Лучшее из переведенного



Mustafa Gül

Atatürk University, Erzurum, Turkey

Osmo Hänninen

University of Kuopio, Finland

Keywords: exercise, training, skeletal muscle, cardiovascular functions, respiration, fatigue


1. Introduction

2. Skeletal Muscle

3. Cardiovascular Adaptation due to Exercise

4. Respiratory Regulation During Exercise

5. Fatigue

6. Conclusion




Biographical Sketches


Skeletal muscle consists of slow-oxidative fibers, fast-oxidative glycolytic fibers, and fast-glycolytic fibers. Slow-oxidative fibers are recruited during low-intensity endurance events, such as marathon running. Fast-oxidative-glycolytic fibers, generating more force but fatiguing easily, are used mainly during shorter, higher-intensity endurance events, such as in a 1 mile run. Fast-glycolytic fibers are predominantly used in highly explosive events, such as the 100 m dash. Endurance training increases the number of mitochondria in the slow-oxidative and fast-oxidative glycolytic fibers and also the capillaries around them. On the other hand, short-duration, high-intensity exercise, such as weight lifting, affects primarily the fast-glycolytic fibers, resulting in muscle hypertrophy. Energy for short-duration and high-intensity exercise is provided by the immediate energy system, including ATP and creatine phosphate, and anaerobic glycolysis, while it is mainly provided by oxidative phosphorylation for endurance-type exercise.

Both heart rate and stroke volume increase proportionally to exercise intensity, the latter leveling off earlier. The increase in stroke volume results from increased contractility of the ventricle and venous return. Most of the increase in cardiac output goes to the exercising muscles, heart, and skin during exercise. Endurance training increases capillary density in muscles and stroke volume but decreases heart rate with no change in cardiac output at rest. Systolic blood pressure increases during exercise with either no change or a slight decrease in diastolic pressure. Plasma volume decreases owing to increased capillary filtration and more oxygen is extracted from the blood by the active muscles during exercise. The respiratory system provides adequate aeration of the blood, even in heavy exercise. Therefore, respiration is mainly controlled by neurogenic mechanisms during exercise. The exercise capacity is usually limited by the ability of the heart to pump blood to the muscles. The respiratory muscles can, however, be weak. Regular aerobic exercise can provide a prolonged, healthy life span by decreasing heart attacks, brain strokes, and excess weight by its beneficial effects on metabolism, circulation, and blood lipid profile.

1. Introduction   

During exercise, many adjustments occur in our body functions. They require a series of interactions involving practically all of the body’s systems, for example:

 skeletal muscles contract and relax moving the body or body parts,

 cardiovascular and respiratory systems work together to provide oxygen to the cells and also to remove CO2,

 skin helps to maintain body temperature by dissipating heat,

 the nervous system coordinates activities, and

 digestive functions are slowed down.

The functions of many of these systems can be observed during exercise. For example, electrical activity of the heart can easily be recorded by heart rate meters, which are already used by many athletes to follow their individual endurance programs.  Electrical activity of the individual muscles can also be recorded during training for later analysis to evaluate the efficacy of the program (see Figure 1).


Figure 1. Measurement of the electrical activity of quadriceps femoris muscles of an athlete with a portable electromyograph. The coach is attaching the surface electrodes before the running test. Surface electrodes cause no pain and do not hamper the performance. The device stores the signals for later computer analysis.

Once the muscle fiber is stimulated by an impulse from the nervous system, contraction processes become activated. They involve specific protein molecules actin and myosin and energy systems to provide the fuel necessary for contraction. As can be seen, physical activity exercise is a complicated process.

Basically, athletic activities can be classified as power, speed, and endurance events. Examples of these are the shot put, the 400 m sprint, and the marathon run, respectively. Skeletal muscle has three energy systems, each of which is used in these three types of activities:

 the immediate energy system, including ATP and creatine phosphate (CP) these two together are also known as the phosphagen system in cytosol;

 anaerobic glycolysis in cytosol; and

 oxidative phosphorylation in mitochondria.

In this article, the functions of skeletal muscle; muscle fiber types and their importance in exercise; muscle fitness, adaptation to activity and energy systems of the skeletal muscle; alterations in cardiovascular functions, such as heart rate, stroke volume, distribution of cardiac output, muscle blood flow, blood pressure, and blood itself during exercise, respiratory adjustments occurring in exercise; and finally fatigue are briefly reviewed.

If physical activity is decreased, skeletal muscles become progressively smaller in diameter. The amount of contractile proteins decreases (called atrophy) owing to the lack of contractions, which may result from denervation, such as in stroke and paralysis or long-term immobilization of the muscle (e.g., because of bone, cartilage, or tendon trauma).

2. Skeletal Muscle   

2.1. Sliding Filaments

Skeletal muscle usually refers to a number of muscle bundles bound together by connective tissue, and usually linked to bones by bundles of collagen fibers tendons located at each end of the muscle. In addition to the elastic components in series like the tendons, the muscles also contain significant amounts of elastic components in parallel with the contractile elements (i.e., muscle fibers). One of the such components is titin. These elastic components store energy, for instance in running, when the leg hits the ground. Their role increases with speed and may mean an increase of 60 70% in efficiency. Each muscle bundle is composed of thousands of individual muscle cells or fibers. Each fiber has a diameter of between 10 and 100 µm and a length that may extend up to 20 cm. Most of the fiber cytoplasm is filled with myofibrils, which extend from one end to the other. The number of myofibrils varies from several hundred to thousands per fiber depending on the fiber diameter.

Each myofibril is divided along its length into sarcomeres, which are the functional units of the contractile system. Each sarcomere contains two types of filaments: thick and thin. The thick filaments are composed almost entirely of the contractile protein myosin, while the thin filaments contain the contractile protein actin, as well as two other proteins: troponin and tropomyosin, which play important roles in regulating contraction.

