Accurate data on the cardiac output in various types and intensities of exercise are not available, due largely to the very great technical difficulties of measurement. Such data as are available must be accepted with some reservation for the same reason. A great deal is known about the changes in heart rate which accompany exercise, but little is known about the equally important adjustments in the stroke volume.
Even without direct measurements, this could be postulated from the enormous increase in oxygen consumption which occurs. Krogh and Lindhard 3 using an indirect Fick method, found that the cardiac output may exceed 20 liters per minute during heavy exercise. In spite of calculations which indicated a possible total blood flow of 30 to 40 liters per minute during running when the oxygen consumption was 4 liters per minute, it is probable that in the average man the cardiac output during work seldom exceeds 20 liters per minute. An example of the enormous increase in cardiac output which can be achieved by exceptional athletes.
The increase in cardiac output which may be attained in exercise is limited by several factors. First, it is obvious that the heart cannot, for more than a few beats, eject more blood than is returned to it by the systemic veins; in other words, cardiac output cannot exceed the venous return. In numerous conditions, such as shock, hemorrhage, the erect posture with no movement, extreme heat, prolonged bed rest, etc., the cardiac output is reduced below normal by an inadequate venous return. Following strenuous exercise, the sudden withdrawal of the pumping effect of skeletal muscle contractions on venous blood flow results in a sharp fall in cardiac output. On the other hand, the available evidence indicates that the normal healthy adult heart is always able to increase its output sufficiently to handle the greatest amount of blood which can be returned to it in maximal exertion. Additional factors which may limit the increase in cardiac output in exercise are the maximal capacity of the heart for dilating and the reduction in diastolic filling of the heart which results from extremely rapid heart rates.
Finally, such adverse conditions as fatigue, lack of sleep, malnutrition and acute infections may seriously reduce the maximal cardiac output of which the subject would otherwise be capable.
Wednesday, February 27, 2008
Basal Values, The Effect of Posture
Basal Values
Under basal conditions, the cardiac output in man averages about 64 ml. per kilogram per minute. 2 It is higher in the adolescent than in the adult and decreases in subjects over forty-five years of age. Sub-basal values are found in the early hours of the morning, during standing and probably also during recovery from heavy exercise. The normal basal cardiac output has an absolute value of 4 liters per minute for an individual of average size and if the pulse rate is 70, the stroke volume is 57 ml.
The Effect of Posture
The cardiac output is usually reduced when the subject stands. Since the pulse rate is usually increased, his must indicate a reduction in stroke volume. This is especially true in prolonged standing without movement and is common after a long period of hot weather. The reduction in stroke volume is due apparently to a decrease in the venous return from the lower part of the body. In the sitting posture, the output is slightly less than when the subject is reclining, but peculiarly enough, the output is not reduced when the subject is in the erect position but leaning against a support.
Miscellaneous Influences
The cardiac output is increased by the taking of food and water and, temporarily, by high altitude. Exposure to cold slows the heart rate but increases the stroke volume, leaving the cardiac output unchanged, unless shivering occurs, when the cardiac output is increased. Exposure to warmth increases resting cardiac output very considerably. The heart rate is increased with a slight reduction in stroke volume. If the heat is severe enough to cause dehydration, cardiac output returns to the basal level. It may fall below the basal level in heat prostration in spite of a rapid heart rate, indicating a reduction in stroke volume due to inadequate venous return to the heart. Cardiac output is diminished by many types of cardiovascular abnormalties.
Under basal conditions, the cardiac output in man averages about 64 ml. per kilogram per minute. 2 It is higher in the adolescent than in the adult and decreases in subjects over forty-five years of age. Sub-basal values are found in the early hours of the morning, during standing and probably also during recovery from heavy exercise. The normal basal cardiac output has an absolute value of 4 liters per minute for an individual of average size and if the pulse rate is 70, the stroke volume is 57 ml.
The Effect of Posture
The cardiac output is usually reduced when the subject stands. Since the pulse rate is usually increased, his must indicate a reduction in stroke volume. This is especially true in prolonged standing without movement and is common after a long period of hot weather. The reduction in stroke volume is due apparently to a decrease in the venous return from the lower part of the body. In the sitting posture, the output is slightly less than when the subject is reclining, but peculiarly enough, the output is not reduced when the subject is in the erect position but leaning against a support.
Miscellaneous Influences
The cardiac output is increased by the taking of food and water and, temporarily, by high altitude. Exposure to cold slows the heart rate but increases the stroke volume, leaving the cardiac output unchanged, unless shivering occurs, when the cardiac output is increased. Exposure to warmth increases resting cardiac output very considerably. The heart rate is increased with a slight reduction in stroke volume. If the heat is severe enough to cause dehydration, cardiac output returns to the basal level. It may fall below the basal level in heat prostration in spite of a rapid heart rate, indicating a reduction in stroke volume due to inadequate venous return to the heart. Cardiac output is diminished by many types of cardiovascular abnormalties.
Heart Murmurs Cardiac Output
Heart Murmurs
Sometimes, due to congenital malformation or disease, the action of the heart valves is impaired. The valve orifices may be narrowed so that the normal flow of blood is impeded, and the valve leaflets may fail to close completely, allowing a leakage of blood in the reverse direction. This abnormal valve action results in distortion of the normal heart sounds or in the appearance of additional sounds. These abnormal heart sounds are called murmurs. The particular valve involved may be determined from the point on the chest wall at which the murmur is heard most clearly. In the case of so-called "functional" murmurs, there is no structural defect to account for the abnormal heart sounds.
Cardiac Output
From a functional standpoint the most important index of heart function is the cardiac output, that is, the volume of blood pumped by each ventricle per minute. Two factors, each of which may vary within wide limits, determine the size of the cardiac output. These are the heart rate and the stroke volume. The heart rate is very easily determined. The stroke volume, on the other hand, must be calculated from the values of the cardiac output and the heart rate. The fundamental importance of the cardiac output as an index of heart function has led to many attempts to devise a method for its measurement. The cardiac output could be calculated from the experimentally determined values of the oxygen content of the mixed venous blood (that is, the venous blood from all parts of the body after it has been mixed in the right heart), the oxygen content of the arterial blood and the oxygen consumption of the body. Suppose, for example, that the oxygen content of the mixed venous blood is 15 volumes per cent, that of the arterial blood 20 volumes per cent and the oxygen consumption is 250 ml. per minute. It is obvious that each 100 ml. of blood yields 5 ml. of oxygen to the tissues, so that of blood is required to furnish 250 ml. of oxygen to the tissues. Since this amount of blood must be pumped by each ventricle per minute, it represents the cardiac output. Until recently this method has not been used for studies on human subjects because of the difficulty in obtaining samples of mixed venous blood. Various procedures for determining the gaseous content of the mixed venous blood by indirect methods have been devised (for details, see textbooks of physiology) but all are open to criticism, especially when attempts are made to measure the cardiac output during exercise. A plastic catheter is inserted into an arm vein and carefully threaded up the vein and into the right heart. Samples of mixed venous blood are thus obtained and their oxygen content determined. The oxygen content of the arterial blood is determined by analysis of samples obtained by arterial puncture and the oxygen consumption of the body is measured with the ordinary clinical B.M.R. apparatus. From these data the cardiac output is calculated as illustrated above.
Sometimes, due to congenital malformation or disease, the action of the heart valves is impaired. The valve orifices may be narrowed so that the normal flow of blood is impeded, and the valve leaflets may fail to close completely, allowing a leakage of blood in the reverse direction. This abnormal valve action results in distortion of the normal heart sounds or in the appearance of additional sounds. These abnormal heart sounds are called murmurs. The particular valve involved may be determined from the point on the chest wall at which the murmur is heard most clearly. In the case of so-called "functional" murmurs, there is no structural defect to account for the abnormal heart sounds.
Cardiac Output
From a functional standpoint the most important index of heart function is the cardiac output, that is, the volume of blood pumped by each ventricle per minute. Two factors, each of which may vary within wide limits, determine the size of the cardiac output. These are the heart rate and the stroke volume. The heart rate is very easily determined. The stroke volume, on the other hand, must be calculated from the values of the cardiac output and the heart rate. The fundamental importance of the cardiac output as an index of heart function has led to many attempts to devise a method for its measurement. The cardiac output could be calculated from the experimentally determined values of the oxygen content of the mixed venous blood (that is, the venous blood from all parts of the body after it has been mixed in the right heart), the oxygen content of the arterial blood and the oxygen consumption of the body. Suppose, for example, that the oxygen content of the mixed venous blood is 15 volumes per cent, that of the arterial blood 20 volumes per cent and the oxygen consumption is 250 ml. per minute. It is obvious that each 100 ml. of blood yields 5 ml. of oxygen to the tissues, so that of blood is required to furnish 250 ml. of oxygen to the tissues. Since this amount of blood must be pumped by each ventricle per minute, it represents the cardiac output. Until recently this method has not been used for studies on human subjects because of the difficulty in obtaining samples of mixed venous blood. Various procedures for determining the gaseous content of the mixed venous blood by indirect methods have been devised (for details, see textbooks of physiology) but all are open to criticism, especially when attempts are made to measure the cardiac output during exercise. A plastic catheter is inserted into an arm vein and carefully threaded up the vein and into the right heart. Samples of mixed venous blood are thus obtained and their oxygen content determined. The oxygen content of the arterial blood is determined by analysis of samples obtained by arterial puncture and the oxygen consumption of the body is measured with the ordinary clinical B.M.R. apparatus. From these data the cardiac output is calculated as illustrated above.
The Heart Cardiac Cycle
The cardiac cycle includes all the events--pressure changes, volume changes and valve action--which occur during one complete period of contraction and relaxation of the heart. Since the complete cycle takes place in a period of one second or less, it is no wonder that early physiologists despaired of ever solving its mysteries. Modern methods of recording rapid changes in volume and pressure have, however, permitted a very exact analysis of events.
A description of the cardiac cycle may begin at any point in the cycle. For convenience, we will start with the phase of diastasis, the period during which the whole heart is completely relaxed. Blood is entering the right auricle from the venae cavae and the left auricle from the pulmonary veins. The auriculo-ventricular (A-V) valves which guard the orifice between the auricle and the ventricle on each side are open and the blood which enters the auricles flows freely through into the relaxed ventricles. The valves leading from the ventricles to the pulmonary artery and the aorta are closed, so that none of the blood entering the ventricles is able to leave. The period of diastasis ends abruptly with the onset of systole (contraction) of the auricles. Filling of the ventricles is already virtually complete when auricular systole occurs, so that it is of minor importance so far as ventricular filling is concerned. Almost immediately after auricular systole is completed, ventricular systole begins. Contraction of the ventricular muscle results in a rapid rise in the pressure of the blood in the ventricle. This very quickly exceeds the auricular pressure (which is always low) and causes a sudden closure of the A-V valves on both sides. The vibrations of these valves as they close set up waves which are transmitted to the surface of the chest, where they may be heard as the first heart sound. As the ventricles continue their contraction the pressure exerted on their contained masses of blood rises steeply, but since all the valves of the heart are closed no blood is pumped out. Since the heart muscle cannot shorten during this period, it is referred to as the isometric phase of systole. As soon as the ventricular pressure rises above the pressure in the pulmonary artery and the aorta, the valves guarding these vessels open and blood is rapidly ejected. During the ejection phase, the ventricular muscle is able to shorten (resulting in a decrease in the size of the ventricular cavities) so that it represents an isotonic contraction.
The termination of ventricular systole marks the onset of ventricular diastole, or relaxation. As the ventricular muscle relaxes, intraventricular pressure falls. When it drops below the pressure in the aorta and the pulmonary artery, the valves guarding their orifices close, giving rise to the second heart sound. The intraventricular pressure continues to fall and eventually drops below intra-auricular pressure, resulting in the opening of the A-V valves. As blood begins to pour from the auricles into the ventricles, the period of diastasis, with which this description of the cardiac cycle began, is reached once more.
A typical cardiac cycle consists, then, of three phases: diastasis (resting period), systole (contraction period) and diastole (relaxation period). Most of the filling of the ventricle occurs during the early part of diastole. This is of importance in the adjustment of heart function in exercise, because the increase in heart rate occurs primarily at the expense of the period of diastasis. When the heart rate becomes excessively high, the filling of the ventricle may be cut short, with a resulting decrease in stroke volume.
A description of the cardiac cycle may begin at any point in the cycle. For convenience, we will start with the phase of diastasis, the period during which the whole heart is completely relaxed. Blood is entering the right auricle from the venae cavae and the left auricle from the pulmonary veins. The auriculo-ventricular (A-V) valves which guard the orifice between the auricle and the ventricle on each side are open and the blood which enters the auricles flows freely through into the relaxed ventricles. The valves leading from the ventricles to the pulmonary artery and the aorta are closed, so that none of the blood entering the ventricles is able to leave. The period of diastasis ends abruptly with the onset of systole (contraction) of the auricles. Filling of the ventricles is already virtually complete when auricular systole occurs, so that it is of minor importance so far as ventricular filling is concerned. Almost immediately after auricular systole is completed, ventricular systole begins. Contraction of the ventricular muscle results in a rapid rise in the pressure of the blood in the ventricle. This very quickly exceeds the auricular pressure (which is always low) and causes a sudden closure of the A-V valves on both sides. The vibrations of these valves as they close set up waves which are transmitted to the surface of the chest, where they may be heard as the first heart sound. As the ventricles continue their contraction the pressure exerted on their contained masses of blood rises steeply, but since all the valves of the heart are closed no blood is pumped out. Since the heart muscle cannot shorten during this period, it is referred to as the isometric phase of systole. As soon as the ventricular pressure rises above the pressure in the pulmonary artery and the aorta, the valves guarding these vessels open and blood is rapidly ejected. During the ejection phase, the ventricular muscle is able to shorten (resulting in a decrease in the size of the ventricular cavities) so that it represents an isotonic contraction.
The termination of ventricular systole marks the onset of ventricular diastole, or relaxation. As the ventricular muscle relaxes, intraventricular pressure falls. When it drops below the pressure in the aorta and the pulmonary artery, the valves guarding their orifices close, giving rise to the second heart sound. The intraventricular pressure continues to fall and eventually drops below intra-auricular pressure, resulting in the opening of the A-V valves. As blood begins to pour from the auricles into the ventricles, the period of diastasis, with which this description of the cardiac cycle began, is reached once more.
A typical cardiac cycle consists, then, of three phases: diastasis (resting period), systole (contraction period) and diastole (relaxation period). Most of the filling of the ventricle occurs during the early part of diastole. This is of importance in the adjustment of heart function in exercise, because the increase in heart rate occurs primarily at the expense of the period of diastasis. When the heart rate becomes excessively high, the filling of the ventricle may be cut short, with a resulting decrease in stroke volume.
General Description of the Heart
The salient anatomical features of the heart may be reviewed. The heart is a hollow muscular organ, subdivided internally into four chambers: the right and left auricles (or atria) and the right and left ventricles. The auricles are thin-walled collecting chambers. They have little contractile power and serve primarily by storing the blood brought to them by the veins during the contraction, or systole, of the ventricles and then passing this blood on to the ventricles during their period of relaxation, or diastole. The ventricles, on the other hand, are thick-walled muscular chambers which exert considerable force during contraction. This contractile force imparts the necessary kinetic energy to the blood to maintain its circulation.
From a functional standpoint, the heart may be divided into the "right heart" (right auricle and ventricle) and the "left heart" (left auricle and ventricle). The right heart receives venous blood from all the systemic veins of the body and pumps it through the pulmonary arteries into the lungs, where oxygen is absorbed and carbon dioxide eliminated. The oxygenated blood is returned through the pulmonary veins to the left heart which in turn pumps it through the aorta into the systemic arteries of the body. The orifices between the auricles and their corresponding ventricles, and the exit of the pulmonary artery and the aorta from their respective ventricles are guarded by valves which permit the flow of blood in one direction only.
The heart muscle itself is not nourished by the blood contained within its chambers, but is supplied by the coronary arteries which leave the aorta just beyond the aortic valves.
The stimulus which causes contraction of the heart muscle at each beat arises within the heart itself, in a specialized muscle mass known as the sine-auricular (S-A) node or "pacemaker." The impulse is conducted to all parts of the heart muscle by way of a specialized conducting system, the auriculo-ventricular (A-V) node and bundle. The rate of beating of the heart is regulated by two sets of nerves, the vagus nerves which slow the rate and the accelerator nerves which increase the rate.
The heart is enclosed in a fibrous sac called the pericardium. A thin film of fluid (the pericardial fluid) separates the heart from the pericardium and minimizes the friction which otherwise would occur during contraction and relaxation of the heart. The pericardium probably serves a protective function in preventing dangerous overdistention of the heart. It is uncertain to what extent the pericardium limits the stroke volume (amount of blood pumped by the heart at each beat) during exercise. While the pericardium is relatively nonelastic and hence resists attempts at sudden stretching, it can be stretched very slowly to permit the normal increase in heart size often seen in athletes or the pathological dilatation of the heart which occurs in certain types of heart disease.
