physiologic responses and long-term adaptations to exercise

ContentsIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

Physiologic Responses to Episodes of Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

Cardiovascular and Respiratory Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

Cardiovascular Responses to Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

Cardiac Output . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

Blood Flow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Oxygen Extraction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Coronary Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Respiratory Responses to Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64

Resistance Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Skeletal Muscle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Skeletal Muscle Energy Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Energy Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Metabolic Rate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

Maximal Oxygen Uptake . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

Lactate Threshold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

Hormonal Responses to Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

Immune Responses to Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

Long-Term Adaptations to Exercise Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

Adaptations of Skeletal Muscle and Bone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

Metabolic Adaptations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

Cardiovascular and Respiratory Adaptations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

Long-Term Cardiovascular Adaptations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

Respiratory Adaptations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

CHAPTER 3PHYSIOLOGIC RESPONSES AND LONG-TERM

ADAPTATIONS TO EXERCISE

Contents, continued

Maintenance, Detraining, and Prolonged Inactivity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

Maintaining Fitness and Muscular Strength . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

Detraining . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

Prolonged Inactivity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

Special Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Disability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Environmental Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Effects of Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Differences by Sex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

Research Needs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

Introduction

When challenged with any physical task, thehuman body responds through a series of

integrated changes in function that involve most, ifnot all, of its physiologic systems. Movement re-quires activation and control of the musculoskeletalsystem; the cardiovascular and respiratory systemsprovide the ability to sustain this movement overextended periods. When the body engages in exer-cise training several times a week or more frequently,each of these physiologic systems undergoes specificadaptations that increase the body’s efficiency andcapacity. The magnitude of these changes dependslargely on the intensity and duration of the trainingsessions, the force or load used in training, and thebody’s initial level of fitness. Removal of the train-ing stimulus, however, will result in loss of theefficiency and capacity that was gained throughthese training-induced adaptations; this loss is aprocess called detraining.

This chapter provides an overview of how thebody responds to an episode of exercise and adaptsto exercise training and detraining. The discussionfocuses on aerobic or cardiorespiratory enduranceexercise (e.g., walking, jogging, running, cycling,swimming, dancing, and in-line skating) and resis-tance exercise (e.g., strength-developing exercises).It does not address training for speed, agility, andflexibility. In discussing the multiple effects ofexercise, this overview will orient the reader to thephysiologic basis for the relationship of physicalactivity and health. Physiologic information perti-nent to specific diseases is presented in the nextchapter. For additional information, the reader isreferred to the selected textbooks shown in thesidebar.

Selected Textbooks on Exercise Physiology

Åstrand PO, Rodahl K. Textbook of work physiology.3rd edition. New York: McGraw-Hill Book Company,1986.

Brooks GA, Fahey TD, White TP. Exercise physiology:human bioenergetics and its applications. 2nd edition.Mountain View, CA: Mayfield Publishing Company,1996.

Fox E, Bowers R, Foss M. The physiological basis forexercise and sport. 5th edition. Madison, WI: Brownand Benchmark, 1993.

McArdle WD, Katch FI, Katch VL. Essentials ofexercise physiology. Philadelphia, PA: Lea andFebiger, 1994.

Powers SK, Howley ET. Exercise physiology: theoryand application to fitness and performance. Dubuque,IA: William C. Brown, 1990.

Wilmore JH, Costill DL. Physiology of sport andexercise. Champaign, IL: Human Kinetics, 1994.

Physiologic Responses to Episodesof ExerciseThe body’s physiologic responses to episodes ofaerobic and resistance exercise occur in the muscu-loskeletal, cardiovascular, respiratory, endocrine,and immune systems. These responses have beenstudied in controlled laboratory settings, where ex-ercise stress can be precisely regulated and physi-ologic responses carefully observed.

Cardiovascular and Respiratory SystemsThe primary functions of the cardiovascular andrespiratory systems are to provide the body with

CHAPTER 3PHYSIOLOGIC RESPONSES AND LONG-TERM

ADAPTATIONS TO EXERCISE

62

Physical Activity and Health

oxygen (O2) and nutrients, to rid the body of carbondioxide (CO2) and metabolic waste products, tomaintain body temperature and acid-base balance,and to transport hormones from the endocrineglands to their target organs (Wilmore and Costill1994). To be effective and efficient, the cardiovascu-lar system should be able to respond to increasedskeletal muscle activity. Low rates of work, such aswalking at 4 kilometers per hour (2.5 miles perhour), place relatively small demands on the cardio-vascular and respiratory systems. However, as therate of muscular work increases, these two systemswill eventually reach their maximum capacities andwill no longer be able to meet the body’s demands.

Cardiovascular Responses to ExerciseThe cardiovascular system, composed of the heart,blood vessels, and blood, responds predictably tothe increased demands of exercise. With few excep-tions, the cardiovascular response to exercise isdirectly proportional to the skeletal muscle oxygendemands for any given rate of work, and oxygenuptake ( ̇VO2) increases linearly with increasing ratesof work.

Cardiac OutputCardiac output (Q̇) is the total volume of bloodpumped by the left ventricle of the heart per minute.It is the product of heart rate (HR, number of beatsper minute) and stroke volume (SV, volume of bloodpumped per beat). The arterial-mixed venous oxygen(A--vO

2) difference is the difference between the oxy-

gen content of the arterial and mixed venous blood. Aperson’s maximum oxygen uptake (V̇O2 max) is afunction of cardiac output (Q̇) multiplied by theA--vO2 difference. Cardiac output thus plays an im-portant role in meeting the oxygen demands forwork. As the rate of work increases, the cardiacoutput increases in a nearly linear manner to meetthe increasing oxygen demand, but only up to thepoint where it reaches its maximal capacity (Q̇ max).

To visualize how cardiac output, heart rate, andstroke volume change with increasing rates of work,consider a person exercising on a cycle ergometer,starting at 50 watts and increasing 50 watts every 2minutes up to a maximal rate of work (Figure 3-1 A,B, and C). In this scenario, cardiac output and heartrate increase over the entire range of work, whereasstroke volume only increases up to approximately 40

Figure 3-1. Changes in cardiac output (A), heart rate (B), and stroke volume (C) with increasing rates of work on the cycle ergometer

(A)

(B)

6

8

10

12

14

16

18

20

22

80

100

120

140

160

180

200

60

70

80

90

100

110

120

25 50 75 100 125 150 175 200

25 50 75 100Power (watts)

Power (watts)

Power (watts)

Stro

ke v

olum

e (m

l/bea

t)C

ardi

ac o

utpu

t (lit

ers/

min

)H

eart

rat

e (b

eats

/min

)

125 150 175 200

25 50 75 100 125 150 175 200

(C)

63

Physiologic Responses and Long-Term Adaptations to Exercise

is generally much higher in these patients, likely owingto a lesser reduction in total peripheral resistance.

For the first 2 to 3 hours following exercise,blood pressure drops below preexercise resting lev-els, a phenomenon referred to as postexercise hy-potension (Isea et al. 1994). The specific mechanismsunderlying this response have not been established.The acute changes in blood pressure after an episodeof exercise may be an important aspect of the role ofphysical activity in helping control blood pressure inhypertensive patients.

Oxygen ExtractionThe A--vO2 difference increases with increasing ratesof work (Figure 3-2) and results from increasedoxygen extraction from arterial blood as it passesthrough exercising muscle. At rest, the A--vO2 differ-ence is approximately 4 to 5 ml of O2 for every 100 mlof blood (ml/100 ml); as the rate of work approachesmaximal levels, the A--vO

2 difference reaches 15 to 16

ml/100 ml of blood.

Coronary CirculationThe coronary arteries supply the myocardium withblood and nutrients. The right and left coronaryarteries curve around the external surface of the heart,then branch and penetrate the myocardial musclebed, dividing and subdividing like branches of a treeto form a dense vascular and capillary network tosupply each myocardial muscle fiber. Generally onecapillary supplies each myocardial fiber in adult hu-mans and animals; however, evidence suggests thatthe capillary density of the ventricular myocardiumcan be increased by endurance exercise training.

At rest and during exercise, myocardial oxygendemand and coronary blood flow are closely linked.This coupling is necessary because the myocardiumdepends almost completely on aerobic metabolismand therefore requires a constant oxygen supply.Even at rest, the myocardium’s oxygen use is highrelative to the blood flow. About 70 to 80 percent ofthe oxygen is extracted from each unit of bloodcrossing the myocardial capillaries; by comparison,only about 25 percent is extracted from each unitcrossing skeletal muscle at rest. In the healthy heart,a linear relationship exists between myocardial oxy-gen demands, consumption, and coronary bloodflow, and adjustments are made on a beat-to-beat

to 60 percent of the person’s maximal oxygen uptake( V̇O2 max), after which it reaches a plateau. Recentstudies have suggested that stroke volume in highlytrained persons can continue to increase up to nearmaximal rates of work (Scruggs et al. 1991; Gledhill,Cox, Jamnik 1994).

