Responses to Acute Exercise
Physical exercise is one of the most ordinary, yet taxing, situations with which the cardiovascular system must cope. The specific alterations in cardiovascular function that occur during exercise depend on several factors including (1) the type of exercise—that is, whether it is predominantly “dynamic” (rhythmic or isotonic) or “static” (isometric), (2) the intensity and duration of the exercise, (3) the age of the individual, and (4) the level of “fitness” of the individual. The example shown in Figure 10–4 is typical of cardiovascular alterations that might occur in a normal, untrained, middle-aged adult doing a dynamic-type exercise such as running or dancing. Note especially that heart rate and cardiac output increase greatly during exercise and that mean arterial pressure and pulse pressure also increase significantly. These alterations ensure that increased metabolic demands of the exercising skeletal muscle are met by appropriate increases in skeletal muscle blood flow. (Use the data in this figure to answer Study Questions 10–5 to 10–8.)
Changes in cardiovascular variables with strenuous exercise.
Many of the adjustments to exercise are due to a large increase in sympathetic activity, which results from the mechanisms outlined in Figure 10–5
. One of the primary disturbances associated with the stress and/or anticipation of exercise originates within the cerebral cortex and exerts an influence on the medullary cardiovascular centers through corticohypothalamic pathways. This set point–raising influence, referred to as the “central command,” causes mean arterial pressure to be regulated to a higher-than-normal level (see Appendix E
, Figure E–1
). Also indicated in Figure 10–5
is the possibility that a second set point–raising influence may reach the cardiovascular centers from chemoreceptors and mechanoreceptors in the active skeletal muscles. Such inputs would also contribute to the elevations in sympathetic activity and mean arterial pressure that accompany exercise.
Cardiovascular mechanisms involved during exercise.
A major primary disturbance on the cardiovascular system during dynamic exercise, however, is the great decrease in total peripheral resistance caused by metabolic vasodilator accumulation and decreased vascular resistance in the active skeletal muscle. As indicated in Figure 10–5
, decreased total peripheral resistance is a pressure-lowering disturbance that elicits a strong increase in sympathetic activity through the arterial baroreceptor reflex.
Although mean arterial pressure is above normal during exercise, the decreased total peripheral resistance causes it to fall below the elevated level to which it would be regulated by the set point–raising influences on the cardiovascular center alone. The arterial baroreceptor reflex pathway responds to this circumstance with a large increase in sympathetic activity. Thus, the arterial baroreceptor reflex is responsible for a large portion of the increase in sympathetic activity that accompanies exercise despite the seemingly contradictory fact that arterial pressure is higher than normal. In fact, were it not for the arterial baroreceptor reflex, the decrease in total peripheral resistance that occurs during exercise would cause mean arterial pressure to fall well below normal.
As discussed in Chapter 9 and indicated in Figures 10–4 and 10–5, cutaneous blood flow may increase during exercise despite a generalized increase in sympathetic vasoconstrictor tone because thermal reflexes can override pressure reflexes in the special case of skin blood flow control. Temperature reflexes, of course, are usually activated during strenuous exercise to dissipate the excess heat being produced by the active skeletal muscles. Often cutaneous flow decreases at the onset of exercise (as part of the generalized increase in arteriolar tone from increased sympathetic vasoconstrictor activity) and then increases later during exercise as body heat builds up.
In addition to the increases in the skeletal muscle and skin blood flow, coronary blood flow increases substantially during strenuous exercise. This is primarily due to local metabolic vasodilation of coronary arterioles as a result of increased cardiac work and myocardial oxygen consumption.
Two important mechanisms that participate in the cardiovascular response to dynamic exercise are not shown in Figure 10–5. The first is the skeletal muscle pump, which was discussed in connection with upright posture. The skeletal muscle pump is a very important factor in promoting venous return during dynamic exercise preventing the reflex-induced increase in cardiac output from drastically lowering central venous pressure. The second factor is the respiratory pump, which also promotes venous return during exercise. Exaggerated respiratory movements that occur during exercise increase the effectiveness of the respiratory pump and thus enhance venous return and cardiac filling.
As indicated in Figure 10–4, the average central venous pressure does not change much, if at all, during strenuous dynamic exercise. This is because the cardiac output and the venous return curves are both shifted upward during exercise. Therefore, the cardiac output and venous return will be elevated without a significant change in central venous pressure. Thus, the increase in stroke volume that accompanies exercise (suggested in this figure by the increase in pulse pressure) largely reflects the increased myocardial contractility and increased ejection fraction with decreased end-systolic ventricular volume.