From a functional standpoint, the heart may be divided into the "right heart" (right auricle and ventricle) and the "left heart" (left auricle and ventricle). The right heart receives venous blood from all the systemic veins of the body and pumps it through the pulmonary arteries into the lungs, where oxygen is absorbed and carbon dioxide eliminated. The oxygenated blood is returned through the pulmonary veins to the left heart which in turn pumps it through the aorta into the systemic arteries of the body. The orifices between the auricles and their corresponding ventricles, and the exit of the pulmonary artery and the aorta from their respective ventricles are guarded by valves which permit the flow of blood in one direction only.
The heart muscle itself is not nourished by the blood contained within its chambers, but is supplied by the coronary arteries which leave the aorta just beyond the aortic valves.
The stimulus which causes contraction of the heart muscle at each beat arises within the heart itself, in a specialized muscle mass known as the sine-auricular (S-A) node or "pacemaker." The impulse is conducted to all parts of the heart muscle by way of a specialized conducting system, the auriculo-ventricular (A-V) node and bundle. The rate of beating of the heart is regulated by two sets of nerves, the vagus nerves which slow the rate and the accelerator nerves which increase the rate.
The heart is enclosed in a fibrous sac called the pericardium. A thin film of fluid (the pericardial fluid) separates the heart from the pericardium and minimizes the friction which otherwise would occur during contraction and relaxation of the heart. The pericardium probably serves a protective function in preventing dangerous overdistention of the heart. It is uncertain to what extent the pericardium limits the stroke volume (amount of blood pumped by the heart at each beat) during exercise. While the pericardium is relatively nonelastic and hence resists attempts at sudden stretching, it can be stretched very slowly to permit the normal increase in heart size often seen in athletes or the pathological dilatation of the heart which occurs in certain types of heart disease.
The Hearth General Features of the Circulation
The tissues of the body require, for their normal functioning, a reasonable degree of constancy with respect to certain factors; among these factors are: temperature, acidity, food supply, and oxygen. The primary function of the circulation of the blood is to ensure the preservation of this constant internal environment by transporting oxygen, food materials and hormones to the tissue cells and by removing the waste products of activity. The interchange of materials between the blood and the tissues occurs in the thin-walled capillaries. The rest of the circulatory system, including the heart, exists solely for the purpose of maintaining the capillary exchange. The heart is a muscular pump which imparts sufficient kinetic energy to the blood to move it through the capillaries. The arteries conduct the blood from the heart to the capillaries and the veins conduct the blood from the capillaries back to the heart again. As will be seen in later chapters, the arteries and veins are not simply passive conducting tubes, but are also responsible, through alterations in their diameters, for the proper distribution of the blood to various organs and tissues in accordance with their metabolic requirements.
From the standpoint of the physiology of exercise, the heart is primarily a respiratory organ. In the periods of rest between bouts of exercise, the muscles are able to store sufficient food materials to initiate exercise and to maintain it until reserves can be mobilized. There is, however, no mechanism for the storage of oxygen in the tissues. Any increase in the oxygen requirement must be satisfied by a corresponding increase in the transport of oxygen to the tissues. This is accomplished in two ways: (1) by diverting blood to the contracting muscles from less active regions and (2) by increasing the volume of blood pumped by the heart per minute. Not only is the flow of blood to the muscles increased when they become active, but in addition a larger volume of oxygen is removed from each volume of blood. Of these adaptive mechanisms, the increased pumping action of the heart is the most important in terms of the share it contributes to the adjustment of oxygen supply to the requirements of the contracting muscles. It is also the most vulnerable link in the chain; the upper limit to the volume of oxygen which can be delivered to active muscles is almost invariably set by the capacity of the heart to increase its output. For these reasons the heart occupies the key position in any scheme of the physiological adjustments in exercise.
From the standpoint of the physiology of exercise, the heart is primarily a respiratory organ. In the periods of rest between bouts of exercise, the muscles are able to store sufficient food materials to initiate exercise and to maintain it until reserves can be mobilized. There is, however, no mechanism for the storage of oxygen in the tissues. Any increase in the oxygen requirement must be satisfied by a corresponding increase in the transport of oxygen to the tissues. This is accomplished in two ways: (1) by diverting blood to the contracting muscles from less active regions and (2) by increasing the volume of blood pumped by the heart per minute. Not only is the flow of blood to the muscles increased when they become active, but in addition a larger volume of oxygen is removed from each volume of blood. Of these adaptive mechanisms, the increased pumping action of the heart is the most important in terms of the share it contributes to the adjustment of oxygen supply to the requirements of the contracting muscles. It is also the most vulnerable link in the chain; the upper limit to the volume of oxygen which can be delivered to active muscles is almost invariably set by the capacity of the heart to increase its output. For these reasons the heart occupies the key position in any scheme of the physiological adjustments in exercise.
Increase in the maximal oxygen intake
Oxygen Intake
The practical advantage to the subject is that a greater proportion of the oxygen requirement for a given task is obtained without the accumulation of lactic acid and the acquisition of an oxygen debt. The average individual with a resting oxygen consumption of 250 ml. per minute may increase this to about 1500 ml. per minute during work, an increase of 600 per cent. In the athlete this margin may be raised to 3 or 4 liters per minute, an increase of 1200 to 1600 per cent.
Oxygen Debt
The maximal oxygen debt which can be tolerated by a subject is usually increased by training. This means, primarily, that the trained individual is able to buffer a larger amount of lactic acid since there is no evidence of any difference in ability to tolerate a higher degree of actual tissue acidity. It might be expected, then, that training would increase the body's supply of buffer alkali, and this seems to be true. An average alkali reserve or 72.12 volumes per cent in highly trained athletes as compared with 65.15 volumes per cent in normal but untrained men. A steady rise in the alkali reserve of dogs subjected to regular exercise on a treadmill for a period of 7 to 9 weeks.
It is probable, however, that an increase in the alkali reserve does not invariably occur. Thus, normal alkali reserves in five young athletes of international renown in distance running. Apparently, then, the ability to accumulate a large oxygen debt must depend partly on other factors as yet unidentified.
The practical advantage to the subject is that a greater proportion of the oxygen requirement for a given task is obtained without the accumulation of lactic acid and the acquisition of an oxygen debt. The average individual with a resting oxygen consumption of 250 ml. per minute may increase this to about 1500 ml. per minute during work, an increase of 600 per cent. In the athlete this margin may be raised to 3 or 4 liters per minute, an increase of 1200 to 1600 per cent.
Oxygen Debt
The maximal oxygen debt which can be tolerated by a subject is usually increased by training. This means, primarily, that the trained individual is able to buffer a larger amount of lactic acid since there is no evidence of any difference in ability to tolerate a higher degree of actual tissue acidity. It might be expected, then, that training would increase the body's supply of buffer alkali, and this seems to be true. An average alkali reserve or 72.12 volumes per cent in highly trained athletes as compared with 65.15 volumes per cent in normal but untrained men. A steady rise in the alkali reserve of dogs subjected to regular exercise on a treadmill for a period of 7 to 9 weeks.
It is probable, however, that an increase in the alkali reserve does not invariably occur. Thus, normal alkali reserves in five young athletes of international renown in distance running. Apparently, then, the ability to accumulate a large oxygen debt must depend partly on other factors as yet unidentified.
Influence of Training on Oxygen Requirement, Oxygen Intake and Oxygen Debt.
The results of training may briefly be summarized as follows:
1. The oxygen requirement for a given task is diminished as a result of more efficient use of muscles and elimination of extraneous movements, and of greater mechanical efficiency of the muscles themselves.
2. The maximal oxygen intake is increased through improved capacity of the heart to pump blood, and through circulatory and respiratory adjustments.
3. The maximal oxygen debt which can be incurred is increased, probably due to an increase in the amount of buffer alkali available for neutralizing lactic acid.
Oxygen Requirement
Training increases the case with which work is performed. It is difficult to determine accurately the relative importance of increased skill and of increased mechanical efficiency of the muscles. In evaluating the influence of training on skill, it is unfair to compare athletes with nonathletes because skill is due partly to inborn aptitude. However, in a given individual, the improvement in skill with training is often striking and may be acquired early in the course of training. Thus in repeated observations on one man the improvement from training appeared to reach a maximum after only a few trial runs scattered over ten days. His net efficiency during this period rose from 17.7 to 20.6 per cent. Improvement in skill and consequent reduction in oxygen requirements are often noted in army recruits learning to march.
Improvement in the mechanical efficiency of muscles is due largely to the increase in diameter of each muscle fiber which results from continued usage. As a result, fewer fibers must contract for the development of a given amount of tension. This change takes place more gradually than does the increase in skill.
1. The oxygen requirement for a given task is diminished as a result of more efficient use of muscles and elimination of extraneous movements, and of greater mechanical efficiency of the muscles themselves.
2. The maximal oxygen intake is increased through improved capacity of the heart to pump blood, and through circulatory and respiratory adjustments.
3. The maximal oxygen debt which can be incurred is increased, probably due to an increase in the amount of buffer alkali available for neutralizing lactic acid.
Oxygen Requirement
Training increases the case with which work is performed. It is difficult to determine accurately the relative importance of increased skill and of increased mechanical efficiency of the muscles. In evaluating the influence of training on skill, it is unfair to compare athletes with nonathletes because skill is due partly to inborn aptitude. However, in a given individual, the improvement in skill with training is often striking and may be acquired early in the course of training. Thus in repeated observations on one man the improvement from training appeared to reach a maximum after only a few trial runs scattered over ten days. His net efficiency during this period rose from 17.7 to 20.6 per cent. Improvement in skill and consequent reduction in oxygen requirements are often noted in army recruits learning to march.
Improvement in the mechanical efficiency of muscles is due largely to the increase in diameter of each muscle fiber which results from continued usage. As a result, fewer fibers must contract for the development of a given amount of tension. This change takes place more gradually than does the increase in skill.
Oxygen Intake and Oxygen Debt as Limiting Factors in Exercise
The maximum effort which can be exerted over a given period of time is limited by the maximum amount of oxygen which the subject can absorb per minute and by the maximum oxygen debt which he is able to contract. Since these are both measurable quantities, it should be possible to predict the limits of exertion for any individual from the results of laboratory tests (neglecting emotional factors). A welltrained athlete may be able to absorb 4 liters of oxygen per minute and to acquire an oxygen debt of 15 liters. It has been firmly established that, when the maximum oxygen debt has been incurred, the body becomes incapable of further effort. These facts permit one to estimate the duration of exertion which is possible when the oxygen requirement is greater than the maximal oxygen intake. 8 Assume that an athlete is able to absorb 4 liters of oxygen per minute and to incur an oxygen debt of 15 liters. If he runs at a speed requiring 5 liters of oxygen per minute, he must go into debt for oxygen at the rate of 1 liter per minute, and this intensity of exertion could be sustained for 15 minutes. If the speed of running is increased until the oxygen requirement is doubled, the excess of oxygen requirement over oxygen intake is 10--4 = 6 liters per minute, and exhaustion would occur at the end of 15/6 = 2.5 minutes.
In running, the oxygen requirement increases as the square or cube of the speed. Therefore doubling the rate of running increases the oxygen requirement per minute from 4 to 16 times. A man does not have time to incur his maximal oxygen debt in short sprints. It has been estimated that 50 to 55 seconds of running at top speed would be required before the maximal oxygen debt would be reached. Since the maximum amount of exertion which is possible before exhaustion occurs is determined by the upper limits of the oxygen intake and the oxygen debt, the question naturally arises as to the factors which set these limits. The factors limiting oxygen intake have been mentioned earlier in this chapter and will be discussed in detail in later chapters. So far as the oxygen debt is concerned, the practical limit seems to be set by the tissue acidity which results from lactic acid accumulation. Since lactic acid is a strong acid, it cannot exist as such in weakly alkaline media such as the blood and tissue fluids. As soon as lactic acid is formed during exercise, it is neutralized or "buffered" by alkali. As a result, the increase in acidity is much less than it would be if the acid remained in the free form. Presumably, the amount of lactic acid which the body can tolerate will depend largely on the amount of buffer alkali available. If this is large, more lactic acid can accumulate before the tissue acidity rises to all intolerable level. Meyerhof showed that the lactic acid concentration in the exhausted isolated muscle is much greater if the muscle is kept in all alkaline medium. Also in man the values of blood lactic acid following exhaustion are much higher if the man started the work with higher alkali reserve. This may mean that it is possible to increase the capacity for work by increasing the alkali reserve. That this is, indeed, true is indicated by experiments which demonstrated that the maximum blood lactic acid concentration following running to exhaustion on a treadmill was increased by the previous administration of a dose of sodium bicarbonate.
In running, the oxygen requirement increases as the square or cube of the speed. Therefore doubling the rate of running increases the oxygen requirement per minute from 4 to 16 times. A man does not have time to incur his maximal oxygen debt in short sprints. It has been estimated that 50 to 55 seconds of running at top speed would be required before the maximal oxygen debt would be reached. Since the maximum amount of exertion which is possible before exhaustion occurs is determined by the upper limits of the oxygen intake and the oxygen debt, the question naturally arises as to the factors which set these limits. The factors limiting oxygen intake have been mentioned earlier in this chapter and will be discussed in detail in later chapters. So far as the oxygen debt is concerned, the practical limit seems to be set by the tissue acidity which results from lactic acid accumulation. Since lactic acid is a strong acid, it cannot exist as such in weakly alkaline media such as the blood and tissue fluids. As soon as lactic acid is formed during exercise, it is neutralized or "buffered" by alkali. As a result, the increase in acidity is much less than it would be if the acid remained in the free form. Presumably, the amount of lactic acid which the body can tolerate will depend largely on the amount of buffer alkali available. If this is large, more lactic acid can accumulate before the tissue acidity rises to all intolerable level. Meyerhof showed that the lactic acid concentration in the exhausted isolated muscle is much greater if the muscle is kept in all alkaline medium. Also in man the values of blood lactic acid following exhaustion are much higher if the man started the work with higher alkali reserve. This may mean that it is possible to increase the capacity for work by increasing the alkali reserve. That this is, indeed, true is indicated by experiments which demonstrated that the maximum blood lactic acid concentration following running to exhaustion on a treadmill was increased by the previous administration of a dose of sodium bicarbonate.
The Oxygen Debt of Exercise
The ability of man to go into debt for oxygen is dependent, at least in part, on the formation of lactic acid. Hence the quantitative relation between the oxygen debt and the amount of lactic acid formed during exercise is of importance in an understanding of the limiting factors in exercise. Since a direct estimation of the total amount of lactic acid in the human body at any one time is, of course, impossible, it is necessary to rely partly on animal experiments and partly on inference from the blood lactic acid concentration. It is still uncertain whether blood lactic acid concentration is a true index of the lactic acid concentration in the corresponding tissues.
The equation for the oxidation of lactic acid may be written: C3H6O3 + 3 O2 → 3 CO2 + 3 H2O. Three molecules of oxygen are required for the oxidation of one molecule of lactic acid. In terms of gram equivalents, 3 × 22.4 liters of oxygen will oxidize 90 grams of lactic acid, or each gram of lactic acid requires 746.7 ml. of oxygen. In isolated frog muscle, only 150 ml. of oxygen are consumed for each grant of lactic acid which disappears, or about one-fifth the theoretical amount. This led to the belief that the oxidation of one-fifth of the lactic acid produced furnishes energy for the reconversion of the other four-fifths to glycogen. There is no direct evidence that any of the lactic acid is oxidized during recovery in oxygen.
It is not lactic acid that is oxidized in recovering muscle, but its equivalent in glucose. In this case all of the lactic acid would be reconverted to glycogen, while a quantity of glucose equivalent to approximately onefifth of the lactic acid so removed is oxidized. A portion of the energy thus liberated is used in the resynthesis of glycogen from lactic acid, while the rest appears as heat. In the exercising human subject, the quantitative relation between oxygen debt and lactic acid production is not so simple as it is in isolated frog muscle. Margaria, Edwards and Dill 6 have made a careful study of the relation of oxygen debt to metabolic rate and to lactic acid production. Some of their results necessitate a considerable revision of Hill's original theory. Two of their findings deserve particular emphasis: (1) in moderate exercise, the oxygen debt may reach 3 or 4 liters with no evidence of lactic acid accumulation, and (2) a considerable fraction (about one-third) of the total oxygen debt is repaid very rapidly (within three minutes) after the cessation of exercise, while repayment of the remainder of the debt may require several hours. Oxygen debts greater than 3 or 4 liters there is a linear relation between oxygen debt and blood lactic acid concentration. From these and other facts, the authors drew the following conclusions: The excess oxygen consumption following exercise is really made up of two fractions: (1) a true "oxygen debt" which is used to repay an oxygen deficit incurred during exercise and (2) an increased "basal" oxygen consumption which may last for several hour's or longer, and is not used for the reversal of any of the reactions which occurred during the exercise. The oxygen debt, in turn, consists of two fractions: (a) the "alactacid" debt, which is not related to the accumulation of lactic acid and is repaid within a few minutes after exercise ceases, and (b) the "lactacid" debt which is proportional to the lactic, acid accumulation and may require an hour or longer for repayment. The excess oxygen consumption of the alaclacid phase probably is used in the oxidation of the same fuels used by the resting muscle, and the resulting energy is perhaps used for the resynthesis of phosphocreatine or of adenosine triphosphate. The lactacid phase certainly represents the excess oxygen consumption which furnishes the energy for the reconversion of lactic acid to glycogen. The reason for the long duration of this phase is uncertain. The conversion of lactic acid to glycogen and the oxidation of glucose are both rapid reactions, while the oxidation of lactic acid is a relatively slow process. For this reason, Margaria and his associates suggest that it may be true, as Hill believed, that the energy for resynthesis of glycogen is derived from the oxidation of a portion of the lactic acid, and not from the oxidation of an equivalent amount of glucose, as indicated by other types of evidence.