In order for the cross bridges to bind to actin, the tropomyosin molecules must be removed from their actin-blocking positions. This occurs when calcium binds to specific binding sites on troponin. Cytosolic calcium-ion concentration determines the number of cross bridges, which can bind to actin and exert force on the thin filaments. Changes in cytosolic calcium concentration are controlled by electrical events occurring in the plasma membrane.

During muscle contraction, cross bridges extending from the surface of the thick filaments make contact with the thin filaments and exert force on them. The actin filaments slide past the myosin filaments by cross-bridge attachments between the two filaments, so that the length of the sarcomere becomes shorter owing to the inward movement of the actin.

The globular end of myosin has an active enzymatic site that catalyzes the breakdown of adenosine triphosphate (ATP), thus releasing the chemical energy stored in ATP needed for the cross-bridge movement. ATP is also needed to pump Ca+2-ions back into the sarcoplasmic reticulum and thus to break the link of myosin and actin at the end of a contraction (see, ExcitationContraction Coupling in Skeletal Muscle).

2.2. Skeletal Muscle Fiber Types

In human beings, all skeletal muscle fibers do not have the same mechanical and metabolic characteristics. Different types of muscle fibers can be identified on the basis of their maximal velocities of shortening (fast and slow) and the major pathway they use to form ATP (oxidative and glycolytic) (see, Muscle Energy Metabolism). Muscle fibers are generally classified as slow-oxidative (SO) and fast-glycolytic fibers. Fast-glycolytic fibers are further classified as fast-oxidative-glycolytic (FOG) and fast-glycolytic (FG) fibers.

Fast and slow fibers contain myosin isozymes that differ in the maximal rates at which they split ATP to release energy for contraction or to allow relaxation. Fibers containing myosin with high ATPase activity are classified as fast fibers, and those containing myosin with a lower ATPase activity are slow fibers.

Slow oxidative fibers contain numerous mitochondria and have a high capacity for oxidative phosphorylation. These fibers may contain significant amounts of lipid but less glycogen. Most ATP produced by such fibers is dependent upon blood oxygen supply and fuel molecules. Numerous capillaries surround these fibers. They also contain large amounts of oxygen-binding myoglobin, which increases the oxygen extraction and provides a small intracellular store of oxygen. Myoglobin gives a dark red color, and thus oxidative fibers are often referred to as red muscle fibers.

In contrast, fast fibers, also called glycolytic fibers, have few mitochondria, but they possess a high concentration of glycolytic enzymes and a large store of glycogen. Corresponding to their limited use of oxygen, relatively few capillaries surround them, and they contain little myoglobin. They are called white muscle fibers owing to their lighter color compared with the red oxidative fibers.

The glycolytic fibers generally have much larger diameters than oxidative fibers. The larger the diameter, the greater the maximal tension it can develop (i.e., the greater its strength).

A motor unit is a single motor neuron and the muscle fibers it innervates. When a single SO motor neuron stimulates its fibers, far fewer muscle fibers contract than when a single FG motor neuron stimulates its fibers. Consequently, FG motor fibers reach peak tension faster and collectively generate more force than SO fibers do.

Skeletal muscle fibers also differ in their capacity to resist fatigue. FG fibers fatigue rapidly, whereas SO fibers are very resistant to fatigue. The fast-oxidative fibers have an intermediate capacity to resist fatigue. The characteristics of skeletal muscle fiber types are summarized in Table 1.

Table 1. Characteristics of muscle fiber types. System 1 is used in the text to classify muscle fibers, but names used in other systems are also shown.

In humans, all muscles have varying percentages of the FG and SO muscle fibers. Depending on the proportions of the fiber types present, muscles can differ considerably in their maximal contraction speed, strength, and fatigability. For instance, the gastrocnemius muscle has a higher preponderance of FG fibers, which gives it the capability of forceful and rapid contraction, used, for example, in jumping. On the other hand, the soleus muscle has more SO muscle fibers and is used for prolonged muscle activity in the legs.

In general, SO muscle fibers have a high level of aerobic endurance. The ability to maintain muscular activity for a prolonged period is known as muscular endurance. Since SO fibers have high aerobic endurance, they are recruited most often during endurance events (e.g., marathon running) and during most daily activities, where the muscle force requirements are low (e.g., walking).

FG muscle fibers, on the other hand, have relatively poor aerobic endurance. The FG fibers are used rather infrequently in normal, low-intensity activity, but they are predominantly used in highly explosive events. They are presumed to become active when the anaerobic threshold is exceeded during exercise; then the lactic acid level starts to increase in blood and in the muscle fibers a bit earlier.

FOG motor units generate considerably more force than SO motor units, but they fatigue easily because of their limited endurance. Thus, FOG fibers appear to be used mainly during shorter, higher-intensity endurance events, such as the 1 mile run or the 400 m swim.

Athletic training has not been shown to change the relative proportions of FG and SO fibers. Instead, this seems to be determined almost entirely by genetic inheritance, and this in turn could determine the basic athletic capabilities of different individuals. In practical terms the motor nerve dictates the type of the muscle fibers in a motor unit. If a nerve innervating a slow motor unit is cut and reunited with another nerve fiber innervating a fast motor unit, this formerly fast motor unit can gradually change and become a slow one.Varying percentages of fiber types in quadriceps muscles of some athletes from different disciplines are shown in Table 2.

Table 2. Percentages of SO versus FG fibers in quadriceps muscles of athletes compared to an average human

Horse races interest many people. Horses also participate in the Olympic Gamesof course not alone. A Finnish horse (fast fibers composing about 70% of their muscle) can run 12.5 m in a second, while a quarter horse (fast fibers composing about 90% of their muscle) can run 20 m in a second clear indications of their different properties, which have developed over generations.