Blood FlowThe pattern of blood flow changes dramatically whena person goes from resting to exercising. At rest, theskin and skeletal muscles receive about 20 percent ofthe cardiac output. During exercise, more blood issent to the active skeletal muscles, and, as bodytemperature increases, more blood is sent to the skin.This process is accomplished both by the increase incardiac output and by the redistribution of blood flowaway from areas of low demand, such as the splanch-nic organs. This process allows about 80 percent of thecardiac output to go to active skeletal muscles andskin at maximal rates of work (Rowell 1986). Withexercise of longer duration, particularly in a hot andhumid environment, progressively more of the car-diac output will be redistributed to the skin to counterthe increasing body temperature, thus limiting boththe amount going to skeletal muscle and the exerciseendurance (Rowell 1986).

Blood PressureMean arterial blood pressure increases in response todynamic exercise, largely owing to an increase insystolic blood pressure, because diastolic blood pres-sure remains at near-resting levels. Systolic bloodpressure increases linearly with increasing rates ofwork, reaching peak values of between 200 and 240millimeters of mercury in normotensive persons. Be-cause mean arterial pressure is equal to cardiac outputtimes total peripheral resistance, the observed increasein mean arterial pressure results from an increase incardiac output that outweighs a concomitant decreasein total peripheral resistance. This increase in meanarterial pressure is a normal and desirable response, theresult of a resetting of the arterial baroreflex to a higherpressure. Without such a resetting, the body wouldexperience severe arterial hypotension during intenseactivity (Rowell 1993). Hypertensive patients typicallyreach much higher systolic blood pressures for a givenrate of work, and they can also experience increases indiastolic blood pressure. Thus, mean arterial pressure

64


basis. The three major determinants of myocardialoxygen consumption are heart rate, myocardialcontractility, and wall stress (Marcus 1983;Jorgensen et al. 1977). Acute increases in arterialpressure increase left ventricular pressure and wallstress. As a result, the rate of myocardial metabolismincreases, necessitating an increased coronary bloodflow. A very high correlation exists between bothmyocardial oxygen consumption and coronary bloodflow and the product of heart rate and systolic bloodpressure (SBP) (Jorgensen et al. 1977). This so-called double product (HR • SBP) is generally usedto estimate myocardial oxygen and coronary bloodflow requirements. During vigorous exercise, allthree major determinants of myocardial oxygen re-quirements increase above their resting levels.

The increase in coronary blood flow during exer-cise results from an increase in perfusion pressure ofthe coronary artery and from coronary vasodilation.Most important, an increase in sympathetic nervoussystem stimulation leads to an increase in circulatingcatecholamines. This response triggers metabolic pro-cesses that increase both perfusion pressure of the

coronary artery and coronary vasodilation to meet theincreased need for blood flow required by the increasein myocardial oxygen use.

Respiratory Responses to ExerciseThe respiratory system also responds when chal-lenged with the stress of exercise. Pulmonary ven-tilation increases almost immediately, largelythrough stimulation of the respiratory centers inthe brain stem from the motor cortex and throughfeedback from the proprioceptors in the musclesand joints of the active limbs. During prolongedexercise, or at higher rates of work, increases in CO2

production, hydrogen ions (H+), and body andblood temperatures stimulate further increases inpulmonary ventilation. At low work intensities, theincrease in ventilation is mostly the result of in-creases in tidal volume. At higher intensities, therespiratory rate also increases. In normal-sized,untrained adults, pulmonary ventilation rates canvary from about 10 liters per minute at rest to morethan 100 liters per minute at maximal rates of work;in large, highly trained male athletes, pulmonary

Figure 3-2. Changes in arterial and mixed venous oxygen content with increasing rates of work on the cycle ergometer

0

2

4

6

8

10

12

14

16

18

20

25 50 75 100

Power (watts)

mixed venous oxygen content

arterial oxygen content

Oxy

gen

cont

ent (

ml/1

00 m

l of b

lood

)

125 150 175 200 225 250 275

A-vO2 difference-

65


ventilation rates can reach more than 200 liters perminute at maximal rates of work.

Resistance ExerciseThe cardiovascular and respiratory responses toepisodes of resistance exercise are mostly similar tothose associated with endurance exercise. One no-table exception is the exaggerated blood pressureresponse that occurs during resistance exercise. Partof this response can be explained by the fact thatresistance exercise usually involves muscle massthat develops considerable force. Such high, isolatedforce leads to compression of the smaller arteries andresults in substantial increases in total peripheralresistance (Coyle 1991). Although high-intensityresistance training poses a potential risk to hyperten-sive patients and to those with cardiovascular dis-ease, research data suggest that the risk is relativelylow (Gordon et al. 1995) and that hypertensivepersons may benefit from resistance training (Tipton1991; American College of Sports Medicine 1993).

Skeletal MuscleThe primary purpose of the musculoskeletal system isto define and move the body. To provide efficient andeffective force, muscle adapts to demands. In responseto demand, it changes its ability to extract oxygen,choose energy sources, and rid itself of waste prod-ucts. The body contains three types of muscle tissue:skeletal (voluntary) muscle, cardiac muscle or myo-cardium, and smooth (autonomic) muscle. This sec-tion focuses solely on skeletal muscle.

Skeletal muscle is composed of two basic types ofmuscle fibers distinguished by their speed of con-traction—slow-twitch and fast-twitch—a character-istic that is largely dictated by different forms of theenzyme myosin adenosinetriphosphatase (ATPase).Slow-twitch fibers, which have relatively slow con-tractile speed, have high oxidative capacity and fa-tigue resistance, low glycolytic capacity, relativelyhigh blood flow capacity, high capillary density, andhigh mitochondrial content (Terjung 1995). Fast-twitch muscle fibers have fast contractile speed andare classified into two subtypes, fast-twitch type “a”(FTa) and fast-twitch type “b” (FTb). FTa fibers havemoderately high oxidative capacity, are relativelyfatigue resistant, and have high glycolytic capacity,relatively high blood flow capacity, high capillary

density, and high mitochondrial content (Terjung1995). FTb fibers have low oxidative capacity, lowfatigue resistance, high glycolytic capacity, and fastcontractile speed. Further, they have relatively lowblood flow capacity, capillary density, and mito-chondrial content (Terjung 1995).

There is a direct relationship between predomi-nant fiber type and performance in certain sports.For example, in most marathon runners, slow-twitchfibers account for up to or more than 90 percent ofthe total fibers in the leg muscles. On the other hand,the leg muscles in sprinters are often more than 80percent composed of fast-twitch fibers. Although theissue is not totally resolved, muscle fiber type ap-pears to be genetically determined; researchers haveshown that several years of either high-intensitysprint training or high-intensity endurance trainingdo not significantly alter the percentage of the twomajor types of fibers (Jolesz and Sreter 1981).

Skeletal Muscle Energy MetabolismMetabolic processes are responsible for generatingadenosine triphosphate (ATP), the body’s energysource for all muscle action. ATP is generated by threebasic energy systems: the ATP-phosphocreatine(ATP-PCr) system, the glycolytic system, and theoxidative system. Each system contributes to energyproduction in nearly every type of exercise. Therelative contribution of each will depend on factorssuch as the intensity of work rate at the onset ofexercise and the availability of oxygen in the muscle.

Energy SystemsThe ATP-PCr system provides energy from the ATPstored in all of the body’s cells. PCr, also found in allcells, is a high-energy phosphate molecule that storesenergy. As ATP concentrations in the cell are reducedby the breakdown of ATP to adenosine diphosphate(ADP) to release energy for muscle contraction, PCr isbroken down to release both energy and a phosphateto allow reconstitution of ATP from ADP. This processdescribes the primary energy system for short, high-intensity exercise, such as a 40- to 200-meter sprint;during such exercise, the system can produce energyat very high rates, and ATP and PCr stores, which aredepleted in 10–20 seconds, will last just long enoughto complete the exercise.

66


At high rates of work, the active muscle cell’soxygen demand exceeds its supply. The cell mustthen rely on the glycolytic energy system to produceATP in the absence of oxygen (i.e., anaerobically).This system can only use glucose, available in theblood plasma and stored in both muscle and the liver asglycogen. The glycolytic energy system is the primaryenergy system for all-out bouts of exercise lastingfrom 30 seconds to 2 minutes, such as an 800-meterrun. The major limitation of this energy system isthat it produces lactate, which lowers the pH of boththe muscle and blood. Once the pH drops below avalue of 6.4 to 6.6, enzymes critical for producingenergy are no longer able to function, and ATPproduction stops (Wilmore and Costill 1994).