Finally, from 4 to 5 per cent 7 of the total recovery oxygen is used by the heart and respiratory muscles and hence is not directly related to the recovery process.
The equation for the oxidation of lactic acid may be written: C3H6O3 + 3 O2 → 3 CO2 + 3 H2O. Three molecules of oxygen are required for the oxidation of one molecule of lactic acid. In terms of gram equivalents, 3 × 22.4 liters of oxygen will oxidize 90 grams of lactic acid, or each gram of lactic acid requires 746.7 ml. of oxygen. In isolated frog muscle, only 150 ml. of oxygen are consumed for each grant of lactic acid which disappears, or about one-fifth the theoretical amount. This led to the belief that the oxidation of one-fifth of the lactic acid produced furnishes energy for the reconversion of the other four-fifths to glycogen. There is no direct evidence that any of the lactic acid is oxidized during recovery in oxygen.
It is not lactic acid that is oxidized in recovering muscle, but its equivalent in glucose. In this case all of the lactic acid would be reconverted to glycogen, while a quantity of glucose equivalent to approximately onefifth of the lactic acid so removed is oxidized. A portion of the energy thus liberated is used in the resynthesis of glycogen from lactic acid, while the rest appears as heat. In the exercising human subject, the quantitative relation between oxygen debt and lactic acid production is not so simple as it is in isolated frog muscle. Margaria, Edwards and Dill 6 have made a careful study of the relation of oxygen debt to metabolic rate and to lactic acid production. Some of their results necessitate a considerable revision of Hill's original theory. Two of their findings deserve particular emphasis: (1) in moderate exercise, the oxygen debt may reach 3 or 4 liters with no evidence of lactic acid accumulation, and (2) a considerable fraction (about one-third) of the total oxygen debt is repaid very rapidly (within three minutes) after the cessation of exercise, while repayment of the remainder of the debt may require several hours. Oxygen debts greater than 3 or 4 liters there is a linear relation between oxygen debt and blood lactic acid concentration. From these and other facts, the authors drew the following conclusions: The excess oxygen consumption following exercise is really made up of two fractions: (1) a true "oxygen debt" which is used to repay an oxygen deficit incurred during exercise and (2) an increased "basal" oxygen consumption which may last for several hour's or longer, and is not used for the reversal of any of the reactions which occurred during the exercise. The oxygen debt, in turn, consists of two fractions: (a) the "alactacid" debt, which is not related to the accumulation of lactic acid and is repaid within a few minutes after exercise ceases, and (b) the "lactacid" debt which is proportional to the lactic, acid accumulation and may require an hour or longer for repayment. The excess oxygen consumption of the alaclacid phase probably is used in the oxidation of the same fuels used by the resting muscle, and the resulting energy is perhaps used for the resynthesis of phosphocreatine or of adenosine triphosphate. The lactacid phase certainly represents the excess oxygen consumption which furnishes the energy for the reconversion of lactic acid to glycogen. The reason for the long duration of this phase is uncertain. The conversion of lactic acid to glycogen and the oxidation of glucose are both rapid reactions, while the oxidation of lactic acid is a relatively slow process. For this reason, Margaria and his associates suggest that it may be true, as Hill believed, that the energy for resynthesis of glycogen is derived from the oxidation of a portion of the lactic acid, and not from the oxidation of an equivalent amount of glucose, as indicated by other types of evidence.
Finally, from 4 to 5 per cent 7 of the total recovery oxygen is used by the heart and respiratory muscles and hence is not directly related to the recovery process.
Economy of Muscular Activity
In activities involving an element of motor skill, the same amount of work is usually performed with a smaller oxygen requirement by the trained athlete. This is due primarily to the fact that the acquisition of motor skill results in the suppression or elimination of extraneous muscular movements which, while contributing nothing to the performance of the task, yet require oxygen.
Environmental Factors
The influence of external temperature and humidity on muscular exercise has been the subject of numerous studies, but the present status of our knowledge leaves much to be desired. The mechanical efficiency of the body is apparently little changed by rather wide changes in external temperature and humidity. Thus, it is found little difference in the oxygen requirement of men working on a bicycle ergometer in the cold room (54°F) and in the warm room (93°F). It is quite possible, however, that in activities requiring skill, high temperatures, by diminishing the accuracy of neuromuscular coordination, might result in a lowered mechanical efficiency. There is no doubt that working capacity (output of work in a given time) is diminished by unfavorable environmental factors, especially by a combination of high temperature and high humidity.
The Steady State
For short periods of time, it is possible to engage in exercise of such severity that the oxygen requirement far exceeds the oxygen intake. In continuous exercise lasting more than a few minutes, however, the oxygen intake must be adequate to meet the oxygen requirement. When this condition exists, the subject is said to be in a "steady state." He is in the state of approximate equilibrium between the processes of breakdown and recovery with respect to his muscle metabolism. When a subject is in genuine steady state, as, for example, at rest or during a long walk at constant speed, the oxygen consumption and carbon dioxide elimination are uniform, the lactate concentration in the blood, the heart rate and respiratory rate and the body temperature are all constant no matter how long, within reasonable limits, the exercise may last. When these "reasonable limits" have been exceeded, exercise may be terminated by accessory factors, such as muscle soreness, blisters or exhaustion of the glycogen reserves.
When a resting subject begins to exercise, the steady state is not achieved immediately. The circulatory and respiratory adjustments which make possible a greater oxygen intake come into play gradually and in heavy work several minutes may be required for the oxygen intake to reach the steady state level. During this preliminary period, a small oxygen debt is incurred which is repaid during the brief recovery period which follows the exercise.
Environmental Factors
The influence of external temperature and humidity on muscular exercise has been the subject of numerous studies, but the present status of our knowledge leaves much to be desired. The mechanical efficiency of the body is apparently little changed by rather wide changes in external temperature and humidity. Thus, it is found little difference in the oxygen requirement of men working on a bicycle ergometer in the cold room (54°F) and in the warm room (93°F). It is quite possible, however, that in activities requiring skill, high temperatures, by diminishing the accuracy of neuromuscular coordination, might result in a lowered mechanical efficiency. There is no doubt that working capacity (output of work in a given time) is diminished by unfavorable environmental factors, especially by a combination of high temperature and high humidity.
The Steady State
For short periods of time, it is possible to engage in exercise of such severity that the oxygen requirement far exceeds the oxygen intake. In continuous exercise lasting more than a few minutes, however, the oxygen intake must be adequate to meet the oxygen requirement. When this condition exists, the subject is said to be in a "steady state." He is in the state of approximate equilibrium between the processes of breakdown and recovery with respect to his muscle metabolism. When a subject is in genuine steady state, as, for example, at rest or during a long walk at constant speed, the oxygen consumption and carbon dioxide elimination are uniform, the lactate concentration in the blood, the heart rate and respiratory rate and the body temperature are all constant no matter how long, within reasonable limits, the exercise may last. When these "reasonable limits" have been exceeded, exercise may be terminated by accessory factors, such as muscle soreness, blisters or exhaustion of the glycogen reserves.
When a resting subject begins to exercise, the steady state is not achieved immediately. The circulatory and respiratory adjustments which make possible a greater oxygen intake come into play gradually and in heavy work several minutes may be required for the oxygen intake to reach the steady state level. During this preliminary period, a small oxygen debt is incurred which is repaid during the brief recovery period which follows the exercise.
Oxygen Requirement and Oxygen Intake
The oxygen requirement of a given act is the volume of oxygen necessary for the performance of the act and for recovery. If the exercise is moderate, this requirement may be satisfied by the oxygen intake and recovery keeps pace with activity. If the exertion is severe, this relation breaks down and an oxygen debt is incurred, In this case, the oxygen requirement of the exercise is the sum of the oxygen intake during exercise anti the oxygen debt which is repaid during recovery.
The oxygen requirement of exercise is determined by a combination of factors, among the most important of which are: the severity or intensity of exercise, its duration, its speed, its economy, and certain environmental conditions, notably temperature and humidity.
Intensity of Work
Tile tension exerted by a contracting muscle is dependent on two factors: the number of fibers contracting and the frequency of their contraction. Muscle tone, which is based on the low frequency activation of a small proportion of the total number of muscle fibers, requires a very small oxygen intake. The same is true of a weak voluntary contraction. If a stronger contraction is needed, additional muscle fibers must be brought into activity and the frequency with which each fiber contracts must be increased; both of these adjustments increase the oxygen requirement of the muscle.
Duration of Work
Within certain limits, the oxygen requirement of work is directly proportional to its duration. If, however, the intensity is great enough, or the duration long enough to induce a state of fatigue, the oxygen requirement per unit of time usually begins to increase rapidly. This is easily explained by recalling the shape or the fatigue curve of an isolated muscle. As a muscle begins to tire the tension developed by each fiber is reduced, and hence more fibers must he brought into activity if the same level of work is to be maintained. The oxygen requirement is increased in proportion to the increased member of active muscle fibers.
Rate or Speed of Work
The relation between the oxygen requirement of work and the speed or performance is complex. For many types of work there is an optimal speed at which the oxygen requirement is minimal. If the work is performed at a slower or a faster rate, the mechanical efficiency is diminished and the oxygen requirement increased. The net result of two opposing factors determines the optimal speed of performance: (a) a rapidly contracting muscle has been shown to develop less tension than does a muscle contracting more slowly due to the limited rate at which the chemical changes underlying muscle contraction can occur; (b) a definite amount of energy is required to maintain tension in a muscle, once it is developed, and the slower the contraction, the greater is the proportion of the total energy used for this purpose (that is, tension must be maintained over a longer period of time in accomplishing a given amount of work at a slower rate of contraction). Factor (a) tends to make work more economical (lower oxygen requirement) at low speeds, while factor (b) results in a smaller oxygen requirement at high speeds. The worker, if left to his own devices, usually automatically adopts the optimal rate of working; this is, of course, impossible in assembly-line work.
There is another important type of work in which there is apparently no optimal speed. This is exemplified by the act of running. Table I indicates that the oxygen requirement of a 120 yard dash increases in direct proportion to the speed. Actually, the difference between these two types of activity is more apparent than real. In running, even at low speeds, the subject is usually exceeding the optimal speed for horizontal locomotion. In walking, on the other hand, there is a definite optimal speed of about 100 yards (120 steps) per minute.
The oxygen requirement of exercise is determined by a combination of factors, among the most important of which are: the severity or intensity of exercise, its duration, its speed, its economy, and certain environmental conditions, notably temperature and humidity.
Intensity of Work
Tile tension exerted by a contracting muscle is dependent on two factors: the number of fibers contracting and the frequency of their contraction. Muscle tone, which is based on the low frequency activation of a small proportion of the total number of muscle fibers, requires a very small oxygen intake. The same is true of a weak voluntary contraction. If a stronger contraction is needed, additional muscle fibers must be brought into activity and the frequency with which each fiber contracts must be increased; both of these adjustments increase the oxygen requirement of the muscle.
Duration of Work
Within certain limits, the oxygen requirement of work is directly proportional to its duration. If, however, the intensity is great enough, or the duration long enough to induce a state of fatigue, the oxygen requirement per unit of time usually begins to increase rapidly. This is easily explained by recalling the shape or the fatigue curve of an isolated muscle. As a muscle begins to tire the tension developed by each fiber is reduced, and hence more fibers must he brought into activity if the same level of work is to be maintained. The oxygen requirement is increased in proportion to the increased member of active muscle fibers.
Rate or Speed of Work
The relation between the oxygen requirement of work and the speed or performance is complex. For many types of work there is an optimal speed at which the oxygen requirement is minimal. If the work is performed at a slower or a faster rate, the mechanical efficiency is diminished and the oxygen requirement increased. The net result of two opposing factors determines the optimal speed of performance: (a) a rapidly contracting muscle has been shown to develop less tension than does a muscle contracting more slowly due to the limited rate at which the chemical changes underlying muscle contraction can occur; (b) a definite amount of energy is required to maintain tension in a muscle, once it is developed, and the slower the contraction, the greater is the proportion of the total energy used for this purpose (that is, tension must be maintained over a longer period of time in accomplishing a given amount of work at a slower rate of contraction). Factor (a) tends to make work more economical (lower oxygen requirement) at low speeds, while factor (b) results in a smaller oxygen requirement at high speeds. The worker, if left to his own devices, usually automatically adopts the optimal rate of working; this is, of course, impossible in assembly-line work.
There is another important type of work in which there is apparently no optimal speed. This is exemplified by the act of running. Table I indicates that the oxygen requirement of a 120 yard dash increases in direct proportion to the speed. Actually, the difference between these two types of activity is more apparent than real. In running, even at low speeds, the subject is usually exceeding the optimal speed for horizontal locomotion. In walking, on the other hand, there is a definite optimal speed of about 100 yards (120 steps) per minute.
Oxygen Requirements of Exercise
The most fundamental problem confronting any organism, from ameba to man, is that of securing an adequate supply of oxygen. The very existence of living organisms depends on the constant availability of free energy, derived ultimately from oxidations. When any organ or system of the body becomes "active" (as when a resting muscle contracts, or when a gland begins to secrete), its oxygen requirement is proportionately increased. The oxygen consumption of the human body under basal conditions (12 to 14 hours after eating and following a 30 minute period of resting in bed, at a comfortable room temperature) is approximately 200 to 250 ml. per minute. During maximal physical exertion this may rise to 4000 ml. per minute, or 15 to 20 times the basal consumption. This remarkable factor of safety involves the coordinated adjustment of the heart and circulation, the blood and the respiratory system.
While all the tissues of the body require oxygen for their continued activity, some are able to function for short periods at a level of intensity which far exceeds their capacity for obtaining oxygen. They do this by calling on anaerobic sources of energy such as the breakdown of glycogen to lactic acid. This is a wasteful procedure, as compared with oxidation, since only a portion of the energy of the fuel is liberated. Nevertheless, it serves an extremely useful function in enabling the organism to meet emergency situations requiring an energy expenditure in excess of that which can be supplied by oxidations alone. It must be emphasized, however, that anaerobic metabolism is not a substitute for oxidation--it merely postpones it. Following a period of activity powered by anaerobic energy, the anaerobic reactions must be reversed in order to restore the fuel supply and to remove acid metabolites, and this is accomplished by oxidative energy. During the period of exercise the subject has gone into debt for oxygen and this debt must be repaid during recovery.
While some of the organs of the body arc able to meet emergencies by incurring an oxygen debt, others, notably the heart and brain, cannot. These vital organs depend entirely on oxidative energy and their function begins to suffer as soon as their oxygen supply falls short of their requirement. The oxygen requirement of the brain is not particularly affected by exercise, lint that of the heart may be tremendously increased, and it will be demonstrated in a later chaplet that the inability of the heart to obtain its full oxygen requirement is one of the most important factors which limits the intensity and duration of exercise.
While all the tissues of the body require oxygen for their continued activity, some are able to function for short periods at a level of intensity which far exceeds their capacity for obtaining oxygen. They do this by calling on anaerobic sources of energy such as the breakdown of glycogen to lactic acid. This is a wasteful procedure, as compared with oxidation, since only a portion of the energy of the fuel is liberated. Nevertheless, it serves an extremely useful function in enabling the organism to meet emergency situations requiring an energy expenditure in excess of that which can be supplied by oxidations alone. It must be emphasized, however, that anaerobic metabolism is not a substitute for oxidation--it merely postpones it. Following a period of activity powered by anaerobic energy, the anaerobic reactions must be reversed in order to restore the fuel supply and to remove acid metabolites, and this is accomplished by oxidative energy. During the period of exercise the subject has gone into debt for oxygen and this debt must be repaid during recovery.
While some of the organs of the body arc able to meet emergencies by incurring an oxygen debt, others, notably the heart and brain, cannot. These vital organs depend entirely on oxidative energy and their function begins to suffer as soon as their oxygen supply falls short of their requirement. The oxygen requirement of the brain is not particularly affected by exercise, lint that of the heart may be tremendously increased, and it will be demonstrated in a later chaplet that the inability of the heart to obtain its full oxygen requirement is one of the most important factors which limits the intensity and duration of exercise.