Muscles also contain totally different types of muscle fibers in their muscle spindles. These structures sense the tension of the muscle. The sensitivity of the muscle spindles can be adjusted by the contraction of their specialized intrafusal muscle fibers. The spindles are in parallel with the main muscle or extrafusal fibers. The gamma-motoneurons control the tension level of the intrafusal muscle fibers in spindles whereas the alfa-motoneurons regulate the extrafusal muscle fibers, which are responsible for the muscle contraction itself.

2.3. Muscle Fitness

The fitness of muscles affects the ability to exercise. The fitness of muscles can be evaluated in several different ways. Fitness clubs provide a number of simple methods.

An indirect way is to measure force/torque output of the upper and lower limbs, as well as upper body and neck, with the aid of different training machines such as isokinetic, isotonic, and isometric training devices. The limitation in these methods is that they define the activity or power output of one specific muscle or muscle group.

Simultaneous surface electromyography helps to describe entire muscle performance, and the participating muscles producing the power output can also be detected easily.

Electrical activity can be recorded without causing pain or disturbing the person by using surface electrodes attached to the skin above the muscle to be studied; as in electrocardiography they are glued to the chest and extremities. When muscles are loaded in standard ways, a linear increase in the electrical activity is observed. A strong person can lift a much heavier load than a weak person, because of the larger muscle fibers in the strong person. A higher electrical activity is generated in the muscles of a weak than in a strong person, if they lift the same load.When muscles fatigue, the electrical activity increases with time, if the muscles work for a long time against the same load. With the increase of electrical activity the low-frequency components of the electromyographic spectrum also increase, while the high-frequency components tend to be blocked out as it is their nature to perform short-lasting tasks.

This shift to lower frequencies can easily be calculated during fatiguing exercise, and simple figures such as median frequency provide the information needed on muscle fitness in, for example, 2 minute test times (see, Figure 2). If trunk muscles are the objects of interest, one can use as a standard load the maintenance in the same position of, for example, the upper body over a table edge, and record the electrical activity from the paraspinal muscles. More specific loading can be run in special training chairs. Trunk muscles are important in every physical activity, and their fitness has a role in the maintenance of balance and standing posture. If trunk muscles are poorly developed, low back pain risk is greater, especially if the person happens to lift something heavy using the wrong techniques.


Figure 2. The decrease of dynamically recorded spectral mean power frequency of electrical activity of the paraspinal muscles on the left side at the level of the fifth lumbar vertebra and first sacral vertebra of fit (A) and less fit (B) male subjects when they have done dynamic back-and-forth movements against load in a back extension training device. The decrease in the less fit person is much faster than in the fit person.

By following electrical activity during training programs one gets objective data on the progress of the exercises as the fitness increases and fatiguing decreases. This method is especially valuable when observing the muscles, which are difficult to test in any other way. The pelvic floor muscles are important. A sedentary life style, decreasing estrogen hormone level because of aging, obesity, and several child deliveries are the most common reasons for decreasing fitness. Urinary incontinence is one of the most annoying problems of middle-aged women, but it is not uncommon in males either. Training of the pelvic floor muscles is one of the great challenges. The use of biofeedback, using electromyographic sensors in the vagina, is a physiological solution. The audiovisual feedback motivates the patient to continue pelvic exercises with a positive treatment response, and an improvement in pelvic muscle condition can be detected after one to three months of doing the exercises.

2.4. Adaptation of the Skeletal Muscle to Exercise

Two types of change can occur in skeletal muscle fibers as a result of exercise or inactivity: (1) alterations in their ATP-forming capacity as a result of increases or decreases of enzymes in the various ATP-producing pathways, and (2) changes in the diameters of the muscle fibers as a result of the formation or loss of myofibrils in the muscle blood flow. Exercise will not change the fiber type distribution in the muscles. Regular exercise causes adaptation in the connective tissue in the muscles and their tendons, too.

2.4.1. Adaptation to Endurance Exercise

Relatively low intensity exercise but of long duration, such as long-distance running and swimming, increases the number of mitochondria and their enzymes in the SO and FOG fibers, which are recruited in this kind of activity; the enzyme activities of antioxidant defense are also increased. All these changes lead to an increase in endurance. Fiber diameter may decrease slightly, and thus there is a small decrease in the strength of the muscles as a result of endurance exercise.

Endurance also depends on the amount of glycogen that has been stored in muscles before the period of exercise. At high exercise levels more ATP is produced per mole of oxygen from glycogen (about 6.5 moles of ATP per mole oxygen consumed) than in burning fatty acids (about 5.6 moles of ATP per mole of oxygen consumed). A person on a high-carbohydrate diet can store far more glycogen in muscles than a person on either a mixed or high-fat diet. After a fast, poor endurance can be expected.

In addition, there is an increase in the number of capillaries around the fibers. As will be discussed later, endurance exercise also produces other changes in the circulatory and respiratory systems, which improve the delivery of oxygen and fuel molecules to the muscles.

In exercise eccentric efforts are more tiring than concentric efforts. In eccentric work, where the muscle resists lengthening, such as in walking downhill, the muscles may suffer from small traumas and aching muscles can be expected.

2.4.2. Adaptation to Short-Duration, High-Intensity Exercise

Short-duration, high-intensity exercise, such as weight lifting, primarily affects the FG fibers. They are recruited when the intensity of contraction exceeds about 40% of the maximal tension produced by the muscle. The diameter of these fibers increases because of the increased synthesis of actin and myosin filaments to form more myofibrils. The hypertrophy results in an increased diameter of the muscle fibers rather than increased numbers of fibers, but this is probably not entirely true because greatly enlarged muscle fibers may develop new fibers via satellite cell activation, thus increasing the number of fibers. In addition, the activity of glycolytic enzymes increases.