The oxidative energy system uses oxygen toproduce ATP within the mitochondria, which arespecial cell organelles within muscle. This processcannot generate ATP at a high enough rate to sustainan all-out sprint, but it is highly effective at lowerrates of work (e.g., long distance running). ATP canalso be produced from fat and protein metabolismthrough the oxidative energy system. Typically, car-bohydrate and fat provide most of the ATP; undermost conditions, protein contributes only 5 to 10percent at rest and during exercise.

Metabolic RateThe rate at which the body uses energy is known asthe metabolic rate. When measured while a person isat rest, the resulting value represents the lowest (i.e.,basal) rate of energy expenditure necessary to main-tain basic body functions. Resting metabolic rate ismeasured under highly controlled resting condi-tions following a 12-hour fast and a good night’ssleep (Turley, McBride, Wilmore 1993). To quantifythe rate of energy expenditure during exercise, themetabolic rate at rest is defined as 1 metabolicequivalent (MET); a 4 MET activity thus representsan activity that requires four times the resting meta-bolic rate. The use of METs to quantify physicalactivity intensity is the basis of the absolute intensityscale. (See Chapter 2 for further information.)

Maximal Oxygen UptakeDuring exercise, ̇VO

2 increases in direct proportion to

the rate of work. The point at which a person’s ̇VO2 isno longer able to increase is defined as the maximal

oxygen uptake ( V̇O2max) (Figure 3-3). A person’s V̇O2max is in part genetically determined; it can beincreased through training until the point that thegenetically possible maximum is reached. ̇VO2max isconsidered the best estimate of a person’s cardio-respiratory fitness or aerobic power (Jorgensen et al.1977).

Lactate ThresholdLactate is the primary by-product of the anaerobicglycolytic energy system. At lower exercise intensi-ties, when the cardiorespiratory system can meet theoxygen demands of active muscles, blood lactatelevels remain close to those observed at rest, becausesome lactate is used aerobically by muscle and isremoved as fast as it enters the blood from themuscle. As the intensity of exercise is increased,however, the rate of lactate entry into the blood frommuscle eventually exceeds its rate of removal fromthe blood, and blood lactate concentrations increaseabove resting levels. From this point on, lactatelevels continue to increase as the rate of work in-creases, until the point of exhaustion. The point atwhich the concentration of lactate in the bloodbegins to increase above resting levels is referred toas the lactate threshold (Figure 3-3).

Lactate threshold is an important marker for endur-ance performance, because distance runners set theirrace pace at or slightly above the lactate threshold(Farrell et al. 1979). Further, the lactate thresholdsof highly trained endurance athletes occur at a muchhigher percentage of their ̇VO

2max, and thus at higher

relative workloads, than do the thresholds of un-trained persons. This key difference is what allowsendurance athletes to perform at a faster pace.

Hormonal Responses to ExerciseThe endocrine system, like the nervous system,integrates physiologic responses and plays an im-portant role in maintaining homeostatic conditionsat rest and during exercise. This system controls therelease of hormones from specialized glands through-out the body, and these hormones exert their actionson targeted organs and cells. In response to anepisode of exercise, many hormones, such as cat-echolamines, are secreted at an increased rate, thoughinsulin is secreted at a decreased rate (Table 3-1).The actions of some of these hormones, as well as

67


their specific responses to exercise, are discussed inmore detail in Chapter 4.

Immune Responses to ExerciseThe immune system is a complex adaptive systemthat provides surveillance against foreign proteins,viruses, and bacteria by using the unique functions ofcells produced by the bone marrow and the thymusgland. By interacting with neural and endocrinefactors, the immune system influences the body’soverall response to exercise (Reichlin 1992). A grow-ing body of literature indicates that the incidence ofsome infections may be influenced by the exercisehistory of the individual (Nieman 1994; Hoffman-Goetz and Pedersen 1994).

Moderate exercise has been shown to bolster thefunction of certain components of the human immunesystem—such as natural killer cells, circulating T- andB-lymphocytes, and cells of the monocyte-macroph-age system—thereby possibly decreasing the inci-dence of some infections (Keast, Cameron, Morton1988; Pedersen and Ullum 1994; Woods and Davis1994) and perhaps of certain types of cancer (Shephardand Shek 1995).

Exercise of high intensity and long duration orexercise that involves excessive training may haveadverse effects on immune function. In general, ahigh-intensity, single episode of exercise results in amarked decline in the functioning of all major cells ofthe immune system (Newsholme and Parry-Billings1994; Shephard and Shek 1995). In addition, over-training may reduce the response of T-lymphocytes tomutagenic stimulation, decrease antibody synthesisand plasma level of immunoglobins and complement,and impair macrophage phagocytosis. The reducedplasma glutamine levels that occur with high-intensityexercise or excessive training are postulated to con-tribute to these adverse effects on the immune system(Newsholme and Parry-Billings 1994).

Long-Term Adaptations toExercise Training

Adaptations of Skeletal Muscle and BoneSkeletal muscle adapts to endurance training chieflythrough a small increase in the cross-sectional areaof slow-twitch fibers, because low- to moderate-

*Lactate threshold (LT) and maximum oxygen uptake ( V̇O2 max) are indicated.

25

30

35

40

45

50

55

0

2

4

6

8

10

12

25 50 75 100Power (watts)

Oxy

gen

upta

ke (m

l/kg/

min

) Blood lactate (m

mol/liter)

125 150 175 200 225 250 275

VO2max

Lactate threshold

Figure 3-3. Changes in oxygen uptake and blood lactate concentrations with increasing rates of work on the cycle ergometer*

.

68


Table 3-1. A summary of hormonal changes during an episode of exercise

ExerciseHormone response Special relationships Probable importance

Catecholamines Increases Greater increase with intense Increased blood glucose;exercise; norepinephrine > increased skeletal muscle andepinephrine; increases less after liver glycogenolysis; increasedtraining lipolysis

Growth hormone (GH) Increases Increases more in untrainedpersons; declines faster in trained Unknownpersons

Adrenocorticotropic Increases Greater increase with intense Increased gluconeogenesis inhormone (ACTH)-cortisol exercise; increases less liver; increased mobilization of

after training with fatty acidssubmaximal exercise

Thyroid-stimulating Increases Increased thyroxine turnoverhormone (TSH)-thyroxine with training but no toxic effects Unknown

are evident

Luteinizing hormone (LH) No change None None

Testosterone Increases None Unknown

Estradiol-progesterone Increases Increases during luteal phase Unknownof the menstrual cycle

Insulin Decreases Decreases less after training Decreased stimulus to use bloodglucose

Glucagon Increases Increases less after training Increased blood glucose viaglycogenolysis andgluconeogenesis

Renin-angiotensin- Increases Same increase after training Sodium retention to maintainaldosterone in rats plasma volume

Antidiuretic hormone Expected None Water retention to maintain(ADH) increase plasma volume

Parathormone Unknown None Needed to establish proper(PTH)-calcitonin bone development

Erythropoietin Unknown None Would be important to increaseerythropoiesis

Prostaglandins May May increase in response to May be local vasodilatorsincrease sustained isometric contractions;

may need ischemic stress

Adapted from Wilmore JH, Costill DL. Physiology of sport and exercise. Champaign, IL: Human Kinetics, 1994, p. 136.

69


intensity aerobic activity primarily recruits thesefibers (Abernethy, Thayer, Taylor 1990). Prolongedendurance training (i.e., months to years) can lead toa transition of FTb fibers to FTa fibers, which have ahigher oxidative capacity (Abernethy, Thayer, Taylor1990). No substantive evidence indicates that fast-twitch fibers will convert to slow-twitch fibers undernormal training conditions (Jolesz and Sreter 1981).Endurance training also increases the number ofcapillaries in trained skeletal muscle, thereby allow-ing a greater capacity for blood flow in the activemuscle (Terjung 1995).

Resistance-trained skeletal muscle exerts con-siderably more force because of both increased musclesize (hypertrophy) and increased muscle fiber re-cruitment. Fiber hypertrophy is the result of in-creases in both the size and number of myofibrils inboth fast-twitch and slow-twitch muscle fibers(Kannus et al. 1992). Hyperplasia, or increased fibernumber, has been reported in animal studies, wherethe number of individual muscle fibers can be counted(Gonyea et al. 1986), and has been indirectly demon-strated during autopsies on humans by using directfiber counts to compare dominant and nondominantpaired muscles (Sjöström et al. 1991).