Influence of Diet on Muscular Efficiency
Many attempts have been made to demonstrate a greater mechanical efficiency of the body (less energy expenditure in the performance of a given amount of work) on a diet in which one or another of the major foodstuffs predominates. The modern opinion, is that the efficiency is practically the same on all diets. There is a slight increase in efficiency following a high carbohydrate diet, but probably not more than 5 per cent.
The influence of diet is more clear-cut on another aspect of muscular activity, the working capacity or ability to perform work without early onset of fatigue. Experiments indicated that a high fat diet resulted in greater distress and an earlier onset of fatigue titan did an average mixed diet. Working at an intensity of 7,800 foot-pounds per minute, was aide to continue three times as long on a carbohydrate diet as on a fat diet. This may be associated with the fact that fat metabolism is more prone to result in the production of acid metabolites than is the metabolism of carbohydrate, and a rise in tissue acidity is generally regarded as favoring the onset of fatigue.
Carbohydrate is of primary importance as a fuel for muscular exercise in man. During prolonged work, eventual depletion of the carbohydrate stores (principally liver and muscle glycogen) may force the muscles to obtain a significant proportion of their energy from fat and protein. This is probably an indirect process, involving a preliminary conversion to carbohydrate before oxidation. Muscular efficiency is slightly greater, and the onset of fatigue is postponed, on a high carbohydrate diet. The blood sugar is normal or elevated in light and moderate work and in strenuous work of short duration, so that "priming" with sugar is of no particular advantage. In prolonged strenuous exertion, exhaustion may result from lowering of the blood sugar brought on by depletion of liver glycogen; the administration of sugar is often very definitely beneficial.There is no evidence that hard physical work necessitates an increased intake of protein.
The influence of diet is more clear-cut on another aspect of muscular activity, the working capacity or ability to perform work without early onset of fatigue. Experiments indicated that a high fat diet resulted in greater distress and an earlier onset of fatigue titan did an average mixed diet. Working at an intensity of 7,800 foot-pounds per minute, was aide to continue three times as long on a carbohydrate diet as on a fat diet. This may be associated with the fact that fat metabolism is more prone to result in the production of acid metabolites than is the metabolism of carbohydrate, and a rise in tissue acidity is generally regarded as favoring the onset of fatigue.
Carbohydrate is of primary importance as a fuel for muscular exercise in man. During prolonged work, eventual depletion of the carbohydrate stores (principally liver and muscle glycogen) may force the muscles to obtain a significant proportion of their energy from fat and protein. This is probably an indirect process, involving a preliminary conversion to carbohydrate before oxidation. Muscular efficiency is slightly greater, and the onset of fatigue is postponed, on a high carbohydrate diet. The blood sugar is normal or elevated in light and moderate work and in strenuous work of short duration, so that "priming" with sugar is of no particular advantage. In prolonged strenuous exertion, exhaustion may result from lowering of the blood sugar brought on by depletion of liver glycogen; the administration of sugar is often very definitely beneficial.There is no evidence that hard physical work necessitates an increased intake of protein.
Utilization of Protein and Fat by Muscle
The metabolism of protein in the body is ordinarily measured by determining the amount of nitrogen excreted in the urine. The fact that exercise increases the excretion of nitrogen has been confirmed by later workers, but the conclusion that this indicates utilization of protein as a fuel by the muscles has been questioned since there is no direct relationship between the amount of nitrogen excreted and the amount of work done.
The possibility that the increased nitrogen excretion may be due to altered kidney function is suggested by the finding of albuminuria following severe exercise. The rise in urinary nitrogen after exercise was abolished by feeding carbohydrate before the exercise. It is possible that in long-continued work, exhaustion of the carbohydrate supplies results in the conversion of protein into carbohydrate, thus making protein an indirect fuel for muscular work.
From a practical viewpoint, the available evidence indicates that protein is of minor importance as a source of muscular energy. There is no scientific support for the idea that athletes and workers doing hard physical labor require a larger protein intake than do sedentary persons. Only when tissues are being built or repaired at an increased rate, as in growing children and convalescent patients, is an increased protein intake necessary. By tile same token, when total muscle mass is being increased by a course of muscle training, there may be some necessity for increasing the protein content of tile diet.
The possibility that the increased nitrogen excretion may be due to altered kidney function is suggested by the finding of albuminuria following severe exercise. The rise in urinary nitrogen after exercise was abolished by feeding carbohydrate before the exercise. It is possible that in long-continued work, exhaustion of the carbohydrate supplies results in the conversion of protein into carbohydrate, thus making protein an indirect fuel for muscular work.
From a practical viewpoint, the available evidence indicates that protein is of minor importance as a source of muscular energy. There is no scientific support for the idea that athletes and workers doing hard physical labor require a larger protein intake than do sedentary persons. Only when tissues are being built or repaired at an increased rate, as in growing children and convalescent patients, is an increased protein intake necessary. By tile same token, when total muscle mass is being increased by a course of muscle training, there may be some necessity for increasing the protein content of tile diet.
Blood Glucose
Regardless of the form in which carbohydrate is ingested, it is converted by the digestive enzymes to glucose or similar "simple sugars" and then absorbed into the blood. If there were no provision for rapid storage of glucose in the tissues, its concentration in the blood would rise steeply following a meal, and much of it would be excreted by the kidney and hence lost to the body. Fortunately, much of the glucose absorbed into the blood is removed by the liver and the skeletal muscles and stored as glycogen. The conversion of glucose to glycogen ("glycogenesis") is regulated by the hormone insulin. In the disease diabetes, insulin is deficient or absent and the blood sugar is characteristically high.
The tissues of the body are constantly removing glucose from the blood to use in their metabolic processes and corresponding amounts of glucose must be added to the blood from reserve stores. This is accomplished by the breakdown of glycogen to glucose ("glycogenolysis") under the influence of another hormone, adrenalin. This reaction occurs primarily in the liver and to a lesser extent in the skeletal muscles. The net result is that glucose is stored as glycogen following meals and then reconverted to glucose at a rate sufficient to balance the withdrawal of glucose from the blood by active tissues.
During light exercise, the ordinary rate of delivery of glucose to the blood from the storage depots is adequate to balance the rate of glucose utilization by the muscles, and the blood sugar level is unchanged. As exercise increases in intensity, especially if it is accompanied by emotional excitement, the secretion of adrenalin by the adrenal glands becomes excessive (insofar as blood sugar regulation is concerned) and glucose is added to the blood from the glycogen storage reservoirs at a faster rate than the metabolic activities of the contracting muscles require. The result is a rise in the blood sugar concentration. This effect is more pronounced in intermittent than in continuous exertion. If the exercise is both strenuous and prolonged (as in a marathon race), the blood sugar level often shows a gradual fall, sometimes to half the normal value. This is interpreted as indicating exhaustion of available glycogen stores.
The foregoing discussion has definite implications for the practical management of the diet of athletes. In the first place, the evidence, though conflicting in certain respects, clearly emphasizes the importance of carbohydrate in the energy metabolism of muscle. There is no evidence to support the common belief that candy and other sweets should be restricted during training, unless they diminish the appetite and thus reduce the food intake at the regular meals. On the other hand, since prolonged and exhausting exercise is required to lower the blood sugar level, there would seem to be no practical advantage in the administration of sugar in various forms before or during most types of athletic contests. Any apparent increase in performance which may result is probably psychological in origin. The situation is somewhat different in the case of exhausting exercise which is prolonged over a period of hours. Here the exhaustion of glycogen reserves and the consequent lowering of the blood sugar may be a dominant factor in bringing about complete exhaustion.
It is worth pointing out that the outstanding symptoms of extreme physical exhaustion such as incoordination of movements, collapse and unconsciousness are referable not to the muscles but to the central nervous system. The brain, unlike skeletal muscles, has no available carbohydrate stores and cannot fall back on the metabolism or other substances when its glucose supply is curtailed. It depends, from moment to moment, on the glucose (and lactic acid) brought to it by the blood; when the blood glucose level falls, brain function is depressed and unconsciousness usually occurs when the blood sugar concentration drops below 40 mg. per cent.
The tissues of the body are constantly removing glucose from the blood to use in their metabolic processes and corresponding amounts of glucose must be added to the blood from reserve stores. This is accomplished by the breakdown of glycogen to glucose ("glycogenolysis") under the influence of another hormone, adrenalin. This reaction occurs primarily in the liver and to a lesser extent in the skeletal muscles. The net result is that glucose is stored as glycogen following meals and then reconverted to glucose at a rate sufficient to balance the withdrawal of glucose from the blood by active tissues.
During light exercise, the ordinary rate of delivery of glucose to the blood from the storage depots is adequate to balance the rate of glucose utilization by the muscles, and the blood sugar level is unchanged. As exercise increases in intensity, especially if it is accompanied by emotional excitement, the secretion of adrenalin by the adrenal glands becomes excessive (insofar as blood sugar regulation is concerned) and glucose is added to the blood from the glycogen storage reservoirs at a faster rate than the metabolic activities of the contracting muscles require. The result is a rise in the blood sugar concentration. This effect is more pronounced in intermittent than in continuous exertion. If the exercise is both strenuous and prolonged (as in a marathon race), the blood sugar level often shows a gradual fall, sometimes to half the normal value. This is interpreted as indicating exhaustion of available glycogen stores.
The foregoing discussion has definite implications for the practical management of the diet of athletes. In the first place, the evidence, though conflicting in certain respects, clearly emphasizes the importance of carbohydrate in the energy metabolism of muscle. There is no evidence to support the common belief that candy and other sweets should be restricted during training, unless they diminish the appetite and thus reduce the food intake at the regular meals. On the other hand, since prolonged and exhausting exercise is required to lower the blood sugar level, there would seem to be no practical advantage in the administration of sugar in various forms before or during most types of athletic contests. Any apparent increase in performance which may result is probably psychological in origin. The situation is somewhat different in the case of exhausting exercise which is prolonged over a period of hours. Here the exhaustion of glycogen reserves and the consequent lowering of the blood sugar may be a dominant factor in bringing about complete exhaustion.
It is worth pointing out that the outstanding symptoms of extreme physical exhaustion such as incoordination of movements, collapse and unconsciousness are referable not to the muscles but to the central nervous system. The brain, unlike skeletal muscles, has no available carbohydrate stores and cannot fall back on the metabolism or other substances when its glucose supply is curtailed. It depends, from moment to moment, on the glucose (and lactic acid) brought to it by the blood; when the blood glucose level falls, brain function is depressed and unconsciousness usually occurs when the blood sugar concentration drops below 40 mg. per cent.
Respiratory Quotient
When foodstuffs are oxidized, oxygen is consumed and carbon dioxide is produced. The ratio of the volume of carbon dioxide produced to the volume of oxygen consumed is called the respiratory quotient (R.Q.); its numerical value varies according to the type of food substance which is being oxidized. Thus, in the oxidation of glucose, represented by the reaction C6H12o6 + 6O2 → 6CO2 + 6H2O, 6 molecules of oxygen are consumed and 6 molecules of carbon dioxide produced, for each molecule of glucose burned. In this case, the ratio =1.00. A similar type of calculation yields values of 0.71 for the R.Q. of fat and of 0.80 for protein. In practice, the expired air of the subject is collected for a given period and the percentage of oxygen and of carbon dioxide determined by analysis. Knowing the composition of the inspired air and the volume and composition of the expired air, the volumes of oxygen consumed and of carbon dioxide produced (and hence the R.Q.) are easily calculated. The grams of protein oxidized are calculated from the urinary nitrogen (1 gram of urinary nitrogen reprethe metabolism of 6.25 grams of protein). The total R.Q. is corrected for protein metabolism by subtracting the oxygen consumed and carbon dioxide produced in the oxidation of protein from the total oxygen consumed and carbon dioxide produced. The resulting ratio of is called the "non-protein" R.Q.; from it the relative proportions of fat and of carbohydrate oxidized are obtained from standard tables. Under resting conditions the R.Q. gives a fairly reliable indication of the relative proportions of carbohydrate, fat, and protein which are being oxidized, although any considerable degree of interconversion of the major foodstuffs will seriously affect the ratio. The respiratory quotient is a reliable index of the fuel used in exercise only when the entire recovery period is included in the study. The reason for this is found in certain of the chemical reactions which accompany exercise and recovery. During moderate to strenuous exercise, more lactic acid is formed in the contracting muscles than can be neutralized by the muscle buffers. Much of the excess lactic acid diffuses into the blood stream where it is buffered by the various blood buffers of which the most abundant is sodium bicarbonate (NaHCO3) according to the reactions:
HL + NaHCO3 → NaL + H2CO3 (L represents the lactate ion)
H2CO3 → C02 + H20
As a result of this reaction, a large amount of carbon dioxide is eliminated in the expired air which did not result directly from oxidation and which, therefore, did not involve a corresponding consumption of oxygen. The ratio will be elevated and is frequently greater than 1.0 (R.Q.'s as high as 2.0 may be obtained during very strenuous exercise).
During recovery the lactate produced during exercise is gradually removed by oxidation, urinary excretion, and reconversion to glycogen. As a result the alkali with which this lactate had been combined is available to combine with carbon dioxide once more, so that much of the carbon dioxide produced by oxidations during the recovery period will be retained in the blood instead of being eliminated in the expired air. Consequently, the ratio will be depressed, and R.Q.'s as low as 0.5 may be obtained. This ratio returns to normal when recovery from exercise is complete. If, however, the expired air is collected from the beginning of exercise to the end of tile recovery period, the excess CO2 elimination during exercise is balanced by a corresponding amount of CO: retention during recovery and the correct R.Q. may be calculated. In practice it is often difficult to determine accurately when recovery has been completed, since the oxygen consumption may remain above the preexercise level for some hours. The adoption of an arbitrary time period of recovery is sometimes necessary, and probably results in only minor inaccuracies in the final calculations.
HL + NaHCO3 → NaL + H2CO3 (L represents the lactate ion)
H2CO3 → C02 + H20
As a result of this reaction, a large amount of carbon dioxide is eliminated in the expired air which did not result directly from oxidation and which, therefore, did not involve a corresponding consumption of oxygen. The ratio will be elevated and is frequently greater than 1.0 (R.Q.'s as high as 2.0 may be obtained during very strenuous exercise).
During recovery the lactate produced during exercise is gradually removed by oxidation, urinary excretion, and reconversion to glycogen. As a result the alkali with which this lactate had been combined is available to combine with carbon dioxide once more, so that much of the carbon dioxide produced by oxidations during the recovery period will be retained in the blood instead of being eliminated in the expired air. Consequently, the ratio will be depressed, and R.Q.'s as low as 0.5 may be obtained. This ratio returns to normal when recovery from exercise is complete. If, however, the expired air is collected from the beginning of exercise to the end of tile recovery period, the excess CO2 elimination during exercise is balanced by a corresponding amount of CO: retention during recovery and the correct R.Q. may be calculated. In practice it is often difficult to determine accurately when recovery has been completed, since the oxygen consumption may remain above the preexercise level for some hours. The adoption of an arbitrary time period of recovery is sometimes necessary, and probably results in only minor inaccuracies in the final calculations.
The Fuel of Muscular Exercise
There are three major types of foodstuffs which can be oxidized in the body, namely: carbohydrates, fats, and proteins. Our problem is to determine the relative importance of each of these as a source of energy for muscular work of varying degrees of intensity and duration. This problem is complicated by the fact that a considerable amount of interconversion of the major foodstuffs occurs in the body. A common example of this process is the conversion of carbohydrate into fat in the commercial "fattening" of livestock. It is now believed that carbohydrates and fats are mutually interconvertible in the body and that the amino acids which make up the protein molecule are likewise capable, after certain metabolic modifications, of being converted to carbohydrate.
This makes it difficult to draw conclusions about oxidative sources of energy from a simple analysis of the constituents of the diet and necessitates the use of indirect methods of study.
A knowledge of the types of foodstuffs undergoing oxidation during muscular exertion is not only important from a nutritional standpoint, but is essential to a clear understanding of the chemical basis of muscle contraction anti of the resulting energy liberation. The experimental investigation of this fundamental problem is still far from complete and quite divergent results have been obtained by different workers.
This makes it difficult to draw conclusions about oxidative sources of energy from a simple analysis of the constituents of the diet and necessitates the use of indirect methods of study.
A knowledge of the types of foodstuffs undergoing oxidation during muscular exertion is not only important from a nutritional standpoint, but is essential to a clear understanding of the chemical basis of muscle contraction anti of the resulting energy liberation. The experimental investigation of this fundamental problem is still far from complete and quite divergent results have been obtained by different workers.
Nature of the Shortening of Muscle
The most obvious feature of the contraction of a muscle is the shortening which occurs. The nature of this shortening has been the subject of many experiments and more speculations, yet a final answer is not available. Recently, a protein called actomyosin, has been isolated from muscle. Threads made from this protein can be made to contract in response to chemical stimulation and it is suggested that this protein may be a prominent constituent of the contractile elements of muscle fibers, the myofibrils.