The result of such high-intensity exercise is to increase the strength of the muscle. Although hypertrophied muscles are powerful, they fatigue rapidly. On the other hand, it should not be overlooked that the basic size of a person’s muscles is determined mainly by heredity plus the level of testosterone secretion, which, in men, causes considerably larger muscles than seen in women.

Because different types of exercise produce quite different changes in the strength and endurance capacity of a muscle, an individual must choose the type of exercise that is compatible with the activity he or she ultimately wishes to perform (i.e., the specificity of training). If a regular pattern of exercise is stopped, the changes in the muscle will slowly revert to their state before starting the training or even below.

2.5. Energy Metabolism of the Skeletal Muscle

2.5.1. Alactic Mechanisms

CP provides a reserve of phosphate energy to regenerate ATP from ADP at the onset of contractile activity (see, Figure 3):


At rest, muscle fibers build up a concentration of CP up to five times that of ATP. At the beginning of contraction, when the concentration of ATP begins to fall and ADP to rise owing to the increased rate of ATP breakdown, the mass action favors the formation of ATP from CP.


Figure 3. Metabolic pathways producing the ATP utilized during muscle contraction and relaxation. While anaerobic breakdown of CP and glycolysis occur in cytosol, oxidative phosphorylation takes place in mitochondria.. Source: Modified from Vander et al. (1990).

Although the formation of ATP from CP is rapid, requiring a single enzymatic reaction (Eq. 1), the amount of ATP that can be formed by this process is limited by the initial concentration of CP. Muscle fibers also contain myokinase, which catalyzes the formation of one ATP and one AMP molecule from two ADP molecules. ATP and CP, together, can provide maximal power for 8 10 s. Thus, the energy from the phosphagen system is used for maximal short bursts of muscle power needed in athletics, such as the 100 m dash, shot put, or weight lifting.

2.5.2. Glycolysis

The glycolytic pathway, although producing only small quantities of ATP from each glucose unit metabolized, can produce large quantities of ATP rapidly when enough enzymes and substrate are available. It can also do so in the absence of oxygen:


The glucose for glycolysis comes either from the blood or the glycogen stores. When the starting material is glycogen, three ATP molecules are produced per glucose unit consumed because of phosphorolytic glycogenolysis. As the intensity of muscle activity increases, more and more ATP is needed with the anaerobic breakdown of muscle glycogen, and the corresponding increase in the production of lactic acid. Anaerobic glycolysis can provide energy for 1.3 1.6 min of maximal muscle activity.

The production of lactic acid lowers the pH in the muscle fibers. This hampers the action of enzymes and causes pain, if the elimination of the lactic acid is too slow compared to the production.

2.5.3. Oxidative Phosphorylation

At moderate levels of exercise, for example, a 5000 m run or marathon, most of the ATP used for muscle contractions is formed by oxidative phosphorylation. Oxidative phosphorylation allows far more energy to be liberated from glucose compared with anaerobic glycolysis only:


Fats can be catabolized only by oxidative mechanisms, and the energy yield is high. Amino acids can also be metabolized in this way. Three metabolic pathways to produce ATP for muscle contraction and also for relaxation are shown in Figure 3.

During the first 5 10 min of moderate exercise, the muscle’s own glycogen is the major fuel consumed. For the next 30 min or so, blood-borne fuels become dominant, and blood glucose and fatty acids contribute approximately equally to the oxygen consumption of the muscle. Beyond this period, fatty acids become progressively more important. It is important to emphasize the interaction of anaerobic and aerobic mechanisms in the production of ATP during exercise. Contribution of anaerobic ATP production is greater in short-term, high-intensity activities, while aerobic metabolism predominates in longer activities with low intensity.

2.5.4. Recovery and Oxygen Debt

After the exercise is over, the oxygen uptake still remains above normal (Table 3). Recently, the term, excess post-exercise oxygen consumption, is also used for oxygen debt. At first it occurs at a very high level while the body is reconstituting the CP and ATP stores, and repaying the stored oxygen tissues, and then for another hour at a lower level while the lactic acid is removed. Therefore, the early and latter portions of the oxygen debt are called the alactacid and lactacid oxygen debts, respectively. The increased body temperature also means a higher rate of metabolism and increased oxygen consumption.

The longer and more intense the exercise, the longer it takes to recover. For example, recovery from exhaustive muscle glycogen depletion often requires days, rather than the seconds, minutes, or hours required for recovery of the CP and ATP stores and lactic acid removal. High intensity exercise probably also causes microtraumas in muscle fibers and their repair takes time.

Table 3. Oxygen debt components. After long-lasting, heavy exercise respiration continues at higher level than normal to meet the increased oxygen needs.

3. Cardiovascular Adaptation due to Exercise   

In order to meet the increased demands placed on the cardiovascular system, numerous changes occur in the cardiovascular functions during exercise.

3.1. Muscle Blood Flow During Exercise

Blood flow in resting skeletal muscle (2 4 ml/100 g × min) increases remarkably during exercise. Muscle contractions temporarily decrease muscle blood flow by compressing the intramuscular blood vessels. However, blood flow increases as much as 30-fold in rhythmically contracting muscles (90 ml g-2 min-1 in a well-trained athlete) (see, Muscle Energy Metabolism). It should also be remembered that during strong tonic muscle contractions, skeletal muscle can rapidly fatigue because of the insufficient delivery of oxygen and nutrients, which is due to the compression on these vessels.