In summary, the profound cardiovascular adjustments to dynamic exercise shown in Figure 10–5
all occur automatically as a consequence of the operation of the normal cardiovascular control mechanisms. The tremendous increase in skeletal muscle blood flow is accomplished largely by increased cardiac output but also in part by diverting flow away from the kidneys and the splanchnic organs.
Static exercise (ie, isometric) presents a much different disturbance on the cardiovascular system than does dynamic exercise. As discussed in the previous section, dynamic exercise produces large reductions in total peripheral resistance because of local metabolic vasodilation in exercising muscles. Static efforts, even of moderate intensity, cause a compression of the vessels in the contracting muscles and a reduction in the blood flow through them. Thus, total peripheral resistance does not usually fall during strenuous static exercise and may even increase significantly. The primary disturbances on the cardiovascular system during static exercise seem to be set point–raising inputs to the medullary cardiovascular centers from the cerebral cortex (central command) and from chemoreceptors and mechanoreceptors in the contracting muscle. These inputs result in another example of what is termed the “exercise pressor response.”
Cardiovascular effects of static exercise include increases in the heart rate, cardiac output, and arterial pressure—all of which are the result of increases in sympathetic drive. Static exercise, however, produces less of an increase in the heart rate and cardiac output and more of an increase in diastolic, systolic, and mean arterial pressure than does dynamic exercise. Because of the higher afterload on the heart during static exercise, cardiac work is significantly higher than during dynamic exercise.
The time course of recovery of the various cardiovascular variables after a bout of exercise depends on many factors, including the type, duration, and intensity of the exercise as well as the overall fitness of the individual. Muscle blood flow normally returns to a resting value within a few minutes after dynamic exercise. However, if an abnormal arterial obstruction prevents a normal active hyperemia from occurring during dynamic exercise, the recovery will take much longer than normal. After isometric exercise, muscle blood flow often rises to near-maximum levels before returning to normal with a time course that varies with the duration and intensity of the effort. Part of the increase in muscle blood flow that follows isometric exercise might be classified as reactive hyperemia in response to the blood flow restriction caused by compressional forces within the muscle during the exercise.
Responses to Chronic Exercise
Physical training or “conditioning” produces substantial beneficial effects on the cardiovascular system. The specific alterations that occur depend on the type of exercise, the intensity and duration of the training period, the age of the individual, and his or her original level of fitness.
In general, however, repeated physical exercise over a period of several weeks is associated with an increase in the individual’s work capacity. Cardiovascular alterations associated with conditioning may include decreases in heart rate, increases in cardiac stroke volume, and decreases in arterial blood pressure at rest. During exercise, a trained individual will be able to achieve a given workload and cardiac output with a lower heart rate and higher stroke volume than will be possible by an untrained individual. These changes produce a general decrease in myocardial oxygen
demand and an increase in the cardiac reserve
(potential for increasing cardiac output) that can be called on during times of stress. Much of the cardiovascular benefit of exercise conditioning can be attributed to a significant increase in circulating blood volume. This is triggered by the repetitive activation of the sympathetic nervous system during training, which promotes the renal fluid retention mechanisms.
Ventricular chamber enlargement often accompanies dynamic exercise conditioning regimens (endurance training), whereas increases in myocardial mass and ventricular wall thickness are more pronounced with static exercise conditioning regimens (strength training). These structural alterations improve the pumping capabilities of the myocardium. However, as described in the next chapter, ventricular chamber enlargement and myocardial hypertrophy are not always hallmarks of improved cardiac performance but may be adaptive responses to various pathological states that, if extreme, may not be helpful.
Exercise training or “conditioning” with a higher-than-normal blood volume represents the opposite end of a functional spectrum from the “deconditioning” effects of long-term bed rest with lower-than-normal blood volume. “Deconditioning” after cessation of an exercise program occurs rapidly as blood volume returns to resting levels.
It is clear that exercise and physical conditioning can significantly reduce the incidence and mortality of cardiovascular disease. Although studies have not established specific mechanisms for these beneficial effects, there is a positive correlation between physical inactivity and the incidence rate and intensity of coronary heart disease. It is increasingly evident that recovery from a myocardial infarction or cardiac surgery is enhanced by an appropriate increase in physical activity. The benefits of cardiac rehabilitation programs include improvement in various indices of cardiac function as well as improvements in physical work capacity, percent body fat, serum lipids, psychological sense of well-being, and quality of life.