A relaxed muscle is like a stretched spring, and contracts when stimulated as a spring does when released. Energy must then be used to cause the muscle to relax (i. e., to stretch the spring) in preparation for another contraction. An opposing view is that shortening of the muscle is the active process which requires energy, and that relaxation occurs passively when stimulation ceases.
Chemical Changes in Muscle During Contraction and Recovery
Muscle is essentially a machine for transforming chemical energy into mechanical energy which can do work.
When an isolated frog muscle is stimulated to the point of fatigue, its glycogen (starch) content is greatly diminished and there is a considerable accumulation of lactic acid. If the muscle is then allowed to rest in an atmosphere of oxygen, the lactic acid disappears and the muscle recovers its irritability. It was then postulated that the source(.e of energy for muscle contraction is the breakdown of glycogen to lactic acid. a process which is anaerobic (i. e., does not require oxygen). During the recovery period, oxygen is necessary to burn the lactic acid.
The lactic acid is foxed after contraction has occurred, so that the breakdown of glycogen to lactic acid must provide energy for recovery of muscle, not for its contraction. The ATP molecule contains a large amount of energy which is released when the molecule is split. This released energy, by its effect on actomyosin, is the basic source of energy for muscle contraction. The oxidation of carbohydrate (glycogen and glucose), through a complex series of reactions, provides the energy for rebuilding the high energy ATP molecules. When abundant oxygen is present, carbohydrate breakdown proceeds to its final end products--carbon dioxide and water. If the oxygen supply is not adequate, carbohydrate breakdown proceeds along a different pathway which results in lactic acid formation. If the lactic acid is allowed to accumulate in excessive amounts, the chemical reactions are interfered with and the muscle can no longer be made to contract. In moderate exercise, energy requirements are fully met by oxidations, and no lactic acid is formed.
A relaxed muscle is like a stretched spring, and contracts when stimulated as a spring does when released. Energy must then be used to cause the muscle to relax (i. e., to stretch the spring) in preparation for another contraction. An opposing view is that shortening of the muscle is the active process which requires energy, and that relaxation occurs passively when stimulation ceases.
Chemical Changes in Muscle During Contraction and Recovery
Muscle is essentially a machine for transforming chemical energy into mechanical energy which can do work.
When an isolated frog muscle is stimulated to the point of fatigue, its glycogen (starch) content is greatly diminished and there is a considerable accumulation of lactic acid. If the muscle is then allowed to rest in an atmosphere of oxygen, the lactic acid disappears and the muscle recovers its irritability. It was then postulated that the source(.e of energy for muscle contraction is the breakdown of glycogen to lactic acid. a process which is anaerobic (i. e., does not require oxygen). During the recovery period, oxygen is necessary to burn the lactic acid.
The lactic acid is foxed after contraction has occurred, so that the breakdown of glycogen to lactic acid must provide energy for recovery of muscle, not for its contraction. The ATP molecule contains a large amount of energy which is released when the molecule is split. This released energy, by its effect on actomyosin, is the basic source of energy for muscle contraction. The oxidation of carbohydrate (glycogen and glucose), through a complex series of reactions, provides the energy for rebuilding the high energy ATP molecules. When abundant oxygen is present, carbohydrate breakdown proceeds to its final end products--carbon dioxide and water. If the oxygen supply is not adequate, carbohydrate breakdown proceeds along a different pathway which results in lactic acid formation. If the lactic acid is allowed to accumulate in excessive amounts, the chemical reactions are interfered with and the muscle can no longer be made to contract. In moderate exercise, energy requirements are fully met by oxidations, and no lactic acid is formed.
Chemical Changes in Muscle During Contraction and Recovery
Muscle may be regarded as a machine which transforms chemical energy into work. The mechanism of this conversion remains obscure despite the enormous amount of research which has been directed toward its solution. Accordingly, the views which are presented here must be regarded as tentative and subject to almost certain modification as new data become available. The difficulty is that, although the time course of tension development and heat production can be followed quite accurately, there are no methods sufficiently accurate and rapid to permit a study of the chemical changes which accompany and follow a single twitch. In fact it is necessary to stimulate a muscle for several seconds involving scores of contractions before the chemical changes become great enough to permit accurate analysis. In the discussion which follows an attempt will be made to correlate some of the more striking chemical changes with the phases of activity and recovery in skeletal muscle under both aerobic and anaerobic conditions.
Carbohydrate Metabolism
The metabolism of carbohydrate in muscle begins with glycogen, a form of animal starch. The exact chemical structure of glycogen is uncertain, but it is known to be built up by the combination of large numbers of glucose molecules with the splitting out of water. Glycogen is the common storage form of carbohydrate in the body, and is found in large amounts particularly in the liver and in skeletal muscles. The lactic acid (an organic acid produced by the partial breakdown of carbohydrate) accumulates in muscles contracting to the point of fatigue and disappears during recovery of the muscles if adequate oxygen is present. Fletcher and Hopkins concluded that lactic acid production (probably from glycogen) is the fundamental chemical reaction producing energy for muscle contraction; they suggested that the development of tension may be due to an action of lactic acid on the colloidal protein contractile substance in muscle. According to this relatively simple theory contraction itself is an anaerobic process, and oxygen is necessary only for the oxidative removal of lactic acid, since its accumulation leads to loss of irritability of muscle.
Much of the lactic acid is formed after contraction and relaxation are over, so that the formation of lactic acid cannot be an immediate source of energy for muscle contraction. Lactic acid production in normal muscle contraction is associated, either directly or indirectly, with the development of tension in anaerobic contractions, but there is no satisfactory evidence that lactic acid is produced under aerobic conditions. Some lactic acid may be formed during short periods of tetanic contraction in intact cat muscle, but there is some doubt whether the oxygen supply was completely adequate in these experiments.
Carbohydrate Metabolism
The metabolism of carbohydrate in muscle begins with glycogen, a form of animal starch. The exact chemical structure of glycogen is uncertain, but it is known to be built up by the combination of large numbers of glucose molecules with the splitting out of water. Glycogen is the common storage form of carbohydrate in the body, and is found in large amounts particularly in the liver and in skeletal muscles. The lactic acid (an organic acid produced by the partial breakdown of carbohydrate) accumulates in muscles contracting to the point of fatigue and disappears during recovery of the muscles if adequate oxygen is present. Fletcher and Hopkins concluded that lactic acid production (probably from glycogen) is the fundamental chemical reaction producing energy for muscle contraction; they suggested that the development of tension may be due to an action of lactic acid on the colloidal protein contractile substance in muscle. According to this relatively simple theory contraction itself is an anaerobic process, and oxygen is necessary only for the oxidative removal of lactic acid, since its accumulation leads to loss of irritability of muscle.
Much of the lactic acid is formed after contraction and relaxation are over, so that the formation of lactic acid cannot be an immediate source of energy for muscle contraction. Lactic acid production in normal muscle contraction is associated, either directly or indirectly, with the development of tension in anaerobic contractions, but there is no satisfactory evidence that lactic acid is produced under aerobic conditions. Some lactic acid may be formed during short periods of tetanic contraction in intact cat muscle, but there is some doubt whether the oxygen supply was completely adequate in these experiments.
The Metabolism of Muscle
When muscles contract, energy is liberated. If a muscle shortens against a load (isotonic contraction) work is done and part of the energy is thus accounted for; the rest appears as heat. If the muscle is unable to shorten (isometric contraction), all the energy which is liberated is eventually dissipated as heat. In either ease, the liberation of energy is the result of certain chemical reactions which occur within the muscle fibers. Since the total energy of contraction appears as heat in an isometric contraction, and since this heat can be measured very accurately, an analysis of the time course of heat liberation in this type of contraction furnishes valuable cities to the nature of the chemical reactions in tile contracting muscle. This is all the more important in view of the fact that the chemical changes themselves are so small and so fleeting that they can be measured accurately only after a tetanus or a series of twitches and little information is ained about tile sequence of these changes. For these reasons, it is well to begin our study of the metabolism of muscle with a brief consideration of the heat liberated during an isometric twitch.
The Heat Production of Muscle
The contraction of muscle is associated with the metabolic breakdown of certain chemical compounds. During recovery these chemical compounds must be rebuilt and waste products removed if the original contractile power of the muscle is to be restored. Both of these processes yield heat. While this heat production serves a useful purpose in maintaining body temperature in cold environments, it is an inevitable by-product of muscular activity which may render exertion in a hot environment disagreeable or even impossible. It represents energy consumed with no mechanical work produced and hence is a measure of the inefficiency of our muscles considered as machines.
When a muscle performs a simple twitch, heat is liberated in two fairly distinct bursts. The first, which is called initial heat, accompanies the development and subsidence of tension. Hartree 1 has shown that the initial heat of a twitch occurs in two phases: (1) the contraction heat, which rises and then falls off during the developmerit of tension, and (2) the relaxation heat, which is liberated during the subsidence of tension. After the contraction is over, there is a second and slower production of heat, the delayed heat, also called the recovery heat since it is due to chemical changes which restore the muscle to the condition in which it was before its response. When a muscle contracts tetanically, there is a further heat production during the maintenance of the contraction.
We usually associate heat production in living tissues with the oxidation of energy-yielding compounds. However, many chemical reactions of a non-oxidative nature also result in the liberation of heat. Heat which is liberated only when oxygen is present must be due to oxidative processes and is frequently called aerobic heat: heat which is liberated in the absence of oxygen must be due Io non-oxidative processes and is referred to as anaerobic heat. A study of the heat production of muscle under both aerobic and anaerobic conditions yields data from which we may draw certain conclusions about the general types of reactions which occur during contraction, relaxalion and recovery in muscle. The lime course and magnitude of the initial heat are essentially the same whether the muscle is contracting in an atmosphere of oxygen or one of nitrogen. Thus, the chemical reactions which are associated with actual contraction and relaxation of the isolated muscle are presumably non-oxidative, or anaerobic. The magnitude of the delayed heat is greatly diminished in the absenee of oxygen, so that oxidation plays an important role in the recovery of muscle from the effects of contraction. Apparently the energy for contraction of muscle is liberated by the "explosive" breakdown of compounds with high potential energy, and oxygen is not necessary for this breakdown. During recovery these compounds must be rebuilt in order that energy may be available for subsequent contractions. This process of rebuilding requires energy which is obtained, at least in part, from oxidations.
The Heat Production of Muscle
The contraction of muscle is associated with the metabolic breakdown of certain chemical compounds. During recovery these chemical compounds must be rebuilt and waste products removed if the original contractile power of the muscle is to be restored. Both of these processes yield heat. While this heat production serves a useful purpose in maintaining body temperature in cold environments, it is an inevitable by-product of muscular activity which may render exertion in a hot environment disagreeable or even impossible. It represents energy consumed with no mechanical work produced and hence is a measure of the inefficiency of our muscles considered as machines.
When a muscle performs a simple twitch, heat is liberated in two fairly distinct bursts. The first, which is called initial heat, accompanies the development and subsidence of tension. Hartree 1 has shown that the initial heat of a twitch occurs in two phases: (1) the contraction heat, which rises and then falls off during the developmerit of tension, and (2) the relaxation heat, which is liberated during the subsidence of tension. After the contraction is over, there is a second and slower production of heat, the delayed heat, also called the recovery heat since it is due to chemical changes which restore the muscle to the condition in which it was before its response. When a muscle contracts tetanically, there is a further heat production during the maintenance of the contraction.
We usually associate heat production in living tissues with the oxidation of energy-yielding compounds. However, many chemical reactions of a non-oxidative nature also result in the liberation of heat. Heat which is liberated only when oxygen is present must be due to oxidative processes and is frequently called aerobic heat: heat which is liberated in the absence of oxygen must be due Io non-oxidative processes and is referred to as anaerobic heat. A study of the heat production of muscle under both aerobic and anaerobic conditions yields data from which we may draw certain conclusions about the general types of reactions which occur during contraction, relaxalion and recovery in muscle. The lime course and magnitude of the initial heat are essentially the same whether the muscle is contracting in an atmosphere of oxygen or one of nitrogen. Thus, the chemical reactions which are associated with actual contraction and relaxation of the isolated muscle are presumably non-oxidative, or anaerobic. The magnitude of the delayed heat is greatly diminished in the absenee of oxygen, so that oxidation plays an important role in the recovery of muscle from the effects of contraction. Apparently the energy for contraction of muscle is liberated by the "explosive" breakdown of compounds with high potential energy, and oxygen is not necessary for this breakdown. During recovery these compounds must be rebuilt in order that energy may be available for subsequent contractions. This process of rebuilding requires energy which is obtained, at least in part, from oxidations.
Phasic Contractions; Reflex and Volitional Movements
Phasic contractions result in movement; they may be either reflex or volitional in origin. A reflex movement is one which occurs as the result of the stimulation of receptors located at or near the surface of the body. Nerve impulses resulting from stimulation of the receptors travel over sensory nerve fibers to the spinal cord. Here the impulses are transmitted either directly or by way of intermediate neurones to the motor nerve cells. Tire central processes of the sensory nerve fibers terminate as tiny knobs or "end-feet" in contact with the dendrites and eell body of the motor neurone. This junction is called a synapse; its very great susceptibility to adverse conditions, including fatigue, is of particular significance to students of exercise physiology. The motor nerve cell discharges over the motor nerve fiber to the muscle where the impulses must cross another type of junction, the motor end plate, which is a specialized mass of tissue intervening between the nerve fiber and the sarcoplasm of the muscle fiber, lake the synapse, but to a lesser degree, the motor end plate is readily rendered non-functional by fatigue and the action of certain drugs. The simple reflex arc as here analyzed consists of the following structures: receptor, sensory nerve fiber, synapse, motor nerve cell and fiber, motor end plate, muscle fiber. The reflexes which utilize this simple type of circuit are called spinal reflexes, since they are mediated through the spinal cord without the intervention of higher centers.
Spinal reflex activity is primitive and unlearned in spite of its seeming purposiveness. The character of the reflex response to stimulation of any particular area of the body surface is determined largely by the type of receptor stimulated. Thus, painful stimulation of the sole of the foot causes flexion of the leg which withdraws the foot from contact with the injurious agent. On the other hand, gentle pressure applied to the same point elicits extension of the leg due to stimulation of pressure receptors just under the skin (this "extensor thrust" reflex is an integral part of the whole reflex mechanism of walking, and is normally operative on contact of the sole of the foot with the ground).
All reflexes are not of this simple spinal type. Some involve higher brain centers (for example, the instantaneous turning of the head toward the source of a sudden, loud noise). Despite their greater complexity of nervous pathways, however, the general principles are the same as for the simpler types: a reflex is an invariable, predictable response to stimulation of a particular type of receptor, and the response always accomplishes a useful purpose which is related to the nature of the stimulus.
Volitional movements are initiated by impulses which are discharged from certain areas of the cerebral cortex. Cortical (volitional) activity differs from reflex activity in several respects, one of the most important of which is that, unlike spinal activity, it is unpredictable. This results from the fact that it is determined not only by the nature of the immediate stimulus (if any) lint also by the stored memories of past experiences.
The region of the cerebral cortex which discharges the impulses witch bring about voluntary movements is called the motor area; it is a narrow strip of tissue located just in front of the central fissure. The motor impulses arise in the large pyramidal cells and are transmitted along a bundle of nerve fibers, the pyramidal tract, down through the brain stem and spinal cord to terminate by synapsing with ventral horn (motor) cells of the spinal cord. Most of the pyramidal tibet's cross to the opposite side in passing through the brain stem, so that the motor area on the left side controls the muscles on the right side of the body, and vice versa.
Electrical stimulation of the motor area reveals that the muscles of each region of the body have their own distinct controlling areas; stimulation of the arm area o the cortex, for example, results in contraction of the arm muscles of the opposite side of the body. The size of the cortical area which controls the activity of a given group of muscles is determined not by the size of the muscle group, but rather by the complexity of its activity. For example, the cortical area which controls tinge/' movements is much larger than the cortical area for the entire trunk musculature. Another very significant fact revealed by electrical stimulation of the motor area is that this area controls the contractions of single, discrete muscles or small groups of muscles---quite different from the complex group contractions which characterize voluntary activity. If, however, the region just in front of the motor area (known as the "pre-motor area") is stimulated, complex group movements (flexion and extension, pronation, and supination) are elicited. Since this type of response cannot be obtained if the connections between the motor and the pre-motor areas are cut, it is evident that impulses originating in the pre-motor area travel to the motor area and there stimulate the pyramidal cells. What is the significance of this indirect method of control? The answer has been obtained from clinical eases in which the pre-motor area has been destroyed. There is no paralysis of voluntary muscles, but the ability to execute complex, learned types of skilled activities, such as playing the piano, is lost. We are now in a position to analyze the way in which motor skills are acquired by practice. In the beginning, performance of the component parts of the activity requires constant attention; it is controlled by the motor area. Gradually, smoothness and accuracy of performance are developed and constant attention is no longer required; control of the activity has now been transferred to the pre-motor area.
