increasing muscle mass & strength. Risks: can cause hypertrophy of internal organs, muscle and joint weakness, diabetes, hypertension, & heart disease.
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Chapter 11. Ergogenic Aids
3. Oral Contraceptives Birth control pills contain synthetic versions of natural estrogens & progesterones. Proposed as ergogenic aids foe women due to its ability to regulate menstrual cycle (function as contraceptives by preventing ovulation). Little research that support as ergogenic aid. May be beneficial for women athletes who suffer from PMS or dysmenorrheal. Risks: nausea, weight gain, fatigue, hypertension, liver tumors, blood clots, stroke, & heart attack.
C. Physiological Agents: 1. Blood doping An artificial increase in a person’s total volume of red blood cells (RBCs) via infusion of RBCs in effort to increase hemoglobin concentration & O 2- carrying capacity of blood.
Proposed ergogenic benefits Theoretically, O2 is carried through the body bond to hemoglobin. It seems logical that increasing the number of RBCs will increase hemoglobin concentration, available to ferry the O 2 to the tissues. Increasing the number of O 2 carriers (hemoglobin) should increase the blood’s oxygen-carrying capacity, allowing more O2 to be delivered to the active tissues. This will results in improvements in VO2max and aerobic endurance performance. Recent research found major increase in maximal O 2 uptake, longer time to exhaustion; enhance performance in cross-country skiing & distance running. Risks: a) Blood clotting due to blood become too viscous. b) Heart failure due to clotting. c) Administration of mislabeled blood & mismatched of reinfused blood could cause allergic reaction such as chill, fever & nausea. d) Transmission of hepatitis. e) Transmission of virus that causes acquired immune deficiency syndrome (AIDS).
2. Erythropoietin (EPO) Hormone that stimulate RBC production. Proposed with the premise that increasing the number of RBCs would increase the blood’s O2-carrying capacity. Proven increase maximal O2 consumption (VO2max) & increased time to exhaustion. Risks: very dangerous because we cannot predict the magnitude of the body’s response to EPO supplementation. Can lead to death if RBCs are overproduced, because increased blood viscosity can cause clotting and heart failure.
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Chapter 11. Ergogenic Aids
3. Oxygen Supplementation During exercise improves endurance performance but is too cumbersome to be practical. Supplementation before or immediately after exercise has not been proven ergogenically effective. Risks: no serious risks associated with brief (2-3 min) periods of O 2 breathing.
4. Aspartic Acid An amino acid involved in the liver’s conversion of ammonia to urea. Because excess ammonia is associated with fatigue, ingestion of aspartates has been postulated to reduce the ammonia that builds up during exercise, thus delaying fatigue. Research on its effectiveness as an ergogenic aid & risk is insufficient.
5. Bicarbonate Loading Bicarbonate is an important component of the body’s buffering system, needed to maintain normal pH by neutralizing excess acid. Proposed to increase the blood’s alkalinity, thus increasing the buffering capacity so that more lactate can be cleared. This would delay the onset of fatigue. Ingest of at least 300 mg·kg-1 body weight can delay fatigue & increase performance in all-out bouts of exercise lasting more than 1 min but less than 7 min. Risks: cause gastrointestinal distress, including cramping, bloating, & diarrhea.
6. Phosphate Loading Ingestion of sodium phosphate has been postulated to improve general CV & metabolic functioning. During exercise, phosphate loading has been proposed to elevate phosphate levels throughout the body, which would increase the potential for oxidative phosphorylation & phosphocreatine synthesis, enhance O2 release to the cells, improve CV response to exercise, improve the body’s buffering capacity, & improve endurance capacity. Research on its effectiveness as an ergogenic aid & risk is limited.
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UNIVERSITI TEKNOLOGI MARA
FACULTY OF SPORT SCIENCE AND RECREATION
SPS 211 EXERCISE PHYSIOLOGY
EXERCISE (Ergogenic Aids) Name : _______________________________________
Group : _________ Date : _______________
Answer ALL questions. 1. Define ergogenic aid and ergolytic substance. a. _____________________________________________________________________________ b. _____________________________________________________________________________
2. What is ‘placebo’? Why must an investigator use ‘placebo’ treatment to evaluate the effectiveness of an ergogenic aid? a. _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________
3. What is “carbo-loading”? Describe its benefit in endurance activities. a. _____________________________________________________________________________ _____________________________________________________________________________ b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
4. What are beta blockers? What are the ergogenic and ergolytic properties? a. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ Ergogenic properties b. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________
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