During both aerobic and resistance exercise,active muscles can undergo changes that lead tomuscle soreness. Some soreness is felt immediatelyafter exercise, and some can even occur during exer-cise. This muscle soreness is generally not physicallylimiting and dissipates rapidly. A more limiting sore-ness, however, may occur 24 to 48 hours followingexercise. This delayed-onset muscle soreness is pri-marily associated with eccentric-type muscle action,during which the muscle exerts force while lengthen-ing, as can happen when a person runs down a steephill or lowers a weight from a fully flexed to a fullyextended position (e.g., the two-arm curl). Delayed-onset muscle soreness is the result of structural dam-age to the muscle; in its most severe form, this damagemay include rupture of the cell membrane and disrup-tion of the contractile elements of individual musclefibers (Armstrong, Warren, Warren 1991). Such dam-age appears to result in an inflammatory response(MacIntyre, Reid, McKenzie 1995).

Total inactivity results in muscle atrophy andloss of bone mineral and mass. Persons who aresedentary generally have less bone mass than thosewho exercise, but the increases in bone mineral and

mass that result from either endurance or resistancetraining are relatively small (Chesnut 1993). Therole of resistance training in increasing or maintain-ing bone mass is not well characterized. Endurancetraining has little demonstrated positive effect onbone mineral and mass. Nonetheless, even smallincreases in bone mass gained from endurance orresistance training can help prevent or delay theprocess of osteoporosis (Drinkwater 1994). (SeeChapter 4 for further information on the effects ofexercise on bone.)

The musculoskeletal system cannot function with-out connective tissue linking bones to bones (liga-ments) and muscles to bones (tendons). Extensiveanimal studies indicate that ligaments and tendonsbecome stronger with prolonged and high-intensityexercise. This effect is the result of an increase in thestrength of insertion sites between ligaments, ten-dons, and bones, as well as an increase in the cross-sectional areas of ligaments and tendons. Thesestructures also become weaker and smaller with sev-eral weeks of immobilization (Tipton and Vailas 1990),which can have important implications for muscu-loskeletal performance and risk of injury.

Metabolic AdaptationsSignificant metabolic adaptations occur in skeletalmuscle in response to endurance training. First, boththe size and number of mitochondria increase sub-stantially, as does the activity of oxidative enzymes.Myoglobin content in the muscle can also be aug-mented, increasing the amount of oxygen stored inindividual muscle fibers (Hickson 1981), but thiseffect is variable (Svedenhag, Henriksson, Sylvén1983). Such adaptations, combined with the increasein capillaries and muscle blood flow in the trainedmuscles (noted in a previous section), greatly enhancethe oxidative capacity of the endurance-trained muscle.

Endurance training also increases the capacity ofskeletal muscle to store glycogen (Kiens et al. 1993).The ability of trained muscles to use fat as an energysource is also improved, and this greater reliance onfat spares glycogen stores (Kiens et al. 1993). Theincreased capacity to use fat following endurancetraining results from an enhanced ability to mobilizefree-fatty acids from fat depots and an improvedcapacity to oxidize fat consequent to the increase inthe muscle enzymes responsible for fat oxidation(Wilmore and Costill 1994).

70


These changes in muscle and in cardiorespi-ratory function are responsible for increases inboth ̇VO

2max and lactate threshold. The endurance-

trained person can thus perform at considerably higherrates of work than the untrained person. Increases inV̇O2max generally range from 15 to 20 percent follow-ing a 6-month training period (Wilmore and Costill1994). However, individual variations in this responseare considerable. In one study of 60- to 71-year-oldmen and women who endurance trained for 9 to 12months, the improvement in ̇VO2max varied from 0to 43 percent; the mean increase was 24 percent

(Kohrt et al. 1991). This variation in response maybe due in part to genetic factors and to initial levelsof fitness. To illustrate the changes that can beexpected with endurance training, a hypotheticalsedentary man’s pretraining values have been com-pared with his values after a 6-month period ofendurance training and with the values of a typicalelite endurance runner (Table 3-2).

Responses to endurance training are similar formen and women. At all ages, women and men showsimilar gains in strength from resistance training(Rogers and Evans 1993; Holloway and Baechle 1990)

Table 3-2. A hypothetical example of alterations in selected physiological variables consequent to a 6-monthendurance training program in a previously sedentary man compared with those of a typical eliteendurance runner

Sedentary man

Variable Pretraining Posttraining Runner

CardiovascularHR at rest (beats • min-1) 71 59 36HR max (beats • min-1) 185 183 174SV rest (ml) 65 80 125SV max (ml) 120 140 200Q̇ rest (L • min-1) 4.6 4.7 4.5Q̇ max (L • min-1) 22.2 25.6 32.5Heart volume (ml) 750 820 1,200Blood volume (L) 4.7 5.1 6.0Systolic BP rest (mmHg) 135 130 120Systolic BP max (mmHg) 210 205 210Diastolic BP rest (mmHg) 78 76 65Diastolic BP max (mmHg) 82 80 65

RespiratoryV̇

E rest (L • min-1) 7 6 6

V̇E rest (L • min-1) 110 135 195

TV rest (L) 0.5 0.5 0.5TV max (L) 2.75 3.0 3.9RR rest (breaths • min-1) 14 12 12RR max (breaths • min-1) 40 45 50

MetabolicA--vO

2 diff rest (ml • 100 ml-1) 6.0 6.0 6.0

A--vO2 diff max (ml • 100 ml-1) 14.5 15.0 16.0

V̇O2 rest (ml • kg-1 • min-1) 3.5 3.5 3.5

V̇O2 max (ml • kg-1 • min-1) 40.5 49.8 76.5Blood lactate rest (mmol • L-1) 1.0 1.0 1.0Blood lactate max (mmol • L-1) 7.5 8.5 9.0

Adapted from Wilmore JH, Costill DL. Physiology of sport and exercise. Champaign, IL: Human Kinetics, 1994, p. 230.

HR = heart rate; max = maximal; SV = stroke volume; Q̇ = cardiac output; BP = blood pressure; V̇E = ventilatory volume; TV = tidal volume;RR = respiration rate; A--vO2 diff = arterial-mixed venous oxygen difference; V̇O2 = oxygen consumption.

71


and similar gains in ̇VO2max from aerobic endurancetraining (Kohrt et al. 1991; Mitchell et al. 1992).

Cardiovascular and Respiratory AdaptationsEndurance training leads to significant cardiovascu-lar and respiratory changes at rest and during steady-state exercise at both submaximal and maximal ratesof work. The magnitude of these adaptations largelydepends on the person’s initial fitness level; on mode,intensity, duration, and frequency of exercise; andon the length of training (e.g., weeks, months, years).

Long-Term Cardiovascular AdaptationsCardiac output at rest and during submaximal exer-cise is essentially unchanged following an endur-ance training program. At or near maximal rates ofwork, however, cardiac output is increased sub-stantially, up to 30 percent or more (Saltin andRowell 1980). There are important differences inthe responses of stroke volume and heart rate totraining. After training, stroke volume is increasedat rest, during submaximal exercise, and duringmaximal exercise; conversely, posttraining heartrate is decreased at rest and during submaximalexercise and is usually unchanged at maximal ratesof work. The increase in stroke volume appears tobe the dominant change and explains most of thechanges observed in cardiac output.

Several factors contribute to the increase instroke volume from endurance training. Endurancetraining increases plasma volume by approximatelythe same percentage that it increases stroke volume(Green, Jones, Painter 1990). An increased plasmavolume increases the volume of blood available toreturn to the right heart and, subsequently, to theleft ventricle. There is also an increase in the end-diastolic volume (the volume of blood in the heartat the end of the diastolic filling period) because ofincreased amount of blood and increased return ofblood to the ventricle during exercise (Seals et al.1994). This acute increase in the left ventricle’send-diastolic volume stretches its walls, resultingin a more elastic recoil.

Endurance training also results in long-termchanges in the structure of the heart that augmentstroke volume. Short-term adaptive responses in-clude ventricular dilatation; this increase in the vol-ume of the ventricles allows end-diastolic volume to

increase without excessive stress on the ventricularwalls. Long-term adaptive responses include hyper-trophy of the cardiac muscle fibers (i.e., increases inthe size of each fiber). This hypertrophy increasesthe muscle mass of the ventricles, permitting greaterforce to be exerted with each beat of the heart.Increases in the thickness of the posterior and septalwalls of the left ventricle can lead to a more forcefulcontraction of the left ventricle, thus emptying moreof the blood from the left ventricle (George, Wolfe,Burggraf 1991).