The initial rise in muscle blood flow is probably a neurally mediated response, since it sometimes increases at or even before the start of exercise. Impulses in the sympathetic vasodilator system may be involved. Local mechanisms maintaining a high blood flow in exercising muscle include increased temperature in active muscles, a fall in tissue PO2, a rise in tissue PCO2, and accumulation of K+ and other vasodilator metabolites, such as lactate and nitric oxide.

In active muscle, temperature rises and further dilates the vessels. Dilation of the arterioles and precapillary sphincters causes a 10 100-fold increase in the number of open capillaries.

Moderately increased arterial blood pressure during exercise increases the capillary pressure. In addition, the increase in blood pressure not only forces more blood through the blood vessels but also stretches the walls of the arterioles, further reducing the vascular resistance. Accumulation of osmotically active metabolites in the interstitial fluid decreases the osmotic gradient across the capillary walls. Lymph flow is also greatly increased and greatly improves the turnover of interstitial fluid.

The decreased pH, increased temperature, and also the increased concentration of 2,3-diphosphoglycerate in red blood cells decrease the O2 affinity of hemoglobin. Thus, more O2 is left in muscle tissue by the blood, which increases the arteriovenous O2 difference up to three-fold. Transport of CO2 out of the muscle tissue is also facilitated. K+ dilates arterioles in exercising muscle, particularly during the early part of exercise. Skeletal muscle O2 consumption increases perhaps 100-fold during exercise because of all these changes.

3.2. Cardiac Functions

3.2.1. Heart Rate

The resting heart rate averages 60 80 beats min1 and can sometimes exceed 100 beats min1 in middle-aged, sedentary individuals. In highly conditioned, endurance-trained athletes lower resting heart rates, in the range of 28 40 beats min1, have been reported (see, Heart).

Before the start of exercise, the heart rate usually increases well above normal resting values. As mentioned above, this anticipatory response is likely to be mediated through the release of the neurotransmitter norepinephrine from the sympathetic nervous system and the hormone epinephrine secreted from the adrenal glands. Vagal tone probably decreases, too.

The increase in heart rate is about proportional to the increase in exercise intensity and oxygen consumption until near the point of exhaustion (see, Figure 4). The poorer the fitness of the person, the faster the heart rate increases. It begins to level off at O2 max. The withdrawal of vagal tone and increased sympathetic stimulation of the heart are responsible for the increased heart rate during exercise. One must remember also that the psychogenic increase in heart rate can be considerable.


Figure 4. The heart rate increases in proportion to the increase in bicycle ergometer load, eventually reaching a maximal rate (HRmax). It increases more in the poorly fit than in the well fit. In a fit person the linear increase with the load increase is more clear.

Maximal heart rate shows a slight but steady decrease of about 1 beat y1, beginning at 10 to 15 years of age. It is a highly reliable value that remains constant from day to day. In adults, maximal heart rate can be estimated as follows:


During a constant level of submaximal exercise, the heart rate increases and then levels off as the oxygen requirements of the activity have been satisfied. For each subsequent increase in intensity, the heart rate will reach a new steady-state value within 1 2 min. However, the more intense the exercise, the longer it takes to achieve this steady-state value.

The concept of steady-state heart rate forms the basis of several tests that have been developed to estimate physical fitness. In these tests, individuals are placed on an exercise device, such as a cycle ergometer or treadmill, and they exercise at standardized load levels. Those in better physical condition, based on their cardiorespiratory endurance capacity, will have lower steady-state heart rates at a given level of work load than those who are less fit.

During prolonged exercise, instead of leveling off, heart rate may continue steadily to increase at the same load level. This phenomenon is called cardiovascular drift, which is caused by decreased venous return to the heart. Heart rate continues to increase in order to maintain cardiac output and blood pressure at the same level despite decreased venous return. Decreased plasma volume, which is caused by filtration of fluid from the blood or by excess sweating during prolonged exercise, may decrease venous return. Decreased sympathetic tone may also play a part in decreased venous return to the heart.

Heart rates are lower during strength exercises, such as in weight lifting, than during endurance exercise, such as running. At the same power output, it is higher during upper-body than lower-body exercise. Upper-body exercise also results in higher oxygen consumption, mean arterial pressure, and total peripheral resistance. The higher circulatory load in upper-body exercise results from the use of a smaller muscle mass, increased intrathoracic pressure, and a less effective muscle pump, all decreasing the venous return of blood to the heart.

Heart rate multiplied by systolic blood pressure gives the rate pressure product (RPP), which provides an estimate of cardiac load during exercise (Eq. 5):


3.2.2. Stroke Volume

Stroke volume is the amount of blood pumped into the periphery by each cardiac systole (see , Heart). Stroke volume increases with increasing rates of work, but only up to exercise intensities between 40 and 60% of maximal capacity. After that, the stroke volume levels off. The probable causes are that high heart rates decrease ventricular filling time and that peripheral shunting of blood to active skeletal muscles decreases the central blood volume, which is necessary to maintain ventricular end-diastolic volume.

The primary factor controlling stroke volume is the extent to which the ventricle stretches. For example, if the ventricle stretches more when it fills with more blood during diastole, it will contract with more force according to the Frank Starling law. However, stroke volume can also increase, if the ventricle’s contractility is greater. Studies indicate that both the Frank Starling mechanism and contractility are important in increasing stroke volume. The Frank Starling mechanism appears to have its greatest influence at lower rates of work, while contractility has its greatest effects at higher exercise intensities.

Decreased total peripheral resistance owing to increased vasodilation of the vessels in active skeletal muscles also contributes to the increase in stroke volume during exercise by facilitating the ejection of blood from the left ventricle.