While the pre-motor area of the cerebral cortex thus initiates the muscle contractions which make up skilled activities and ensures that they are performed in proper sequence, other portions of the nervous system are required to adjust the strength, duration and range of muscle movements. The cerebellum, through its connections with the motor areas or' the cortex on the one hand, and with the proprioceptors of the muscles and joints on the other, is the key structure in this coordination. As a muscle begins to contract its muscle spindles and tendon organs are stimulated, and some of the impulses are transmitted up the spinal cord to the cerebellum. In this way the cerebellum is kept constantly informed of the strength of muscle contractions and of the range of movement at the joints. Through its connections with the motor arcas of the cortex, it is then able to increase or decrease cortical motor activity and thus adjust the strength, dural ion and range of muscle movements to the requirements of the act. With training visual memory may largely supplant tile more primitive cerebral mechanism.
Adjustment of the range or extent of movement necessary to accomplish a given act is largely a matter of experience. We learn to correlate our visual impressions of the necessary range of movemerit with the corresponding proprioceptive impulses from the muscle spindles, so that eventually we are able to make this adjustment in the absence of visual stimulation. For example, in learning to type, we must guide the movement of our fingers to the appropriate keys by sight. With practice proprioceptive impulses are sufficient to guide our movements. If the cerebellum is injured proprioceptive information is faulty, and our tendency is to over-reach or underreach the keys; constant visual guidance becomes necessary.
There is evidence that the sensory receptors in the muscles and joints may suffer fatigue in exhausting exercise. This may partially account for the faulty neuromuscular coordination which is often associated with extreme fatigue.
Spinal reflex activity is primitive and unlearned in spite of its seeming purposiveness. The character of the reflex response to stimulation of any particular area of the body surface is determined largely by the type of receptor stimulated. Thus, painful stimulation of the sole of the foot causes flexion of the leg which withdraws the foot from contact with the injurious agent. On the other hand, gentle pressure applied to the same point elicits extension of the leg due to stimulation of pressure receptors just under the skin (this "extensor thrust" reflex is an integral part of the whole reflex mechanism of walking, and is normally operative on contact of the sole of the foot with the ground).
All reflexes are not of this simple spinal type. Some involve higher brain centers (for example, the instantaneous turning of the head toward the source of a sudden, loud noise). Despite their greater complexity of nervous pathways, however, the general principles are the same as for the simpler types: a reflex is an invariable, predictable response to stimulation of a particular type of receptor, and the response always accomplishes a useful purpose which is related to the nature of the stimulus.
Volitional movements are initiated by impulses which are discharged from certain areas of the cerebral cortex. Cortical (volitional) activity differs from reflex activity in several respects, one of the most important of which is that, unlike spinal activity, it is unpredictable. This results from the fact that it is determined not only by the nature of the immediate stimulus (if any) lint also by the stored memories of past experiences.
The region of the cerebral cortex which discharges the impulses witch bring about voluntary movements is called the motor area; it is a narrow strip of tissue located just in front of the central fissure. The motor impulses arise in the large pyramidal cells and are transmitted along a bundle of nerve fibers, the pyramidal tract, down through the brain stem and spinal cord to terminate by synapsing with ventral horn (motor) cells of the spinal cord. Most of the pyramidal tibet's cross to the opposite side in passing through the brain stem, so that the motor area on the left side controls the muscles on the right side of the body, and vice versa.
Electrical stimulation of the motor area reveals that the muscles of each region of the body have their own distinct controlling areas; stimulation of the arm area o the cortex, for example, results in contraction of the arm muscles of the opposite side of the body. The size of the cortical area which controls the activity of a given group of muscles is determined not by the size of the muscle group, but rather by the complexity of its activity. For example, the cortical area which controls tinge/' movements is much larger than the cortical area for the entire trunk musculature. Another very significant fact revealed by electrical stimulation of the motor area is that this area controls the contractions of single, discrete muscles or small groups of muscles---quite different from the complex group contractions which characterize voluntary activity. If, however, the region just in front of the motor area (known as the "pre-motor area") is stimulated, complex group movements (flexion and extension, pronation, and supination) are elicited. Since this type of response cannot be obtained if the connections between the motor and the pre-motor areas are cut, it is evident that impulses originating in the pre-motor area travel to the motor area and there stimulate the pyramidal cells. What is the significance of this indirect method of control? The answer has been obtained from clinical eases in which the pre-motor area has been destroyed. There is no paralysis of voluntary muscles, but the ability to execute complex, learned types of skilled activities, such as playing the piano, is lost. We are now in a position to analyze the way in which motor skills are acquired by practice. In the beginning, performance of the component parts of the activity requires constant attention; it is controlled by the motor area. Gradually, smoothness and accuracy of performance are developed and constant attention is no longer required; control of the activity has now been transferred to the pre-motor area.
While the pre-motor area of the cerebral cortex thus initiates the muscle contractions which make up skilled activities and ensures that they are performed in proper sequence, other portions of the nervous system are required to adjust the strength, duration and range of muscle movements. The cerebellum, through its connections with the motor areas or' the cortex on the one hand, and with the proprioceptors of the muscles and joints on the other, is the key structure in this coordination. As a muscle begins to contract its muscle spindles and tendon organs are stimulated, and some of the impulses are transmitted up the spinal cord to the cerebellum. In this way the cerebellum is kept constantly informed of the strength of muscle contractions and of the range of movement at the joints. Through its connections with the motor arcas of the cortex, it is then able to increase or decrease cortical motor activity and thus adjust the strength, dural ion and range of muscle movements to the requirements of the act. With training visual memory may largely supplant tile more primitive cerebral mechanism.
Adjustment of the range or extent of movement necessary to accomplish a given act is largely a matter of experience. We learn to correlate our visual impressions of the necessary range of movemerit with the corresponding proprioceptive impulses from the muscle spindles, so that eventually we are able to make this adjustment in the absence of visual stimulation. For example, in learning to type, we must guide the movement of our fingers to the appropriate keys by sight. With practice proprioceptive impulses are sufficient to guide our movements. If the cerebellum is injured proprioceptive information is faulty, and our tendency is to over-reach or underreach the keys; constant visual guidance becomes necessary.
There is evidence that the sensory receptors in the muscles and joints may suffer fatigue in exhausting exercise. This may partially account for the faulty neuromuscular coordination which is often associated with extreme fatigue.
Postural Mechanisms and Their Control
Skeletal muscles normally display a firmness which is due to a slight sustained contraction of a fraction of the muscle fibers (muscle lone or tonus). This tone is most pronounced in those muscles which keep the head erect and the jaw closed, and which prevent the body from sagging at the hip and knee joints, that is, in those muscles which maintain the body in the erect position against the force of gravity. Hence, they are commonly referred to as the antigravity muscles.
Muscle tone is reflex in nature. The sensory side of the reflex has its origin in receptors (specialized sensory nerve endings) located in the muscle itself (muscle spindles) and in the tendon which the muscle attaches to bone (tendon organs). Sensory receptors of this type, which are stimulated tension or pressure, are called proprioceptors. When a muscle is stretched, certain of these receptors are stimulated and nerve impulses are transmitted to the central nervous system where they stimulate the motor nerve cells which supply this same muscle. The discharge of these nerve cells results in contraction of the muscle, the strength of the contraction being proportional to the degree of stretching of the muscle. This stretch reflex is one of the basic elements in the origin of muscle tone. Since it is especially well developed in the extensor (antigravity) muscles, it plays an important part in the maintenance of body posture. For example, if the body is to be held erect, the tendency to flex the hip and knee joints under the influence of gravity must be counteracted. If the knee joint begins to buckle, the extensor muscles of the knee joint are stretched and their proprioceptors are stimulated. The resulting reflex contraction of the extensor muscles then straightens the knee joint and preserves the upright posture.
While muscle tone and the basic patterns of posture involve local reflexes, they are definitely under the influence of higher portions of the nervous system. If man is deprived of these higher centers he is unable to maintain normal posture, even though the basic reflex mechanisms are still intact. Also, loss of consciousness, as in fainting or in sleep, abolishes the normal control of posture and the body crumples under its own weight. A detailed analysis of the control of posture by the higher nervous centers is beyond the scope of this book. Suffice it to say that some of these influences increase muscle tone while others diminish it and that many portions of the brain are involved, among them being the cerebral cortex, the cerebellum and the proprioceptors of the inner ear.
Another group of postural reactions which is of paramount importance in sports is concerned with the maintenance of equilibrium or balance. In complex motor skill activities it is essential that the body should be in the correct posture for the performance of the necessary movements. A boxer who is staggered by a blow, or a football player who stumbles while running, "automatically" makes compensatory movements which tend to restore the normal erect posture. These movements are not "thought out"; they can occur in the absence of the cerebral cortex so that they must be considered as complex reflex patterns.
There are three major sources of sensory impulses which initiate these reflex movements: (1) visual stimulation, (2) proprioceptors in the inner ear (the semicircular canals and the otolith organs) and (3) stretch receptors (muscle spindles) in the neck muscles. The example of the football player who stumbles and begins to fall may clarify the operation of the balance mechanisms. The abnormal position of the head in space results in stimulation of nerve endings in the retina of the eye and in the otolith organs of the inner ear. The reflex thus initiated tends to restore the head to its normal position in space through contraction of the appropriate neck muscles. Contraction of the neck muscles causes stimulation of the muscle spindles in these muscles and initiates reflex movements of the arms, the trunk and the legs which serve to restore the rest of the body to its normal upright position. The abnormal movement of the head during falling and also during the performance of gymnastic maneuvers, such as turning somersaults or cartwheels, initiates reflexes originating in the semicircular canals of the inner ear which produce the same types of corrective movements as those described above.
Postural tone is a characteristic of muscles which are engaged in maintaining the body in some static position or attitude. When movement occurs, this posture must temporarily give way, else it might retard the prompt execution of the movement. Accordingly it is found that phasic contractions (those which result in movement as opposed to posture) are accompanied by a temporary decrease in the tone of the antagonistic muscles. This phenomenon is known as reciprocal inhibition of antagonistic muscles. For perfect neuromuscular coordination it is essential that the speed and degree of relaxation of muscles opposing a movement be accurately adjusted to the speed and range of contraction of the muscles effecting a movement. A failure of antagonistic muscles to relax promptly is one of the factors which results in poor performance in exercise which is not preceded by a "warming up" period.
Muscle tone is reflex in nature. The sensory side of the reflex has its origin in receptors (specialized sensory nerve endings) located in the muscle itself (muscle spindles) and in the tendon which the muscle attaches to bone (tendon organs). Sensory receptors of this type, which are stimulated tension or pressure, are called proprioceptors. When a muscle is stretched, certain of these receptors are stimulated and nerve impulses are transmitted to the central nervous system where they stimulate the motor nerve cells which supply this same muscle. The discharge of these nerve cells results in contraction of the muscle, the strength of the contraction being proportional to the degree of stretching of the muscle. This stretch reflex is one of the basic elements in the origin of muscle tone. Since it is especially well developed in the extensor (antigravity) muscles, it plays an important part in the maintenance of body posture. For example, if the body is to be held erect, the tendency to flex the hip and knee joints under the influence of gravity must be counteracted. If the knee joint begins to buckle, the extensor muscles of the knee joint are stretched and their proprioceptors are stimulated. The resulting reflex contraction of the extensor muscles then straightens the knee joint and preserves the upright posture.
While muscle tone and the basic patterns of posture involve local reflexes, they are definitely under the influence of higher portions of the nervous system. If man is deprived of these higher centers he is unable to maintain normal posture, even though the basic reflex mechanisms are still intact. Also, loss of consciousness, as in fainting or in sleep, abolishes the normal control of posture and the body crumples under its own weight. A detailed analysis of the control of posture by the higher nervous centers is beyond the scope of this book. Suffice it to say that some of these influences increase muscle tone while others diminish it and that many portions of the brain are involved, among them being the cerebral cortex, the cerebellum and the proprioceptors of the inner ear.
Another group of postural reactions which is of paramount importance in sports is concerned with the maintenance of equilibrium or balance. In complex motor skill activities it is essential that the body should be in the correct posture for the performance of the necessary movements. A boxer who is staggered by a blow, or a football player who stumbles while running, "automatically" makes compensatory movements which tend to restore the normal erect posture. These movements are not "thought out"; they can occur in the absence of the cerebral cortex so that they must be considered as complex reflex patterns.
There are three major sources of sensory impulses which initiate these reflex movements: (1) visual stimulation, (2) proprioceptors in the inner ear (the semicircular canals and the otolith organs) and (3) stretch receptors (muscle spindles) in the neck muscles. The example of the football player who stumbles and begins to fall may clarify the operation of the balance mechanisms. The abnormal position of the head in space results in stimulation of nerve endings in the retina of the eye and in the otolith organs of the inner ear. The reflex thus initiated tends to restore the head to its normal position in space through contraction of the appropriate neck muscles. Contraction of the neck muscles causes stimulation of the muscle spindles in these muscles and initiates reflex movements of the arms, the trunk and the legs which serve to restore the rest of the body to its normal upright position. The abnormal movement of the head during falling and also during the performance of gymnastic maneuvers, such as turning somersaults or cartwheels, initiates reflexes originating in the semicircular canals of the inner ear which produce the same types of corrective movements as those described above.
Postural tone is a characteristic of muscles which are engaged in maintaining the body in some static position or attitude. When movement occurs, this posture must temporarily give way, else it might retard the prompt execution of the movement. Accordingly it is found that phasic contractions (those which result in movement as opposed to posture) are accompanied by a temporary decrease in the tone of the antagonistic muscles. This phenomenon is known as reciprocal inhibition of antagonistic muscles. For perfect neuromuscular coordination it is essential that the speed and degree of relaxation of muscles opposing a movement be accurately adjusted to the speed and range of contraction of the muscles effecting a movement. A failure of antagonistic muscles to relax promptly is one of the factors which results in poor performance in exercise which is not preceded by a "warming up" period.
Warming Up Performance is improved
Warming Up
Performance is improved if the muscles have been slightly warmed up just before the activity. Most baseball pitchers, for example, work better on warm days. Failure to warm up before vigorous activity may lead to an actual tearing loose of muscle fibers from their tendinous attachments.
Observations on the contraction of isolated muscles provide a clue to the nature of the warming up process. If the muscle is warmed, the speed with which the muscle contracts and relaxes and the force of contraction are all increased. If a previously inactive muscle is stimulated repeatedly, the first few contractions are often small and irregular and relaxation is incomplete. After this, the contractions become stronger and relaxation is complete. It is probable that warming up is due in part to these changes in the muscle itself, involving a local rise in temperature and the accumulation of metabolic products. It is possible that the viscosity of the muscle is thereby decreased, allowing contraction and relaxation to occur with greater promptness. In the body these same factors also increase the local blood flow through the muscle by dilating the small blood vessels. This improves the functional condition of the muscle by increasing its oxygen supply.
The muscles most frequently torn during strenuous activity which has not been preceded by a warming up period are the antagonists to the strong contracting muscles. These "cold" antagonistic muscles relax slowly and incompletely when the agonists contract and thus retard free movement and accurate coordination. At the same time, the force of contraction of the agonists and the momentum of the moving part exert a terrific strain on the unyielding antagonists with consequent tearing of the muscle fibers or their tendinous attachments.
Performance is improved if the muscles have been slightly warmed up just before the activity. Most baseball pitchers, for example, work better on warm days. Failure to warm up before vigorous activity may lead to an actual tearing loose of muscle fibers from their tendinous attachments.
Observations on the contraction of isolated muscles provide a clue to the nature of the warming up process. If the muscle is warmed, the speed with which the muscle contracts and relaxes and the force of contraction are all increased. If a previously inactive muscle is stimulated repeatedly, the first few contractions are often small and irregular and relaxation is incomplete. After this, the contractions become stronger and relaxation is complete. It is probable that warming up is due in part to these changes in the muscle itself, involving a local rise in temperature and the accumulation of metabolic products. It is possible that the viscosity of the muscle is thereby decreased, allowing contraction and relaxation to occur with greater promptness. In the body these same factors also increase the local blood flow through the muscle by dilating the small blood vessels. This improves the functional condition of the muscle by increasing its oxygen supply.
The muscles most frequently torn during strenuous activity which has not been preceded by a warming up period are the antagonists to the strong contracting muscles. These "cold" antagonistic muscles relax slowly and incompletely when the agonists contract and thus retard free movement and accurate coordination. At the same time, the force of contraction of the agonists and the momentum of the moving part exert a terrific strain on the unyielding antagonists with consequent tearing of the muscle fibers or their tendinous attachments.
Muscular Pain, Soreness and Stiffness
During and following strenuous muscular exercise, particularly in untrained objects, there may be muscular pain, soreness and stiffness.
Muscular pain commonly occurs during exercise, while soreness and stiffness usually appear some hours later. It is well known that when muscles are forced to work without adequate blood supply (for example, rapid flexion and extension of the fingers with the circulation occluded by a blood pressure cuff) severe pain results. The inadequate blood flow results in failure of complete removal of the products of muscle metabolism, and it is probable that the pain of strenuous exercise is due to accumulation of acid metabolites which irritate the receptor organs of pain located in the muscles.