Endurance training increases the number of cap-illaries in trained skeletal muscle, thereby allowing agreater capacity for blood flow in the active muscle(Terjung 1995). This enhanced capacity for bloodflow is associated with a reduction in total peripheralresistance; thus, the left ventricle can exert a moreforceful contraction against a lower resistance toflow out of the ventricle (Blomqvist and Saltin 1983).

Arterial blood pressure at rest, blood pressureduring submaximal exercise, and peak blood pres-sure all show a slight decline as a result of endurancetraining in normotensive individuals (Fagard andTipton 1994). However, decreases are greater inpersons with high blood pressure. After endurancetraining, resting blood pressure (systolic/diastolic)will decrease on average -3/-3 mmHg in persons withnormal blood pressure; in borderline hypertensivepersons, the decrease will be -6/-7 mmHg; and inhypertensive persons, the decrease will be -10/-8mmHg (Fagard and Tipton 1994). (See Chapter 4 forfurther information.)

Respiratory AdaptationsThe major changes in the respiratory system from en-durance training are an increase in the maximal rate ofpulmonary ventilation, which is the result of increasesin both tidal volume and respiration rate, and anincrease in pulmonary diffusion at maximal rates ofwork, primarily due to increases in pulmonary bloodflow, particularly to the upper regions of the lung.

Maintenance, Detraining, andProlonged InactivityMost adaptations that result from both enduranceand resistance training will be reversed if a personstops or reduces training. The greatest deterioration

72


in physiologic function occurs during prolonged bedrest and immobilization by casts. A basic mainte-nance training program is necessary to prevent theselosses in function.

Maintaining Fitness and Muscular StrengthMuscle strength and cardiorespiratory capacity aredependent on separate aspects of exercise. After a per-son has obtained gains in V̇O

2max by performing

cardiorespiratory exercise six times per week, twoto four times per week is the optimal frequency oftraining to maintain those gains (Hickson andRosenkoetter 1981). Further, a substantial part ofthe gain can be retained when the duration of eachsession is reduced by as much as two-thirds, butonly if the intensity during these abbreviated ses-sions is maintained at ≥70 percent of V̇O2max(Hickson et al. 1985). If training intensity is reducedby as little as one-third, however, a substantialreduction in ̇VO2max can be expected over the next15 weeks (Hickson et al. 1985).

In previously untrained persons, gains in mus-cular strength can be sustained by as little as a singlesession per week of resistance training, but only ifthe intensity is not reduced (Graves et al. 1988).

DetrainingWith complete cessation of exercise training, a sig-nificant reduction in V̇O

2max and a decrease in

plasma volume occur within 2 weeks; all prior func-tional gains are dissipated within 2 to 8 months, evenif routine low- to moderate-intensity physical activ-ity has taken the place of training (Shephard 1994).Muscular strength and power are reduced at a muchslower rate than V̇O2max, particularly during thefirst few months after an athlete discontinues resis-tance training (Fleck and Kraemer 1987). In fact, nodecrement in either strength or power may occur forthe first 4 to 6 weeks after training ends (Neufer et al.1987). After 12 months, almost half of the strengthgained might still be retained if the athlete remainsmoderately active (Wilmore and Costill 1994).

Prolonged InactivityThe effects of prolonged inactivity have been studiedby placing healthy young male athletes and sedentaryvolunteers in bed for up to 3 weeks after a controlperiod during which baseline measurements were

made. The resulting detrimental changes in physi-ologic function and performance are similar to thoseresulting from reduced gravitational forces duringspace flight and are more dramatic than those result-ing from detraining studies in which routine dailyactivities in the upright position (e.g., walking, stairclimbing, lifting, and carrying) are not restricted.

Results of bed rest studies show numerous physi-ologic changes, such as profound decrements incardiorespiratory function proportional to the dura-tion of bed rest (Shephard 1994; Saltin et al. 1968).Metabolic disturbances evident within a few days ofbed rest include reversible glucose intolerance andhyperinsulinemia in response to a standard glucoseload, reflecting cell insulin resistance (Lipman et al.1972); reduced total energy expenditure; negativenitrogen balance, reflecting loss of muscle protein;and negative calcium balance, reflecting loss of bonemass (Bloomfield and Coyle 1993). There is also asubstantial decrease in plasma volume, which affectsaerobic power.

From one study, a decline in V̇O2max of 15 per-

cent was evident within 10 days of bed rest andprogressed to 27 percent in 3 weeks; the rate of loss wasapproximately 0.8 percent per day of bed rest(Bloomfield and Coyle 1993). The decrement in ̇VO2maxfrom bed rest and reduced activity results from adecrease in maximal cardiac output, consequent to areduced stroke volume. This, in turn, reflects thedecrease in end-diastolic volume resulting from areduction in total blood and plasma volume, andprobably also from a decrease in myocardial contrac-tility (Bloomfield and Coyle 1993). Maximal heartrate and A--vO

2 difference remain unchanged

(Bloomfield and Coyle 1993). Resting heart rateremains essentially unchanged or is slightly in-creased, whereas resting stroke volume and cardiacoutput remain unchanged or are slightly decreased.However, the heart rate for submaximal exertion isgenerally increased to compensate for the sizablereduction in stroke volume.

Physical inactivity associated with bed rest orprolonged weightlessness also results in a progres-sive decrement in skeletal muscle mass (disuseatrophy) and strength, as well as an associatedreduction in bone mineral density that is approxi-mately proportional to the duration of immobiliza-tion or weightlessness (Bloomfield and Coyle 1993).The loss of muscle mass is not as great as that which

73


occurs with immobilization of a limb by a plastercast, but it exceeds that associated with cessation ofresistance exercise training. The muscle groupsmost affected by prolonged immobilization are theantigravity postural muscles of the lower extremi-ties (Bloomfield and Coyle 1993). The loss of nor-mal mechanical strain patterns from contraction ofthese muscles results in a corresponding loss ofdensity in the bones of the lower extremity, particu-larly the heel and the spine (Bloomfield and Coyle1993). Muscles atrophy faster than bones lose theirdensity. For example, 1 month of bed rest by healthyyoung men resulted in a 10 to 20 percent decreasein muscle fiber cross-sectional area and a 21 percentreduction in peak isokinetic torque of knee exten-sors (Bloomfield and Coyle 1993), whereas a simi-lar period of bed rest resulted in a reduction in bonemineral density of only 0.3 to 3 percent for thelumbar spine and 1.5 percent for the heel.

Quantitative histologic examination of musclebiopsies of the vastus lateralis of the leg followingimmobilization shows reduced cross-sectional areafor both slow-twitch and fast-twitch fibers, actualnecrotic changes in affected fibers, loss of capillarydensity, and a decline in aerobic enzyme activity,creatinine phosphate, and glycogen stores (Bloomfieldand Coyle 1993). On resuming normal activity,reversibility of these decrements in cardiorespiratory,metabolic, and muscle function is fairly rapid (withindays to weeks) (Bloomfield and Coyle 1993). Bycontrast, the reversal of the decrement of bone min-eral density requires weeks to months.

Special ConsiderationsThe physiologic responses to exercise and physi-ologic adaptations to training and detraining, re-viewed in the preceding sections, can be influencedby a number of factors, including physical disability,environmental conditions, age, and sex.

DisabilityAlthough there is a paucity of information aboutphysiologic responses to exercise among personswith disabilities, existing information supports thenotion that the capacity of these persons to adapt toincreased levels of physical activity is similar to thatof persons without disabilities. Many of the acute

effects of physical activity on the cardiovascular,respiratory, endocrine, and musculoskeletal systemshave been demonstrated to be similar among personswith disabilities, depending on the specific nature ofthe disability. For example, physiologic responses toexercise have been studied among persons withparaplegia (Davis 1993), quadriplegia (Figoni 1993),mental retardation (Fernhall 1993), multiple sclero-sis (Ponichtera-Mulcare 1993), and postpolio syn-drome (Birk 1993).

Environmental ConditionsThe basic physiologic responses to an episode ofexercise vary considerably with changes in environ-mental conditions. As environmental temperatureand humidity increase, the body is challenged tomaintain its core temperature. Generally, as thebody’s core temperature increases during exercise,blood vessels in the skin begin to dilate, divertingmore blood to the body’s surface, where body heatcan be passed on to the environment (unless envi-ronmental temperature exceeds body temperature).Evaporation of water from the skin’s surface signifi-cantly aids in heat loss; however, as humidity in-creases, evaporation becomes limited.

These methods for cooling can compromise car-diovascular function during exercise. Increasingblood flow to the skin creates competition with theactive muscles for a large percentage of the cardiacoutput. When a person is exercising for prolongedperiods in the heat, stroke volume will generallydecline over time consequent to dehydration andincreased blood flow in the skin (Rowell 1993;Montain and Coyle 1992). Heart rate increases sub-stantially to try to maintain cardiac output to com-pensate for the reduced stroke volume.