Stroke volume is probably the most important factor determining individual differences in . Athletes have a higher exercise cardiac output, since they have a higher stroke volume. For example, while both a sedentary man and a champion cross-country skier are reported to have maximal heart rates of 185 beats/min, their maximal stroke volumes have been found to be, for example, 90 and 173 ml respectively. Thus, the maximal cardiac output of the untrained man is 16.6 L min1, while it is 32 L min1 in the skier.

3.2.3. Cardiac Output

Cardiac output increases directly with exercise intensity (see, Heart):



 = cardiac output, HR = heart rate, and SV = stroke volume

The resting value of cardiac output is approximately 5 L min1. Cardiac output increases directly with increasing exercise intensity to between 20 to 40 L min1, since the major purpose of the increase in cardiac output is to meet the muscles’ increased demand for oxygen during exercise. The absolute value varies with body size and endurance conditioning (see , Muscle Energy Metabolism).

Enhanced sympathetic activity to the heart is not sufficient to account for the elevated cardiac output that occurs in exercise. Cardiac output can be increased at high levels only if venous return to the heart is simultaneously increased. Otherwise, the shortened filling time resulting from the high heart rate would lower the end-diastolic volume and in turn, stroke volume. The factors promoting venous return during exercise are:

          skeletal muscle pump,

          increased inspiration depth and frequency,

          sympathetically mediated increase in venous tone, and

          increased blood flow through the dilated skeletal muscle arterioles.

Most of the increase in cardiac output goes to the exercising muscles, but there are also increases in flow to the skin, required for conducting heat away from the body’s core to the environment, and to the heart, required for the additional work performed by the heart in pumping the increased cardiac output (see, Muscle Energy Metabolism).

In both skeletal and cardiac muscle, arteriolar dilation is mediated by local metabolic factors, whereas the dilation in skin is achieved by decreased activity of the sympathetic neurons. While arteriolar dilation is occurring in these beds during exercise, arteriolar contraction is occurring in the spleen, kidneys, and gastrointestinal organs, secondary to increased activity of the sympathetic neurons.

Coronary blood flow increases with intensity during exercise. Warming up before endurance exercise is important in facilitating an increase not only in coronary blood flow but also in the skeletal muscles during the early stages of exercise. Ischemic changes such as ST segment depression in an electrocardiogram with sudden exercise are usually benign in healthy people, but they could be dangerous in people with heart disease.

The effects of endurance training are increased capillary density in muscles, increased stroke volume, and decreased heart rate with no change in cardiac output at rest. At maximal workloads, trained individuals have an increased cardiac output owing to an increased maximal stroke volume, since maximal heart rate is not altered by training.

In upright exercise, the stroke volume normally reaches its maximum by the time the cardiac output has increased only halfway to its maximum. Any further increase in cardiac output during strenuous exercise must occur by increasing the heart rate.

Training also increases blood volume and the concentrations of oxidative enzymes and mitochondria in the exercised muscle. It is still uncertain what the most effective relative combinations of intensity and duration of exercise are. Walking is effective, if the starting fitness is poor. Too high an intensity is not optimal for the adaptive responses to happen. It is possible that the oxygen-derived radicals, which are generated during exercise-induced oxygen metabolism, have a significant role in the adaptation.

3.3. Blood Pressure

Blood pressure is a function of cardiac output and peripheral resistance (see, Heart) (Eq.7):



 = cardiac output (L/min); TPR = total peripheral resistance (dyne s cm5); 1 mmHg = 0.133 kPa, and 1 pascal (Pa) = kg m1 s2.

During exercise peripheral resistance decreases because of the dilation of arterioles in active skeletal and cardiac muscles and skin. Vasoconstriction in other organs is not enough to compensate for the vasodilation in active muscles and skin. The net result is a marked decrease in total peripheral resistance during exercise.

Even though peripheral resistance may fall to one-third of resting during exercise, systolic blood pressure increases during exercise. Cardiac output increases greatly during exercise, more than compensating for the fall in peripheral resistance.

With whole body endurance activity, systolic blood pressure increases in direct proportion to increased exercise intensity. A systolic pressure that starts from 16 kPa (120 mmHg) at rest can exceed 27 kPa (200 mmHg) at exhaustion. Systolic pressures of 32 33 kPa (240 250 mmHg) have been reported in normal, healthy, highly trained athletes at maximal levels of exercise.

Regardless of the intensity, diastolic pressure changes little if any during endurance exercise. There is either no change or a slight decrease of less than 1.33 kPa (10 mmHg) in diastolic pressure during exercise. Increases in diastolic pressure of 2 kPa (15 mmHg) or more are considered abnormal responses to exercise and exercise needs to be stopped immediately.

Blood pressure responses to resistance exercise, such as weight lifting, are exaggerated. The use of upper-body musculature, as opposed to lower-body musculature, causes a greater blood pressure response at the same absolute rate of energy expenditure during exercise.

3.4. Changes in Blood During Exercise

As metabolism increases during exercise, the functions of the blood become more vital for efficient performance. Training also increases tissue oxygenation by causing changes in the blood. The aggregation of red cells as well as trombocytes is diminished and the rheological properties of blood are promoted (see, Blood Rheology and Hemodynamics). The nitric oxide synthesis is favored in vessel walls (see, Muscle Energy Metabolism).

Arteriovenous oxygen difference increases approximately three-fold from rest to maximal levels of exercise (from 6 to 16 ml of oxygen per 100 ml blood). The active muscles need more oxygen, so more oxygen is extracted from the blood during exercise owing to increased oxygen pressure gradient. The venous oxygen content drops. However, venous blood oxygen content in the right atrium rarely drops below 2 4 ml oxygen per 100 ml of blood. The blood, which returns to the heart from the active tissues, mixes with blood returning from less active organs.