Fluid collects in muscles during activity and a number of hours may be required for its reabsorption into the blood stream. The resulting swelling of the muscle causes it to become shorter and thicker and more resistant to stretching. This gives rise to a sensation of stiffness when the muscle is stretched during the contraction of antagonistic muscles.
The cause of muscle soreness is not completely understood. Two types of muscle soreness have been postulated:
(1) general soreness due to the presence of diffusible metabolic waste products which usually disappears within three or four hours after the cessation of exercise, and (2) localized soreness or lameness which appears eight to twenty-four hours after exercise and may persist for several days. The second type of soreness is probably due to the rupture of muscle fibers or of the sarcolemma which transmits the contraction to the tendon. The less frequently used fibers and the sarcolemma covering them are probably more susceptible to strain than are the fibers more frequently used in ordinary contractions. The generalized type of soreness is alleviated by light work which hastens the circulatory removal of the metabolic waste products, while the localized lameness, which is due to actual injury, needs rest with heat and only enough exercise to prevent adhesions between the injured muscle fibers.
Muscular pain commonly occurs during exercise, while soreness and stiffness usually appear some hours later. It is well known that when muscles are forced to work without adequate blood supply (for example, rapid flexion and extension of the fingers with the circulation occluded by a blood pressure cuff) severe pain results. The inadequate blood flow results in failure of complete removal of the products of muscle metabolism, and it is probable that the pain of strenuous exercise is due to accumulation of acid metabolites which irritate the receptor organs of pain located in the muscles.
Fluid collects in muscles during activity and a number of hours may be required for its reabsorption into the blood stream. The resulting swelling of the muscle causes it to become shorter and thicker and more resistant to stretching. This gives rise to a sensation of stiffness when the muscle is stretched during the contraction of antagonistic muscles.
The cause of muscle soreness is not completely understood. Two types of muscle soreness have been postulated:
(1) general soreness due to the presence of diffusible metabolic waste products which usually disappears within three or four hours after the cessation of exercise, and (2) localized soreness or lameness which appears eight to twenty-four hours after exercise and may persist for several days. The second type of soreness is probably due to the rupture of muscle fibers or of the sarcolemma which transmits the contraction to the tendon. The less frequently used fibers and the sarcolemma covering them are probably more susceptible to strain than are the fibers more frequently used in ordinary contractions. The generalized type of soreness is alleviated by light work which hastens the circulatory removal of the metabolic waste products, while the localized lameness, which is due to actual injury, needs rest with heat and only enough exercise to prevent adhesions between the injured muscle fibers.
Muscle Tone, Muscle Fatigue, Cause of Fatigue
Muscles in the body are normally firm to the touch. This is due to the continuous slight contraction of a small fraction of the component fibers producing what is known as muscle tone. This tone disappears when the nerve supply to the muscle is destroyed, as occurs in poliomyelitis, so that it is clearly due to the constant arrival of low frequency, asynchronous impulses from the spinal cord. This concept of the nature of muscle tone has been questioned because no electrical potentials could be recorded from electrodes thrust into resting muscles.
Muscle Fatigue
When an excised muscle is stimulated repeatedly at a frequency of about once per second, the height of each contraction eventually begins to decrease. Not only is the amount of shortening diminished, but also the relaxation becomes slower and incomplete (contracture). Finally the muscle fails to respond even to the strongest stimulation, that is, its irritability is completely lost. This diminished capacity for response which results from previous activity is called fatigue.
Cause of Fatigue
If a fatigue excised muscle is cut across and the cut surface tested with litmus paper, it is found that the interior of the muscle is acid. Since the normal muscle gives an alkaline reaction with litmus, it is apparent that fatigue is associated with an accumulation of acid. Chemical analysis reveals that the amount of glycogen (energy-yielding carbohydrate) is less in the fatigued muscle than in the normal muscle. These experiments suggest that fatigue may be due to the accumulation of acid waste products which decrease the irritability of the muscle or to exhaustion of stored fuel supplies. The accumulation of acid waste products (largely lactic acid) in the excised muscle is due in large part to the absence of a normal circulation of blood. As a result the amount of oxygen supplied to the muscle is not sufficient to oxidize the lactic acid nor can it be removed from the muscle by diffusion into the circulating blood. Conditions, are, of course different in the case of muscles in the body. Here the fuel is constantly being replenished by way of the blood; the oxygen supply is adequate to oxidize most, if not all, of the lactic acid produced and much of that which is not oxidized nor reconverted to glycogen diffuses into the blood and is carried away from the muscle. As a result, muscles in the body can perform large amounts of work before their capacity for response is abolished by fatigue. In fact, it is doubtful whether the muscle fatigue of this degree ever occurs in normal exercise.
Site of Fatigue
If the motor nerve of a muscle-nerve preparation is stimulated repeatedly, the muscle eventually fails to contract. If the stimulating electrode is now placed directly on the muscle, contractions of almost normal height are obtained showing that the muscle itself is not fatigued. Since nerve fibers have been shown to be practically nonfatiguable, the fatigue in this case must be in the junction between the nerve and the muscle, the neuromuscular junction or motor end plate. This junction is also the site of action of numerous drugs and chemical agents which may influence muscular work in the body.
If a muscle in the body is voluntarily fatigued by repeated contraction and the motor nerve then stimulated electrically through the skin, strong contractions of the "fatigued" muscle may be obtained. In this case the fatigue cannot have been in the muscle, its nerve or the neuromuscular junction, but rather in the brain or in the spinal cord from which the motor nerve arises.
Muscle Fatigue
When an excised muscle is stimulated repeatedly at a frequency of about once per second, the height of each contraction eventually begins to decrease. Not only is the amount of shortening diminished, but also the relaxation becomes slower and incomplete (contracture). Finally the muscle fails to respond even to the strongest stimulation, that is, its irritability is completely lost. This diminished capacity for response which results from previous activity is called fatigue.
Cause of Fatigue
If a fatigue excised muscle is cut across and the cut surface tested with litmus paper, it is found that the interior of the muscle is acid. Since the normal muscle gives an alkaline reaction with litmus, it is apparent that fatigue is associated with an accumulation of acid. Chemical analysis reveals that the amount of glycogen (energy-yielding carbohydrate) is less in the fatigued muscle than in the normal muscle. These experiments suggest that fatigue may be due to the accumulation of acid waste products which decrease the irritability of the muscle or to exhaustion of stored fuel supplies. The accumulation of acid waste products (largely lactic acid) in the excised muscle is due in large part to the absence of a normal circulation of blood. As a result the amount of oxygen supplied to the muscle is not sufficient to oxidize the lactic acid nor can it be removed from the muscle by diffusion into the circulating blood. Conditions, are, of course different in the case of muscles in the body. Here the fuel is constantly being replenished by way of the blood; the oxygen supply is adequate to oxidize most, if not all, of the lactic acid produced and much of that which is not oxidized nor reconverted to glycogen diffuses into the blood and is carried away from the muscle. As a result, muscles in the body can perform large amounts of work before their capacity for response is abolished by fatigue. In fact, it is doubtful whether the muscle fatigue of this degree ever occurs in normal exercise.
Site of Fatigue
If the motor nerve of a muscle-nerve preparation is stimulated repeatedly, the muscle eventually fails to contract. If the stimulating electrode is now placed directly on the muscle, contractions of almost normal height are obtained showing that the muscle itself is not fatigued. Since nerve fibers have been shown to be practically nonfatiguable, the fatigue in this case must be in the junction between the nerve and the muscle, the neuromuscular junction or motor end plate. This junction is also the site of action of numerous drugs and chemical agents which may influence muscular work in the body.
If a muscle in the body is voluntarily fatigued by repeated contraction and the motor nerve then stimulated electrically through the skin, strong contractions of the "fatigued" muscle may be obtained. In this case the fatigue cannot have been in the muscle, its nerve or the neuromuscular junction, but rather in the brain or in the spinal cord from which the motor nerve arises.
Summation of Contractions Tetanus
When a muscle is stimulated twice in such rapid succession that the second stimulus falls during the response to the first, the tension developed is greater than in the single twitch. In some way, as yet not clearly understood, the tension developed as a result of the second stimulus adds to the tension remaining from the first stimulus. If a continuous series of rapidly repeated stimuli is sent into a muscle there is not sufficient time for relaxation between successive contractions and the result is a steady, prolonged contraction known as tetanus. The tension developed during tetanus may be three or four times that of a simple twitch in the muscle. If the rate of stimulation is not rapid enough to produce complete tetanus, there may be partial relaxation between contractions The result is a jerky type of contraction known as incomplete tetanus.
The All-or-none Law and the Motor Unit
If a muscle is stimulated with gradually increasing strengths of current, the tension developed increases progressively up to a certain point; beyond this point there is no increase in tension with further increase in stimulus strength. With increasing strength of stimulation the tension developed by each muscle fiber remains constant, but more fibers are activated. When a muscle is stimulated each fiber contracts maximally or not at all (the "all-or-none law"). It must be remembered, however, that the amount of tension developed by a maximal contraction will vary with such factors as fatigue and training.
It was mentioned earlier that in the body muscles contract only in response to nerve impulses from motor nerve cells in the spinal cord, and further that each motor nerve cell, through terminal branching of its nerve fiber (axon), supplies a large number (100 to 150) of muscle fibers; the motor nerve cell with its nerve fiber and the group of muscle cells supplied by its branches comprise the motor unit. The group of nerve cells in the spinal cord which together give rise to the motor nerve fibers to an entire skeletal muscle is called the motor pool. If the motor pool of a given muscle consists, for example, of 300 nerve cells, the tension developed by the muscle during contraction may theoretically be increased by 300 steps, each representing the activation of an additional motor unit.
Since the tension developed by each motor unit also varies according to the frequency of stimulation, which determines whether the response will be either a series of simple twitches, an incomplete tetanus or a complete tetanus, we have an additional means of varying the tension developed by the muscle. In brief, then, the strength of contraction of a muscle in the body can be varied by two means: (1) variation in the number of motor units activated and (2) variation in the frequency of stimulation of each active motor unit.
One additional point requires consideration. If an isolated muscle is stimulated maximally (that is, with a current sufficiently strong to stimulate every fiber in the muscle) but at a low frequency, the resulting contraction will be jerky because of the partial relaxation between contractions. Since voluntary and reflex contractions in the body are normally smooth, it was thought at one time that they must be invariably tetanic in nature. It is now known, however, that complete tetanus occurs in very powerful contractions and that most contractions involve incomplete tetanus in a variable proportion of the motor units. The smoothness of the contraction is due to the fact that the different motor units are not activated simultaneously; at any instant, the muscle fibers of some units are contracting while those of other units are relaxing. This asynchronous activity of the motor units results in smooth contractions even when the force of contraction is weak. If, as happens in certain nervous disorders, the contractions of the different motor units become synchronized, a jerky type of contraction known as a tremor results.
We are now in a position to understand the mechanism of adjustment of the strength of contraction of muscles to the task required. For example, it is obvious that a more powerful contraction is required to lift a 50 pound weight than to lift a 1 pound weight. A weak voluntary (or reflex) contraction is the result of partial tetanus in a fraction of the motor units responding asynchronously. A very powerful contraction is the result of more nearly complete tetanus in a larger fraction of the motor units of a muscle.
The All-or-none Law and the Motor Unit
If a muscle is stimulated with gradually increasing strengths of current, the tension developed increases progressively up to a certain point; beyond this point there is no increase in tension with further increase in stimulus strength. With increasing strength of stimulation the tension developed by each muscle fiber remains constant, but more fibers are activated. When a muscle is stimulated each fiber contracts maximally or not at all (the "all-or-none law"). It must be remembered, however, that the amount of tension developed by a maximal contraction will vary with such factors as fatigue and training.
It was mentioned earlier that in the body muscles contract only in response to nerve impulses from motor nerve cells in the spinal cord, and further that each motor nerve cell, through terminal branching of its nerve fiber (axon), supplies a large number (100 to 150) of muscle fibers; the motor nerve cell with its nerve fiber and the group of muscle cells supplied by its branches comprise the motor unit. The group of nerve cells in the spinal cord which together give rise to the motor nerve fibers to an entire skeletal muscle is called the motor pool. If the motor pool of a given muscle consists, for example, of 300 nerve cells, the tension developed by the muscle during contraction may theoretically be increased by 300 steps, each representing the activation of an additional motor unit.
Since the tension developed by each motor unit also varies according to the frequency of stimulation, which determines whether the response will be either a series of simple twitches, an incomplete tetanus or a complete tetanus, we have an additional means of varying the tension developed by the muscle. In brief, then, the strength of contraction of a muscle in the body can be varied by two means: (1) variation in the number of motor units activated and (2) variation in the frequency of stimulation of each active motor unit.
One additional point requires consideration. If an isolated muscle is stimulated maximally (that is, with a current sufficiently strong to stimulate every fiber in the muscle) but at a low frequency, the resulting contraction will be jerky because of the partial relaxation between contractions. Since voluntary and reflex contractions in the body are normally smooth, it was thought at one time that they must be invariably tetanic in nature. It is now known, however, that complete tetanus occurs in very powerful contractions and that most contractions involve incomplete tetanus in a variable proportion of the motor units. The smoothness of the contraction is due to the fact that the different motor units are not activated simultaneously; at any instant, the muscle fibers of some units are contracting while those of other units are relaxing. This asynchronous activity of the motor units results in smooth contractions even when the force of contraction is weak. If, as happens in certain nervous disorders, the contractions of the different motor units become synchronized, a jerky type of contraction known as a tremor results.
We are now in a position to understand the mechanism of adjustment of the strength of contraction of muscles to the task required. For example, it is obvious that a more powerful contraction is required to lift a 50 pound weight than to lift a 1 pound weight. A weak voluntary (or reflex) contraction is the result of partial tetanus in a fraction of the motor units responding asynchronously. A very powerful contraction is the result of more nearly complete tetanus in a larger fraction of the motor units of a muscle.
The Contraction of Muscle
An intact skeletal muscle in the body normally contracts only in response to stimuli (nerve impulses) reaching it from the central nervous system. This stimulus-response mechanism is highly complex and is more easily understood after a consideration of the simpler response if an isolated muscle to direct electrical stimulation.
The Simple Muscle Twitch
If the gastrocnemius muscle of a frog is isolated, one end secured in a rigid clamp and the other end attached to a muscle lever, the response of the muscle to stimulation may be recorded on a moving strip of smoked paper. Electrical shocks are used for stimulation, because of the ease of adjustment of strength, duration and frequency, and because they do not injure the muscle.
If a single shock is applied to the muscle a simple muscle twitch results. Although it is unlikely that this simple type of contraction ever occurs in the body, it is none-the-less deserving of study, because it is the building stone of more complex reactions. Inspection of a typical record shows that the twitch may be divided into three intervals: the latent period, the period of contraction, and the period of relaxation.
The latent period is the time which elapses between the application of the stimulus and the first appearance of shortening (or the exertion of tension in the case of an isometric twitch). Most of the latent period recorded in ordinary laboratory experiments is due to instrumental inertia. With highly accurate techniques the true latent period is less than 1 millisecond (0.001 second). However, the actual latent period of muscle contractions in the body is considerably longer, since bony levers with a high degree of inertia must be activated.
The rising phase of the contraction curve represents shortening of the muscle and the more prolonged falling phase indicates the slower relaxation process. Both the relative and the absolute durations of the different phases vary with certain factors, such as fatigue and temperature changes. While the form of the contraction curve is similar for all skeletal muscles, the total duration of the twitch is very different for different types of muscles. Thus the extraocular muscles which move the eyeball are extremely rapid (twitch duration = 7.5 msec.), while at the other extreme the soleus, a red muscle, has a very long twitch duration (94 to 120 msec.).
There is a clear relation between the speed of contraction and the function of a muscle. The pale (white) muscles contract and relax rapidly and are ordinarily involved in acts requiring rapid movement. The red muscles, on the other hand, contract and relax slowly so that the tension developed in a single twitch is maintained over a longer period of time; this makes them well adapted for their role in maintaining posture with minimal expenditure of energy. Flexor muscles contain predominantly pale fibers which are designed for speed and are easily fatigued. Extensor muscles contain predominantly red fibers which are slower in their action but are capable of greater endurance. Because of their slower relaxation time the extensor muscles are frequently pulled in exercise, especially when not properly warmed. Thus, warming up should precede strenuous physical activity. Fast movements of light objects are most easily made with flexors. Slower or sustained activities are most easily performed with the extensors.
The Simple Muscle Twitch
If the gastrocnemius muscle of a frog is isolated, one end secured in a rigid clamp and the other end attached to a muscle lever, the response of the muscle to stimulation may be recorded on a moving strip of smoked paper. Electrical shocks are used for stimulation, because of the ease of adjustment of strength, duration and frequency, and because they do not injure the muscle.
If a single shock is applied to the muscle a simple muscle twitch results. Although it is unlikely that this simple type of contraction ever occurs in the body, it is none-the-less deserving of study, because it is the building stone of more complex reactions. Inspection of a typical record shows that the twitch may be divided into three intervals: the latent period, the period of contraction, and the period of relaxation.