High air temperature is not the only factor thatstresses the body’s ability to cool itself in the heat.High humidity, low air velocity, and the radiant heatfrom the sun and reflective surfaces also contributeto the total effect. For example, exercising underconditions of 32˚C (90˚F) air temperature, 20 per-cent relative humidity, 3.0 kilometers per hour (4.8miles per hour) air velocity, and cloud cover is muchmore comfortable and less stressful to the body thanthe same exercise under conditions of 24˚C (75˚F)air temperature, 90 percent relative humidity, no airmovement, and direct exposure to the sun.

74


Children respond differently to heat than adultsdo. Children have a higher body surface area to bodymass ratio (surface area/mass), which facilitates heatloss when environmental temperatures are belowskin temperature. When environmental tempera-ture exceeds skin temperature, children are at aneven greater disadvantage because these mecha-nisms then become avenues of heat gain. Childrenalso have a lower rate of sweat production; eventhough they have more heat-activated sweat glands,each gland produces considerably less sweat thanthat of an adult (Bar-Or 1983).

The inability to maintain core temperature canlead to heat-related injuries. Heat cramps, character-ized by severe cramping of the active skeletal muscles,is the least severe of three primary heat disorders.Heat exhaustion results when the demand for bloodexceeds what is available, leading to competition forthe body’s limited blood supply. Heat exhaustion isaccompanied by symptoms including extreme fa-tigue, breathlessness, dizziness, vomiting, fainting,cold and clammy or hot and dry skin, hypotension,and a weak, rapid pulse (Wilmore and Costill 1994).Heatstroke, the most extreme of the three heat disor-ders, is characterized by a core temperature of 40˚C(104˚F) or higher, cessation of sweating, hot and dryskin, rapid pulse and respiration, hypertension, andconfusion or unconsciousness. If left untreated, heat-stroke can lead to coma, then death. People experi-encing symptoms of heat-related injury should betaken to a shady area, cooled with by whatever meansavailable, and if conscious given nonalcoholic bever-ages to drink. Medical assistance should be sought.To reduce the risk of developing heat disorders, aperson should drink enough fluid to try to matchthat which is lost through sweating, avoid extremeheat, and reduce the intensity of activity in hotweather. Because children are less resistant to theadverse effects of heat during exercise, special atten-tion should be given to protect them when theyexercise in the heat and to provide them with extrafluids to drink.

Stresses associated with exercising in the ex-treme cold are generally less severe. For most situa-tions, the problems associated with cold stress can beeliminated by adequate clothing. Still, cold stress caninduce a number of changes in the physiologic re-sponse to exercise (Doubt 1991; Jacobs, Martineau,

Vallerand 1994; Shephard 1993). These include theincreased generation of body heat by vigorous activ-ity and shivering, increased production of catechola-mines, vasoconstriction in both the cutaneous andnonactive skeletal muscle beds to provide insulationfor the body’s core, increased lactate production, anda higher oxygen uptake for the same work (Doubt1991). For the same absolute temperature, exposureto cold water is substantially more stressful thanexposure to cold air because the heat transfer inwater is about 25 times greater than in air (Toner andMcArdle 1988). Because the ratio of surface area tomass is higher in children than in adults, childrenlose heat at a faster rate when exposed to the samecold stress. The elderly tend to have a reducedresponse of generating body heat and are thus moresusceptible to cold stress.

Altitude also affects the body’s physiologic re-sponses to exercise. As altitude increases, barometricpressure decreases, and the partial pressure of inhaledoxygen is decreased proportionally. A decreased par-tial pressure of oxygen reduces the driving force tounload oxygen from the air to the blood and from theblood to the muscle, thereby compromising oxygendelivery (Fulco and Cymerman 1988). V̇O

2max is

significantly reduced at altitudes greater than 1,500meters. This effect impairs the performance of endur-ance activities. The body makes both short-term andlong-term adaptations to altitude exposure that en-able it to at least partially adapt to this imposed stress.Because oxygen delivery is the primary concern, theinitial adaptation that occurs within the first 24 hoursof exposure to altitude is an increased cardiac outputboth at rest and during submaximal exercise. Ventila-tory volumes are also increased. An ensuing reductionin plasma volume increases the concentration of redblood cells (hemoconcentration), thus providing moreoxygen molecules per unit of blood (Grover, Weil,Reeves 1986). Over several weeks, the red blood cellmass is increased through stimulation of the bonemarrow by the hormone erythropoietin.

Exercising vigorously outdoors when air qual-ity is poor can also produce adverse physiologicresponses. In addition to decreased tolerance forexercise, direct respiratory effects include increasedairway reactivity and potential exposure to harmfulvapors and airborne dusts, toxins, and pollens(Wilmore and Costill 1994).

75


Effects of AgeWhen absolute values are scaled to account fordifferences in body size, most differences in physi-ologic function between children and adults dis-appear. The exceptions are notable. For the sameabsolute rate of work on a cycle ergometer, chil-dren will have approximately the same metaboliccost, or ̇VO

2 demands, but they meet those demands

differently. Because children have smaller hearts,their stroke volume is lower than that for adults forthe same rate of work. Heart rate is increased tocompensate for the lower stroke volume; but be-cause this increase is generally inadequate, cardiacoutput is slightly lower (Bar-Or 1983). The A--vO2

difference is therefore increased to compensate forthe lower cardiac output to achieve the same V̇O2.The V̇O2max, expressed in liters per minute, in-creases during the ages of 6–18 years for boys and6–14 years for girls (Figure 3-4) before it reaches aplateau (Krahenbuhl, Skinner, Kohrt 1985). Whenexpressed relative to body weight (milliliters perkilogram per minute), ̇VO2max remains fairly stablefor boys from 6–18 years of age but decreases

steadily for girls during those years (Figure 3-4)(Krahenbuhl, Skinner, Kohrt 1985). Most likely,different patterns of physical activity contribute tothis variation because the difference in aerobiccapacity between elite female endurance athletesand elite male endurance athletes is substantiallyless than the difference between boys and girls ingeneral (e.g., 10 percent vs. 25 percent) (Wilmoreand Costill 1994).

The deterioration of physiologic function withaging is almost identical to the change in functionthat generally accompanies inactivity. Maximal heartrate and maximal stroke volume are decreased inolder adults; maximal cardiac output is thus de-creased, which results in a ̇VO

2max lower than that

of a young adult (Raven and Mitchell 1980). Thedecline in ̇VO2max approximates 0.40 to 0.50 milli-liters per kilogram per minute per year in men,according to data from cross-sectional studies; thisrate of decline is less in women (Buskirk andHodgson 1987). Through training, both older menand women can increase their V̇O2max values byapproximately the same percentage as those seen

Data were taken from Krahenbuhl GS, Skinner JS, Kohrt WM 1985 and Bar-Or O 1983.

*Values are expressed in both liters per minute andrelative to body weight (milliliters per kilogram per minute).

0.0

0.5

1.0

1.5

2.0

Max

imal

oxy

gen

upta

ke (l

iters

/min

) Maxim

al oxygen uptake (ml/kg/m

in)

2.5

3.0

3.5

4.0

0

10

20

30

40

50

60

Boys, L/min

Boys, ml/kg

Girls, ml/kg

Girls, L/min

6 7 8 9 10 11 12Age (years)

13 14 15 16 17 18

Figure 3-4. Changes in VO2 max with increasing age from 6 to 18 years of age in boys and girls*. .

76


in younger adults (Kohrt et al. 1991). The inter-relationships of age, V̇O2max, and training statusare evident when the loss in V̇O

2max with age is

compared for active and sedentary individuals(Figure 3-5).

When the cardiorespiratory responses of an olderadult are compared with those of a young or middle-aged adult at the same absolute submaximal rate ofwork, stroke volume for an older person is generallylower and heart rate is higher from the attempt tomaintain cardiac output. Because this attempt isgenerally insufficient, the A--vO2 difference mustincrease to provide the same submaximal oxygenuptake (Raven and Mitchell 1980; Thompson andDorsey 1986). Some researchers have shown, how-ever, that cardiac output can be maintained at bothsubmaximal and maximal rates of work through ahigher stroke volume in older adults (Rodeheffer etal. 1984).