In the beginning of exercise, there is an immediate loss of blood plasma to the interstitial fluid space. This probably results from two factors. The increased hydrostatic pressure within the capillaries forces water out from the vascular compartment. In addition, more metabolic waste products accumulate in the interstitial space in active muscles, increasing osmotic pressure, which attracts more fluid to the muscle. Reduction in plasma volume of 10 20% or higher can occur during prolonged exercise.

Since plasma volume is reduced, hemoconcentration occurs during exercise increasing hematocrits from 40 to 50%. Even without an increase in the total number of red blood cells, higher hemoglobin concentration, owing to decreased plasma volume, increases the oxygen-carrying capacity of blood substantially during exercise.


Heat loss is a problem in long-duration activities (see, Thermoregulation). Blood flow to active skeletal muscles decreases to allow more blood to be diverted to the skin for temperature regulation. However, body fluid changes and temperature regulation are of little practical importance in short-lasting activities. In marathon runs the ability to maintain proper body temperature is very important. If both the environmental temperature and humidity are high, the body temperature may increase too high to permit finishing the run.

At rest, arterial blood pH is about 7.4. It changes very little from rest up to an exercise intensity of about 50% of maximal aerobic capacity. Above this level, pH starts to decrease primarily because of the increased lactate production, owing to increased reliance on anaerobic metabolism.

A summary of the cardiovascular changes in moderate exercise is shown in Table 4.

Table 4. A summary of the cardiovascular changes in moderate exercise, which involves large muscle groups for an extended period of time.

3.5. , the Best Measure of Cardiovascular Capacity

 is the product of maximum cardiac output and maximum oxygen difference (Eq. 8):



 = maximal oxygen uptake, expressed in ml min1

 = maximal cardiac output, expressed in ml min1

 = maximum arteriovenous oxygen difference, expressed in ml O2 dl1

 is the point at which oxygen consumption fails to rise despite an increased exercise intensity or power output. After  has been reached, exercise can still be sustained by anaerobic metabolism.

 is the best predictor of cardiovascular capacity. Biochemical factors such as oxidative enzyme activity and mitochondrial volume, are better predictors of endurance, which is the ability to sustain a particular level of physical effort.

The oxygen consumption capacity of a muscle varies according to fiber type. The ability of the mitochondria to extract oxygen from blood is approximately three to five times greater in slow fibers compared to fast fibers.

Cardiac output is the most important factor determining . Cardiac output can increase by 20% in endurance training. This accounts for most of the training-induced change in , since there is little difference in  between endurance athletes and sedentary people.

Even though having a high  is important for endurance, it is not the only requirement for success. The ability to continue exercising at a high level of O2 consumption, speed, and lactic acid clearance capacity are also among the important factors for athletic success.

4. Respiratory Regulation During Exercise  

During exercise, O2 extraction from blood increases three-fold accompanied by a 30-fold or greater increase in blood flow. Thus, the metabolic rate of muscle may rise as much as 100-fold during exercise.

4.1. Increased Alveolar-Capillary PO2 Gradient, Blood Flow, and CO2 Removal

The amount of O2 entering the blood in the lungs increases during exercise. The PO2 of blood flowing into the pulmonary capillaries falls from 5.3 to 3.3 kPa (from 40 to 25 mmHg) or less, so that the alveolar-capillary PO2 gradient is increased, and more O2 enters the blood. Blood flow per minute is also increased from 5.5 L min1 to as much as 2035 L min1. The total amount of O2 entering the blood therefore increases from 250 ml min1 at rest to values as high as 4000 ml min1. The amount of CO2 removed from each unit of blood is also increased.

The increase in O2 uptake is proportionate to workload up to a maximum level. With the increase of workload, there is a point where the blood lactate level starts to rise (lactate threshold). When aerobic re-synthesis of energy stores cannot keep pace with their utilization, lactate formation in muscles increases and an oxygen debt occurs. In practical terms the anaerobic threshold is reached, when the blood lactate level exceeds 4 mmole L-1. The anaerobic threshold can be observed in the changes in the respiratory parameters and in electromyographic recordings of muscles without taking blood samples, which causes some pain.

4.2. Changes in Respiratory Quotient (RQ) During Exercise

Respiratory quotient (RQ) is the ratio of the volume of CO2 produced to the volume of O2 consumed per unit of time. At rest it can be, for example, 0.8. When glucose metabolism dominates it is 1. In poorly fit persons the glucose metabolism exceeds the rate of fat metabolism already at low load levels. In highly fit endurance athletes the ability to use fatty acids in energy production continues at high load levels. During exercise the RQ rises, values perhaps reaching even 1.52.0, because of the extra CO2 produced by buffering of lactic acid during strenuous exercise. The RQ falls to 0.5 or less during the repayment of the O2 debt after exercise.

4.3. Control of Ventilation During Exercise

Ventilation increases as the exercise starts, but it does not reach the level needed immediately, only gradually. The immediate needs of energy are met by energy-rich phosphates and then by their resynthesis using oxygen, which is contained in tissue fluids or stored in oxygen-carrying proteins (see, Figure 5).


Figure 5. Changes in ventilation during exercise. Notice the abrupt increase and decrease at the onset and end of exercise, respectively. During the recovery period the small oxygen debt phase is visible.

There is an abrupt increase in ventilation at the onset of exercise and an equally abrupt decrease at the end. This suggests a conditioned, or learned response. Markedly decreased oxygen pressure of the arterial blood and increased CO2 pressure of the venous blood may be expected during exercise because of the increased metabolism of the skeletal muscles. However, both of them remain nearly normal, demonstrating the extreme ability of the respiratory system to provide adequate aeration of the blood, even in heavy exercise. Thus, the blood gases do not have to become abnormal for respiration to be stimulated in exercise.