The latent period is the time which elapses between the application of the stimulus and the first appearance of shortening (or the exertion of tension in the case of an isometric twitch). Most of the latent period recorded in ordinary laboratory experiments is due to instrumental inertia. With highly accurate techniques the true latent period is less than 1 millisecond (0.001 second). However, the actual latent period of muscle contractions in the body is considerably longer, since bony levers with a high degree of inertia must be activated.
The rising phase of the contraction curve represents shortening of the muscle and the more prolonged falling phase indicates the slower relaxation process. Both the relative and the absolute durations of the different phases vary with certain factors, such as fatigue and temperature changes. While the form of the contraction curve is similar for all skeletal muscles, the total duration of the twitch is very different for different types of muscles. Thus the extraocular muscles which move the eyeball are extremely rapid (twitch duration = 7.5 msec.), while at the other extreme the soleus, a red muscle, has a very long twitch duration (94 to 120 msec.).
There is a clear relation between the speed of contraction and the function of a muscle. The pale (white) muscles contract and relax rapidly and are ordinarily involved in acts requiring rapid movement. The red muscles, on the other hand, contract and relax slowly so that the tension developed in a single twitch is maintained over a longer period of time; this makes them well adapted for their role in maintaining posture with minimal expenditure of energy. Flexor muscles contain predominantly pale fibers which are designed for speed and are easily fatigued. Extensor muscles contain predominantly red fibers which are slower in their action but are capable of greater endurance. Because of their slower relaxation time the extensor muscles are frequently pulled in exercise, especially when not properly warmed. Thus, warming up should precede strenuous physical activity. Fast movements of light objects are most easily made with flexors. Slower or sustained activities are most easily performed with the extensors.
Organization of Muscle Fibers in a Muscle
Groups of 100 to 150 muscle fibers are bound together with connective tissue to form a unit known as a fasciculus. Groups of fasciculi are bound together into still larger units which in turn are bound together to form the muscle itself; it is likewise invested with a connective tissue sheath. At each end of the muscle this connective tissue merges with tile tendon bundles which attach to the bone.
Nerve and Blood Supply of Skeletal Muscles
The sarcolemma of each muscle fiber insulates it from adjacent fibers, so that excitalion of one fiber does not directly affect neighboring fibers. Hence, each muscle fiber must be supplied with a separate motor nerve twig. A motor nerve supplying a muscle is composed of numerous nerve fibers, each originating from a separate nerve cell in the spinal cord. In the substance of the muscle each nerve fiber breaks up into many branches and each branch penetrates the sarcolemma of a single muscle fiber to terminate in a specialized mass of protoplasm known as a motor end plate. When a single motor nerve cell in the spinal cord discharges impulses to a muscle, all the muscle fibers supplied by branches of tile corresponding nerve fiber are stimulated and contract together. This group of muscle fibers, which forms the smallest functional unit under normal conditions, is believed to correspond to the fasciculus mentioned above. A single motor nerve cell in the spinal cord together with its nerve fiber and the group of muscle fibers supplied by its branches form the basic neuromuscular unit commonly referred to as the motor unit.
In addition to the motor nerve supply, skeletal muscles are also supplied with sensory nerve endings, some of which lie between the groups of muscle fibers while others are associated with muscle tendons. These sensory nerve endings are stimulated by changes in tension in the muscle (contraction, relaxation, stretching) and send impulses to the central nervous system. These impulses play an important role in maintaining muscle tone, in informing the central nervous system of the position of parts of the body with respect to one another and in adjusting the rate and extent of muscle movements.
Each muscle receives blood through one or more arteries. These arteries break up into profuse capillary networks in the connective tissue surrounding each muscle fiber. Under resting conditions many of these capillaries are closed, but they open when the muscle undergoes vigorous contraction. In this way the blood supply to a muscle is adjusted in accordance with the degree of muscular activity.
Nerve and Blood Supply of Skeletal Muscles
The sarcolemma of each muscle fiber insulates it from adjacent fibers, so that excitalion of one fiber does not directly affect neighboring fibers. Hence, each muscle fiber must be supplied with a separate motor nerve twig. A motor nerve supplying a muscle is composed of numerous nerve fibers, each originating from a separate nerve cell in the spinal cord. In the substance of the muscle each nerve fiber breaks up into many branches and each branch penetrates the sarcolemma of a single muscle fiber to terminate in a specialized mass of protoplasm known as a motor end plate. When a single motor nerve cell in the spinal cord discharges impulses to a muscle, all the muscle fibers supplied by branches of tile corresponding nerve fiber are stimulated and contract together. This group of muscle fibers, which forms the smallest functional unit under normal conditions, is believed to correspond to the fasciculus mentioned above. A single motor nerve cell in the spinal cord together with its nerve fiber and the group of muscle fibers supplied by its branches form the basic neuromuscular unit commonly referred to as the motor unit.
In addition to the motor nerve supply, skeletal muscles are also supplied with sensory nerve endings, some of which lie between the groups of muscle fibers while others are associated with muscle tendons. These sensory nerve endings are stimulated by changes in tension in the muscle (contraction, relaxation, stretching) and send impulses to the central nervous system. These impulses play an important role in maintaining muscle tone, in informing the central nervous system of the position of parts of the body with respect to one another and in adjusting the rate and extent of muscle movements.
Each muscle receives blood through one or more arteries. These arteries break up into profuse capillary networks in the connective tissue surrounding each muscle fiber. Under resting conditions many of these capillaries are closed, but they open when the muscle undergoes vigorous contraction. In this way the blood supply to a muscle is adjusted in accordance with the degree of muscular activity.
Types of Contractile Tissues in the Body
The contractile tissues of the body arc composed of cells which are able to exert tension by decreasing their length. In the human body there are three principal types of contractile tissue: skeletal muscle, heart muscle and smooth muscle, each of which has certain distinct structural and functional features. The characteristic result of the shortening of muscle is movement, either of parts of the skeleton (skeletal muscle), or of the contents of hollow organs (heart muscle and smooth muscle). Skeletal muscle is characterized structurally by the presence of distinct cross striations; hence, it is frequently called striated muscle. It contracts and relaxes much more rapidly than do the other types of muscle and normally becomes active only in response to stimulation from the central nervous system. Smooth muscle has no cross striations; it contracts and relaxes very sluggishly and is capable of contracting in the absence of stimulation from the central nervous system, although its activity may be increased or decreased by extraneous nerves. It is usually found in the walls of hollow organs or tubes such as the digestive tract, the blood vessels, the ureters and urinary bladder, and the uterus. When the muscle cells contract, the volume of these hollow organs is decreased and their contents are moved onward. Heart muscle is intermediate between skeletal muscle and smooth muscle, both structurally and functionally; like skeletal muscle its cells are cross striated, and like smooth muscle it is capable of contracting in the absence of extraneous nervous stimulation. Unlike skeletal or smooth muscle, heart muscle cells are not separated from one another, but form a continuous network or syncytium, so that all its fibers contract at each beat of the heart.
Structure of Skeletal Muscle
A skeletal muscle, such as the biceps, is composed of thousands of muscle fibers bound together with connective tissue. Each fiber is an elongated cell varying in length from 1 to 40 mm. The thickness of the fibers varies from 10 to 100 μ or more (1 μ=0.001 mm.); apparently the thickness depends not on the length of the fiber, but on the type of animal and the particular muscle. In a given animal the more primitive muscles, such as those of the eye, have thinner fibers. Fibers of varying diameter may be found in the same muscle, perhaps indicating different amounts of usage since the thickness of fibers is known to increase under the influence of strenuous muscular activity.
Each muscle fiber is covered by a thin structureless membrane, the sarcolemma. The fiber itself consists of two parts: (1) a protoplasmic mass, the sarcoplasm, and (2) very thin cross-striated fibrils, the myofibrils, which are arranged parallel to one another in the sarcoplasm. A great deal of discussion has centered around the existence of myofibrils in living muscle cells (many workers claiming that they arc artifacts resulting from killing and staining procedures) and their possible role in the contraction process. Their existence in living muscle cells is now apparently well established and most authorities attribute to them a fundamental role in the contraction process. If a single fiber from a fresh muscle is examined under the microscope both longitudinal and transverse striations are seen. The transverse striation of the muscle fiber results from the fact that each myofibril consists of alternate light and dark segments and the corresponding segments of adjacent fibrils lie at the same level, forming light and dark bands passing completely across the fiber. During contraction complex changes occur in the position and relative thickness of these light and dark bands. These changes, representing reorientation of molecules in the myofibrils, are believed to be the fundamental basis of contraction.
The cytoplasm of the muscle fiber which fills the spaces between the myofibrils is called sarcoplasm. The relative amount of sarcoplasm in the fiber varies. In some fibers it is more abundant and contains pigment granules (muscle hemoglobin) which give it a reddish appearance (red muscle), while in others it is less abundant and the fiber is paler (white muscle). Red muscles are capable of slow, powerful contractions and are not easily fatigued. The diaphragm and the extensor (postural) muscles are composed predominantly of red fibers. White fibers are specialized for speed rather than strength of contraction and predominate in the flexor muscles. In man both types of fibers enter into the composition of every muscle; the relative proportions varying according to the function of the particular muscle. Recently it has been found that if the tendon of a red muscle is cut and then sewed to the tendon stump of a pale muscle (i.e., forced to take over the function of a pale muscle), its hemoglobin content and resistance to fatigue gradually diminish. This indicates that the appearance and endurance of a muscle are largely the result of the type of work it must perform.
Structure of Skeletal Muscle
A skeletal muscle, such as the biceps, is composed of thousands of muscle fibers bound together with connective tissue. Each fiber is an elongated cell varying in length from 1 to 40 mm. The thickness of the fibers varies from 10 to 100 μ or more (1 μ=0.001 mm.); apparently the thickness depends not on the length of the fiber, but on the type of animal and the particular muscle. In a given animal the more primitive muscles, such as those of the eye, have thinner fibers. Fibers of varying diameter may be found in the same muscle, perhaps indicating different amounts of usage since the thickness of fibers is known to increase under the influence of strenuous muscular activity.
Each muscle fiber is covered by a thin structureless membrane, the sarcolemma. The fiber itself consists of two parts: (1) a protoplasmic mass, the sarcoplasm, and (2) very thin cross-striated fibrils, the myofibrils, which are arranged parallel to one another in the sarcoplasm. A great deal of discussion has centered around the existence of myofibrils in living muscle cells (many workers claiming that they arc artifacts resulting from killing and staining procedures) and their possible role in the contraction process. Their existence in living muscle cells is now apparently well established and most authorities attribute to them a fundamental role in the contraction process. If a single fiber from a fresh muscle is examined under the microscope both longitudinal and transverse striations are seen. The transverse striation of the muscle fiber results from the fact that each myofibril consists of alternate light and dark segments and the corresponding segments of adjacent fibrils lie at the same level, forming light and dark bands passing completely across the fiber. During contraction complex changes occur in the position and relative thickness of these light and dark bands. These changes, representing reorientation of molecules in the myofibrils, are believed to be the fundamental basis of contraction.
The cytoplasm of the muscle fiber which fills the spaces between the myofibrils is called sarcoplasm. The relative amount of sarcoplasm in the fiber varies. In some fibers it is more abundant and contains pigment granules (muscle hemoglobin) which give it a reddish appearance (red muscle), while in others it is less abundant and the fiber is paler (white muscle). Red muscles are capable of slow, powerful contractions and are not easily fatigued. The diaphragm and the extensor (postural) muscles are composed predominantly of red fibers. White fibers are specialized for speed rather than strength of contraction and predominate in the flexor muscles. In man both types of fibers enter into the composition of every muscle; the relative proportions varying according to the function of the particular muscle. Recently it has been found that if the tendon of a red muscle is cut and then sewed to the tendon stump of a pale muscle (i.e., forced to take over the function of a pale muscle), its hemoglobin content and resistance to fatigue gradually diminish. This indicates that the appearance and endurance of a muscle are largely the result of the type of work it must perform.
Heart Size, Negro vs. White, Superior ability of Negroes
Heart Size
Heart size is related to constitutional type and thoracic circumference. Measurements of heart size in 233 athletes by orthodiagrams indicate moderate hypertrophy as compared with Hodges-Eyster standards. Such hypertrophy is judged to be normal for athletes. 30 If the larger than average heart is associated with a high vital capacity, the athlete usually also has a slower than average pulse rate and low blood pressure and possesses a large capacity for performance of work.
Negro vs. White
Negroes show a higher rate of sickness absenteeism in industry, but as the occupations and socio-economic status of the Negro and white males become more nearly alike the excess of the frequency rate of disabilities among Negroes tends to decrease, if not to disappear entirely. Negroes can stand humid heat better than white workers. The rate of sickness absenteeism in very humid climates is lower in Negroes than in whites.
The superior ability of Negroes to work in the heat is due in part to greater efficiency, a higher ratio of body surface to weight, the secretion of a more dilute sweat and a greater water intake. Negro and white sharecroppers and a group of northern whites were tested during a summer in Mississippi. Subjects walked for 2 hours on a motor driven treadmill at a rate which elevated the metabolism to 7 times basal. Room temperature averaged 88° F. and humidity 79 per cent. This work raised the body temperature of the partially acclimatized northern white men to intolerable levels, increased their heart rates to nearly maximal values and forced most of the men to discontinue the walk before the end of the two hours. Negro sharecroppers who were acclimatized by field work performed the walk without marked elevation of body temperature or heart rate. They perspired less but drank more water than did the northern whites. White sharecroppers, also accustomed to field work, were intermediate between the other groups in adaptability to the conditions of the experiment. The superiority of the Negro sharecroppers was related to lower energy requirements in performing the walk. Negro servants were no more successful than northern whites in regulating body temperature, but were able to sweat at much higher rates. Most of the Negroes reached an equilibrium with a rectal temperature of about 101° F. and a pulse rate of 150 as compared with about 102° F. and 170 in the white workers. Sweating was of the order of one to two liters an hour. The major item was superior cardiovascular condition. Final mechanical efficiencies were 25.6 per cent in Negroes and 27.5 per cent in whites. Of 23 Negroes, two were below the white average, and of 7 whites, one was better than the average Negro.
In maximal work Negroes reach a greater blood lactate concentration, have a slightly lower maximum oxygen consumption and breathe more rapidly, thus using a smaller fraction of the vital capacity as tidal air. The higher blood lactate indicates greater motivation. Psychological explanation on a similar basis is advanced for the frequent supremacy of the Negro in athletic competition.
Heart size is related to constitutional type and thoracic circumference. Measurements of heart size in 233 athletes by orthodiagrams indicate moderate hypertrophy as compared with Hodges-Eyster standards. Such hypertrophy is judged to be normal for athletes. 30 If the larger than average heart is associated with a high vital capacity, the athlete usually also has a slower than average pulse rate and low blood pressure and possesses a large capacity for performance of work.
Negro vs. White
Negroes show a higher rate of sickness absenteeism in industry, but as the occupations and socio-economic status of the Negro and white males become more nearly alike the excess of the frequency rate of disabilities among Negroes tends to decrease, if not to disappear entirely. Negroes can stand humid heat better than white workers. The rate of sickness absenteeism in very humid climates is lower in Negroes than in whites.
The superior ability of Negroes to work in the heat is due in part to greater efficiency, a higher ratio of body surface to weight, the secretion of a more dilute sweat and a greater water intake. Negro and white sharecroppers and a group of northern whites were tested during a summer in Mississippi. Subjects walked for 2 hours on a motor driven treadmill at a rate which elevated the metabolism to 7 times basal. Room temperature averaged 88° F. and humidity 79 per cent. This work raised the body temperature of the partially acclimatized northern white men to intolerable levels, increased their heart rates to nearly maximal values and forced most of the men to discontinue the walk before the end of the two hours. Negro sharecroppers who were acclimatized by field work performed the walk without marked elevation of body temperature or heart rate. They perspired less but drank more water than did the northern whites. White sharecroppers, also accustomed to field work, were intermediate between the other groups in adaptability to the conditions of the experiment. The superiority of the Negro sharecroppers was related to lower energy requirements in performing the walk. Negro servants were no more successful than northern whites in regulating body temperature, but were able to sweat at much higher rates. Most of the Negroes reached an equilibrium with a rectal temperature of about 101° F. and a pulse rate of 150 as compared with about 102° F. and 170 in the white workers. Sweating was of the order of one to two liters an hour. The major item was superior cardiovascular condition. Final mechanical efficiencies were 25.6 per cent in Negroes and 27.5 per cent in whites. Of 23 Negroes, two were below the white average, and of 7 whites, one was better than the average Negro.
In maximal work Negroes reach a greater blood lactate concentration, have a slightly lower maximum oxygen consumption and breathe more rapidly, thus using a smaller fraction of the vital capacity as tidal air. The higher blood lactate indicates greater motivation. Psychological explanation on a similar basis is advanced for the frequent supremacy of the Negro in athletic competition.
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