The deterioration in physiological function nor-mally associated with aging is, in fact, caused by acombination of reduced physical activity and the

aging process itself. By maintaining an activelifestyle, or by increasing levels of physical activ-ity if previously sedentary, older persons canmaintain relatively high levels of cardiovascularand metabolic function, including V̇O2max (Kohrtet al. 1991), and of skeletal muscle function (Rogersand Evans 1993). For example, Fiatarone and col-leagues (1994) found an increase of 113 percent inthe strength of elderly men and women (mean age of87.1 years) following a 10-week training program ofprogressive resistance exercise. Cross-sectional thighmuscle area was increased, as was stair-climbingpower, gait velocity, and level of spontaneous activ-ity. Increasing endurance and strength in the elderlycontributes to their ability to live independently.

Differences by SexFor the most part, women and men who participatein exercise training have similar responses in car-diovascular, respiratory, and metabolic function(providing that size and activity level are normal-ized). Relative increases in V̇O2max are equivalent

Figure 3-5. Changes in VO2 max with aging, comparing an active population and sedentary population (the figure also illustrates the expected increase in VO2 max when a previously sedentary person begins an exercise program)

0

10

20

30

40

50

60

70

20 30 40 50

Age (years)

60 70 80

VO

2 m

ax (m

l•kg

-1•

min

-1)

Active adults Reduction in activity plus “aging”

Sedentary adults

Expected increase in VO2 max resulting from an exercise intervention

Reduction in activity plus weight gain

.

..

.

Adapted, by permission, from Buskirk ER, Hodgson JL. Federation Proceedings 1987.

.

77


for women and men (Kohrt et al. 1991; Mitchell etal. 1992). Some evidence suggests that older womenaccomplish this increase in ̇VO

2max mainly through

an increase in the A--vO2 difference, whereas youngerwomen and men have substantial increases in strokevolume, which increases maximal cardiac output(Spina et al. 1993). With resistance training, womenexperience equivalent increases in strength (Rogersand Evans 1993; Holloway and Baechle 1990),although they gain less fat-free mass due to lessmuscle hypertrophy.

Several sex differences have been noted in theacute response to exercise. At the same absoluterate of exercise, women have a higher heart rateresponse than men, primarily because of a lowerstroke volume. This lower stroke volume is a func-tion of smaller heart size and smaller blood volume.In addition, women have less potential to increasethe A--vO2 difference because of lower hemoglobincontent. Those differences, in addition to greaterfat mass, result in a lower ̇VO2max in women, evenwhen normalized for size and level of training(Lewis, Kamon, Hodgson 1986).

Conclusions1. Physical activity has numerous beneficial physi-

ologic effects. Most widely appreciated are itseffects on the cardiovascular and musculo-skeletal systems, but benefits on the functioningof metabolic, endocrine, and immune systemsare also considerable.

2. Many of the beneficial effects of exercise train-ing—from both endurance and resistance ac-tivities—diminish within 2 weeks if physicalactivity is substantially reduced, and effectsdisappear within 2 to 8 months if physicalactivity is not resumed.

3. People of all ages, both male and female, undergobeneficial physiologic adaptations to physicalactivity.

Research Needs1. Explore individual variations in response to

exercise.

2. Better characterize mechanisms through whichthe musculoskeletal system responds differen-tially to endurance and resistance exercise.

3. Better characterize the mechanisms by whichphysical activity reduces the risk of cardiovasculardisease, hypertension, and non–insulin-dependent diabetes mellitus.

4. Determine the minimal and optimal amount ofexercise for disease prevention.

5. Better characterize beneficial activity profiles forpeople with disabilities.

ReferencesAbernethy PJ, Thayer R, Taylor AW. Acute and chronic

responses of skeletal muscle to endurance and sprintexercise: a review. Sports Medicine 1990;10:365–389.

American College of Sports Medicine. Position stand:physical activity, physical fitness, and hypertension.Medicine and Science in Sports and Exercise 1993;25:i–x.

Armstrong RB, Warren GL, Warren JA. Mechanisms ofexercise-induced muscle fibre injury. Sports Medicine1991;12:184–207.

Bar-Or O. Pediatric sports medicine for the practitioner:from physiologic principles to clinical applications. NewYork: Springer-Verlag, 1983.

Birk TJ. Poliomyelitis and the post-polio syndrome: exer-cise capacities and adaptations—current research, fu-ture directions, and widespread applicability. Medicineand Science in Sports and Exercise 1993;25:466–472.

Blomqvist CG, Saltin B. Cardiovascular adaptations tophysical training. Annual Review of Physiology1983;45:169–189.

Bloomfield SA, Coyle EF. Bed rest, detraining, and reten-tion of training-induced adaptation. In: Durstine JL,King AC, Painter PL, Roitman JL, Zwiren LD, editors.ACSM’s resource manual for guidelines for exercise test-ing and prescription. 2nd ed. Philadelphia: Lea andFebiger, 1993:115–128.

Buskirk ER, Hodgson JL. Age and aerobic power: the rateof change in men and women. Federation Proceedings1987;46:1824–1829.

Chesnut CH III. Bone mass and exercise. American Journalof Medicine 1993;95(5A Suppl):34S–36S.

78


Coyle EF. Cardiovascular function during exercise: neuralcontrol factors. Sports Science Exchange 1991;4:1–6.

Davis GM. Exercise capacity of individuals with para-plegia. Medicine and Science in Sports and Exercise1993;25:423–432.

Doubt TJ. Physiology of exercise in the cold. SportsMedicine 1991;11:367–381.

Drinkwater BL. Physical activity, fitness, and osteoporosis.In: Bouchard C, Shephard RJ, Stephens T, editors.Physical activity, fitness, and health: international proceed-ings and consensus statement. Champaign, IL: HumanKinetics, 1994:724–736.

Fagard RH, Tipton CM. Physical activity, fitness, andhypertension. In: Bouchard C, Shephard RJ, Stephens T,editors. Physical activity, fitness, and health: internationalproceedings and consensus statement. Champaign, IL:Human Kinetics, 1994:633–655.

Farrell PA, Wilmore JH, Coyle EF, Billing JE, Costill DL.Plasma lactate accumulation and distance runningperformance. Medicine and Science in Sports 1979;11:338–344.

Fernhall B. Physical fitness and exercise training of indi-viduals with mental retardation. Medicine and Sciencein Sports and Exercise 1993;25:442–450.

Fiatarone MA, O’Neill EF, Ryan ND, Clements KM, SolaresGR, Nelson ME, et al. Exercise training and nutritionalsupplementation for physical frailty in very elderlypeople. New England Journal of Medicine 1994;330:1769–1775.

Figoni SF. Exercise responses and quadriplegia. Medicineand Science in Sports and Exercise 1993;25:433–441.

Fleck SJ, Kraemer WJ. Designing resistance training pro-grams. Champaign, IL: Human Kinetics, 1987:264.

Fulco CS, Cymerman A. Human performance and acutehypoxia. In: Pandolf KB, Sawka MN, Gonzalez RR,editors. Human performance physiology and environ-mental medicine at terrestrial extremes. Indianapolis:Benchmark Press, 1988:467–495.

George KP, Wolfe LA, Burggraf GW. The “athletic heartsyndrome”: a critical review. Sports Medicine1991;11:300–331.

Gledhill N, Cox D, Jamnik R. Endurance athletes’ strokevolume does not plateau: major advantage is diastolicfunction. Medicine and Science in Sports and Exercise1994;26:1116–1121.

Gonyea WJ, Sale DG, Gonyea FB, Mikesky A. Exercise-induced increases in muscle fiber number. EuropeanJournal of Applied Physiology 1986;55:137–141.

Gordon NF, Kohl HW III, Pollock ML, VaandragerH, Gibbons LW, Blair SN. Cardiovascular safety ofmaximal strength testing in healthy adults. AmericanJournal of Cardiology 1995;76:851–853.

Graves JE, Pollock ML, Leggett SH, Braith RW, CarpenterDM, Bishop LE. Effect of reduced training frequencyon muscular strength. International Journal of SportsMedicine 1988;9:316–319.

Green HJ, Jones LL, Painter DC. Effects of short-termtraining on cardiac function during prolonged exer-cise. Medicine and Science in Sports and Exercise1990;22:488–493.

Grover RF, Weil JV, Reeves JT. Cardiovascular adaptationto exercise at high altitude. Exercise and Sport SciencesReviews 1986;14:269–302.

Hickson RC. Skeletal muscle cytochrome c and myoglo-bin, endurance, and frequency of training. Journal ofApplied Physiology 1981;51:746–749.

Hickson RC, Foster C, Pollock ML, Galassi TM, Rich S.Reduced training intensities and loss of aerobic power,endurance, and cardiac growth. Journal of AppliedPhysiology 1985;58:492–499.

Hickson RC, Rosenkoetter MA. Reduced training fre-quencies and maintenance of increased aerobic power.Medicine and Science in Sports and Exercise 1981;13:13–16.