Since the arterial PCO2 does not change during moderate exercise, there is no accumulation of excess H+ resulting from CO2 accumulation. But during strenuous exercise, there is an increase in arterial H+ concentration owing to the generation and release of lactic acid from the muscle into the blood. This change in H+ concentration may partly be responsible for stimulating hyperventilation during severe exercise.

Respiration is rather stimulated mainly by neurogenic mechanisms in exercise. Part of this stimulation results from direct stimulation of the respiratory center by branches coming off from the axons descending from the brain to motor neurons supplying exercising muscles. It is believed that afferent pathways from the receptors in joints and muscles also play a significant role in stimulating respiration during exercise.

An increase in body temperature also frequently occurs as a result of increased physical activity and contributes to stimulation of alveolar ventilation. The increased plasma concentrations of epinephrine and norepinephrine probably contribute to stimulation of ventilation during exercise.

4.4. Exercise Capacity Limiting Factor

The actual pulmonary ventilation during maximal exercise is still 50% of the maximal breathing capacity of a man. Furthermore, hemoglobin in arterial blood is saturated even during the most severe exercise. Therefore, the respiratory system may not be a factor limiting exercise capacity in healthy subjects. The fitness of respiratory muscles can, however, be a problem in nonfit persons. The factor limiting the exercise capacity is the ability of the heart to pump blood to the muscles, which in turn affects the maximal transport rate of O2. The cardiovascular fitness is a common problem. The mitochondria in the exercising muscle are the final users of oxygen, and better determinants of endurance.

5. Fatigue  

Everybody experiences muscle fatigue, but there are still some aspects that are not understood well about this phenomenon.

Fatigue can have a central component (i.e., in the central nervous system). There must be the motivation to continue the exercise or competition. Humans are social animals and companionship is an important factor in training. In principle the motoneurons commanding the motor units can also have importance in fatigue. The neurons are releasing acetylcholine in every command cycle. Acetylcholine stores are limited and its synthesis requires both energy and raw materials of which choline stores are smaller than those of acetic acid. The next steps, which can take part in the fatigue, are the neuromuscular junctions where the acetylcholine is transferring the command to the muscle fibers, to be split thereafter. The cell membrane of the fiber and its ion transporters may be  another source of fatigue. The necessary ions and their balance may be a weak point. The potassium level is high in muscle fibers, but it is released when the action potential spreads all over the plasma membrane of the muscle fiber, and it can thus diffuse further away if the re-uptake is too slow. The ion transporters require energy, as also do the intracellular calcium transporters in the sarcoplasmic reticulum membrane. It is also possible that the ion transporters or their lipid environment in the membranes become modified. Energy is provided by the cytoplasmic glycolysis and the mitochondrial oxidation of energy fuels. The catalytic proteins may become less functional because of modification when they operate. One reason is the accumulation of lactic acid and the lowering of pH, if the load has been so high that glycolysis takes place too fast compared with the mitochondrial oxidation owing to the limitation in oxygen availability. Even if then oxygen supply is good, but the load level is high (e.g., 75 80 % of the maximal oxygen uptake in an athlete), the fatigue will stop the performance owing to the shortage of glycogen in the muscle fibers, although the blood glucose level is still normal. This indicates the importance of the role of subject’s diet before strenuous endurance events. Eating immediately before exercise is not, however, recommended, because then circulation is directed to the abdominal area and is not available in the muscles. Glycogen stores must be filled a sufficient time in advance.

The increased usage of oxygen and oxygen-derived radicals may cause damage to all muscle fiber functions if the antioxidant defense systems fail to protect the enzymes, membrane lipids, and ion transporters. It is clear that the antioxidant defense is one of the weak points, since experiments with rats have shown that lowered level of glutathione is directly related to endurance time. The escape of mitochondrial and cytoplasmic proteins to plasma during heavy exercise indicates that the mitochondria can be damaged, as can also the plasma membrane of the muscle fibers (see, Muscle Energy Metabolism).

6. Conclusion   

Endurance training can increase capillary density in muscles and even the size of coronary arteries, providing increased circulation capacity. It can also reduce both systolic and diastolic blood pressures by approximately 1 1.3 kPa (8 10 mmHg) in individuals with moderate hypertension. Exercise exerts a beneficial effect on blood lipid levels. Although the decrease in total cholesterol and low density lipoprotein-cholesterol levels with endurance training are relatively small, there appear to be relatively major increases in high density lipoprotein-cholesterol and major decreases in triglycerides. Exercise also plays an important role in the control and reduction of body weight and in the control of diabetes. By these and many other beneficial effects, regular exercise can not only reduce the risk of heart attacks and brain strokes, but it promotes the quality of life with increased physical as well as mental capacity. Furthermore, it can also provide a prolonged, healthy life span.

Exercise-related research has rapidly transitioned from an organ to a subcellular/molecular focus within the last three decades. Thus, future research in exercise will probably continue to be heavily influenced by new technologies (e.g., gene-chip microarrays) and other molecular biology tools. These developments will possibly drive the emerging fields of exercise-related functional genomics (the dissecting of a gene’s identity and function) and proteomics (the study of the properties of proteins).


Authors thank Dr. Peter M. Tiidus from Wilfrid Laurier University, Canada, for critical reading of the text.




: Arteriovenous oxygen difference. The difference in oxygen content between arterial and mixed venous blood, which reflects the amount of oxygen removed by the tissues.


: A thin protein filament that acts with myosin filaments to produce muscle action.


: Adenosin-diphosphate, a high-energy phosphate compound from which ATP is formed.


: In the presence of oxygen.

Aerobic metabolism

: A process occurring in the mitochondria that uses oxygen to produce energy (ATP), also known as cellular respiration.


: In the absence of oxygen.


: A

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