Hoffman-Goetz L, Pedersen BK. Exercise and the immunesystem: a model of the stress response? ImmunologyToday 1994;15:382–387.

Holloway JB, Baechle TR. Strength training for femaleathletes: a review of selected aspects. Sports Medicine1990;9:216–228.

Isea JE, Piepoli M, Adamopoulos S, Pannarale G, SleightP, Coats AJS. Time course of haemodynamic changesafter maximal exercise. European Journal of ClinicalInvestigation 1994;24:824–829.

Jacobs I, Martineau L, Vallerand AL. Thermoregulatorythermogenesis in humans during cold stress. Exerciseand Sport Sciences Reviews 1994;22:221–250.

Jolesz F, Sreter FA. Development, innervation, and activity–pattern induced changes in skeletal muscle. AnnualReview of Physiology 1981;43:531–552.

Jorgensen CR, Gobel FL, Taylor HL, Wang Y. Myocardialblood flow and oxygen consumption during exercise.Annals of the New York Academy of Sciences 1977;301:213–223.

79


Kannus P, Jozsa L, Renström P, Järvinen M, Kvist M,Lehto M, et al. The effects of training, immobiliza-tion, and remobilization on musculoskeletal tissue.Scandinavian Journal of Medicine and Science in Sports1992;2:100–118.

Keast D, Cameron K, Morton AR. Exercise and the im-mune response. Sports Medicine 1988;5:248–267.

Kiens B, Éssen-Gustavsson B, Christensen NJ, Saltin B.Skeletal muscle substrate utilization during submaximalexercise in man: effect of endurance training. Journal ofPhysiology 1993;469:459–478.

Kohrt WM, Malley MT, Coggan AR, Spina RJ, Ogawa T,Ehsani AA, et al. Effects of gender, age, and fitness levelon response of V̇O

2 max to training in 60–71 yr olds.

Journal of Applied Physiology 1991;71:2004–2011.

Krahenbuhl GS, Skinner JS, Kohrt WM. Developmentalaspects of maximal aerobic power in children. Exerciseand Sport Sciences Reviews 1985;13:503–538.

Lewis DA, Kamon E, Hodgson JL. Physiological differ-ences between genders: implications for sports condi-tioning. Sports Medicine 1986;3:357–369.

Lipman RL, Raskin P, Love T, Triebwasser J, Lecocq FR,Schnure JJ. Glucose intolerance during decreasedphysical activity in man. Diabetes 1972;21:101–107.

MacIntyre DL, Reid WD, McKenzie DC. Delayed musclesoreness: the inflammatory response to muscle injuryand its clinical implications. Sports Medicine 1995;20:24–40.

Marcus ML. The coronary circulation in health and disease.New York: McGraw Hill, 1983.

Mitchell JH, Tate C, Raven P, Cobb F, Kraus W, MoreadithR, et al. Acute response and chronic adaptation toexercise in women. Medicine and Science in Sports andExercise 1992;24(6 Suppl):S258–S265.

Montain SJ, Coyle EF. Influence of graded dehydration onhyperthermia and cardiovascular drift during exercise.Journal of Applied Physiology 1992;73:1340–1350.

Neufer PD, Costill DL, Fielding RA, Flynn MG, KirwanJP. Effect of reduced training on muscular strength andendurance in competitive swimmers. Medicine andScience in Sports and Exercise 1987;19:486–490.

Newsholme EA, Parry-Billings M. Effects of exercise on theimmune system. In: Bouchard C, Shephard RJ, StephensT, editors. Physical activity, fitness, and health: interna-tional proceedings and consensus statement. Champaign,IL: Human Kinetics, 1994:451–455.

Nieman DC. Exercise, infection, and immunity. Interna-tional Journal of Sports Medicine 1994;15(3 Suppl):S131–S141.

Pedersen BK, Ullum H. NK cell response to physicalactivity: possible mechanisms of action. Medicine andScience in Sports and Exercise 1994;26:140–146.

Ponichtera-Mulcare JA. Exercise and multiple sclerosis.Medicine and Science in Sports and Exercise 1993;25:451–465.

Raven PB, Mitchell J. The effect of aging on the cardiovas-cular response to dynamic and static exercise. In:Weisfeldt ML, editor. The aging heart. New York:Raven Press, 1980:269–296.

Reichlin S. Neuroendocrinology. In: Wilson JD, FosterDW, editors. Williams’ textbook of endocrinology. 8thed. Philadelphia: W.B. Saunders, 1992:201.

Rodeheffer RJ, Gerstenblith G, Becker LC, Fleg JL,Weisfeldt ML, Lakatta EG. Exercise cardiac outputis maintained with advancing age in healthy humansubjects: cardiac dilatation and increased strokevolume compensate for a diminished heart rate.Circulation 1984;69:203–213.

Rogers MA, Evans WJ. Changes in skeletal muscle withaging: effects of exercise training. Exercise and SportSciences Reviews 1993;21:65–102.

Rowell LB. Human cardiovascular control. New York:Oxford University Press, 1993.

Rowell LB. Human circulation regulation during physicalstress. New York: Oxford University Press, 1986.

Saltin B, Blomqvist G, Mitchell JH, Johnson RL, WildenthalK, Chapman CB. Response to exercise after bed restand after training: a longitudinal study of adaptivechanges in oxygen transport and body composition.Circulation 1968;38(Suppl 7):1–78.

Saltin B, Rowell LB. Functional adaptations to physicalactivity and inactivity. Federation Proceedings 1980;39:1506–1513.

Scruggs KD, Martin NB, Broeder CE, Hofman Z, ThomasEL, Wambsgans KC, et al. Stroke volume duringsubmaximal exercise in endurance-trained normo-tensive subjects and in untrained hypertensive sub-jects with beta blockade (propranolol and pindolol).American Journal of Cardiology 1991;67:416–421.

Seals DR, Hagberg JM, Spina RJ, Rogers MA, SchechtmanKB, Ehsani AA. Enhanced left ventricular perfor-mance in endurance trained older men. Circulation1994;89:198–205.

80


Shephard RJ. Aerobic fitness and health. Champaign, IL:Human Kinetics, 1994.

Shephard RJ. Metabolic adaptations to exercise in thecold: an update. Sports Medicine 1993;16:266–289.

Shephard RJ, Shek PN. Cancer, immune function, andphysical activity. Canadian Journal of Applied Physiology1995;20:1–25.

Sjöström M, Lexell J, Eriksson A, Taylor CC. Evidence offibre hyperplasia in human skeletal muscles fromhealthy young men? A left-right comparison of thefibre number in whole anterior tibialis muscles. Euro-pean Journal of Applied Physiology 1991;62:301–304.

Spina RJ, Ogawa T, Miller TR, Kohrt WM, Ehsani AA.Effect of exercise training on left ventricular perfor-mance in older women free of cardiopulmonary dis-ease. American Journal of Cardiology 1993;71:99–104.

Svedenhag J, Henriksson J, Sylvén C. Dissociation oftraining effects on skeletal muscle mitochondrial en-zymes and myoglobin in man. Acta PhysiologicaScandinavica 1983;117:213–218.

Terjung RL. Muscle adaptations to aerobic training. SportsScience Exchange 1995;8:1–4.

Thompson PD, Dorsey DL. The heart of the mastersathlete. In: Sutton JR, Brock RM, editors. Sports medi-cine for the mature athlete. Indianapolis: BenchmarkPress, 1986:309–318.

Tipton CM. Exercise, training, and hypertension: anupdate. Exercise and Sport Sciences Reviews 1991;19:447–505.

Tipton CM, Vailas AC. Bone and connective tissue adap-tations to physical activity. In: Bouchard C, ShephardRJ, Stephens T, Sutton JR, McPherson BD, editors.Exercise, fitness, and health: a consensus of current knowl-edge. Champaign, IL: Human Kinetics, 1990:331–344.

Toner MM, McArdle WD. Physiological adjustments ofman to the cold. In: Pandolf KB, Sawka MN, GonzalezRR, editors. Human performance physiology and envi-ronmental medicine at terrestrial extremes. Indianapolis:Benchmark Press, 1988:361–399.

Turley KR, McBride PJ, Wilmore JH. Resting metabolicrate measured after subjects spent the night at home vsat a clinic. American Journal of Clinical Nutrition1993;58:141–144.

Wilmore JH, Costill DL. Physiology of sport and exercise.Champaign, IL: Human Kinetics, 1994.

Woods JA, Davis JM. Exercise, monocyte/macrophagefunction, and cancer. Medicine and Science in Sportsand Exercise 1994;26:147–157.

physiologic responses and long-term adaptations to exercise

Documents