During exercise, when a large portion of the body musculature is involved, such as in running or swimming, there is a significant reduction in total vascular resistance. However, it is important to note that arterial pressure actually increases with the onset of exercise, and the increase in blood pressure correlates with the intensity of the exercise performed. This increase in blood pressure is due to the fact that the increase in cardiac output is proportionally greater than the decrease in total peripheral resistance (TPR). The sympathetic nervous system, as well as the release of catecholamines from the adrenal medulla, causes vasoconstriction in the inactive tissues, which helps maintain normal or increased blood pressure. When sympathetic nerve fibers are blocked or sympathectomy is performed, arterial pressure decreases (hypotension) during exercise. 

During exercise, sympathetic neural activity also causes vasoconstriction in active skeletal muscles when additional muscles are recruited. In experiments where one leg is working at maximum levels and then the other leg starts to work, blood flow actually decreases in the first working leg. Additionally, the levels of norepinephrine in the blood significantly rise during exercise, with most of it being released from sympathetic nerves to the active muscles. 

As the body temperature rises during exercise, the skin vessels dilate in response to thermal stimulation of the heat-regulating center in the hypothalamus, leading to a further decrease in total peripheral resistance. However, the reduction in total peripheral resistance would decrease blood pressure if not for the increased cardiac output and the constriction of arterioles in the renal, splanchnic, and other tissues. 

In general, during exercise, the arterial pressure increases due to the increase in cardiac output. However, this effect is counteracted by an overall decrease in total peripheral resistance, resulting in only a slight increase in mean blood pressure. Vasoconstriction in the inactive vascular beds helps maintain normal arterial blood pressure to ensure adequate perfusion of the active tissues. The actual arterial pressure reached during exercise represents a balance between cardiac output and total peripheral resistance. Systolic pressure usually increases more than diastolic pressure, leading to an increase in pulse pressure. This larger pulse pressure is primarily due to a greater stroke volume, as well as more rapid ejection of blood by the left ventricle and reduced peripheral runoff during the brief ventricular ejection period. 

During exhaustive exercise, the compensatory mechanisms start to fail. The heart rate reaches a maximum level of approximately 180 beats per minute, and the stroke volume plateaus. This may cause the heart rate to decrease, resulting in a drop in blood pressure. Dehydration is also common in individuals who engage in intense exercise. The sympathetic vasoconstrictor activity overrides the vasodilator influence on the skin vessels, leading to a decrease in the rate of heat loss. Since body temperature naturally rises during exercise, a reduction in heat loss through cutaneous vasoconstriction can result in very high body temperatures and acute distress during severe exercise. Increased production of lactic acid and CO2 leads to a decrease in tissue pH and blood pH. This reduced pH may play a crucial role in determining the maximum amount of exercise an individual can tolerate. Exercise tolerance is often determined by subjective feelings of muscle pain, exhaustion, and loss of will to continue. A summary of the neural and local effects of exercise on the cardiovascular system can be found in Fig. 19.19. 

When exercise is stopped, the heart rate and cardiac output rapidly decrease as the sympathetic drive to the heart is essentially removed. However, total peripheral resistance remains low for some time after exercise has ceased, possibly due to the accumulation of vasodilator metabolites in the muscles during the exercise period. As a result of the reduced cardiac output and persistent vasodilation in the muscles, arterial pressure often falls below preexercise levels for brief periods. The baroreceptor reflexes then stabilize blood pressure at normal levels.
If exercise involves a large proportion of the body musculature, as in running or swimming, the reduction in total vascular resistance can be considerable. Nevertheless, arterial pressure starts to rise with the onset of exercise, and the increase in blood pressure approximately parallels the severity of the exercise performed (see
Fig. 19.17 ). Therefore, the increase in cardiac output is proportionally greater than the decrease in TPR. The vasoconstriction produced in the inactive tissues by the sympathetic nervous system (and to some extent by the release of catecholamines from the adrenal medulla) is important for maintenance of normal or increased blood pressure. Sympathectomy or drug-induced blockade of the adrenergic sympathetic nerve fibers decreases arterial pressure (hypotension) during exercise.
Sympathetic neural activity also elicits vasoconstriction in active skeletal muscle when additional muscles are recruited. In experiments in which one leg is working at maximal levels and then the other leg starts to work, blood flow decreases in the first working leg. Furthermore, blood levels of norepinephrine rise significantly during exercise, and most of the norepinephrine is released from sympathetic nerves to the active muscles.
As body temperature rises during exercise, the skin vessels dilate in response to thermal stimulation of the heat-regulating center in the hypothalamus, and TPR decreases further. This reduction in TPR would reduce blood pressure were it not for the increased cardiac output and the constriction of arterioles in the renal, splanchnic, and other tissues.
In general, Pa rises during exercise as a result of the increase in cardiac output. However, the effect of enhanced cardiac output is offset by an overall decrease in TPR, and therefore mean blood pressure increases only slightly. Vasoconstriction in the inactive vascular beds helps maintain normal arterial blood pressure for adequate perfusion of the active tissues. The actual Pa attained during exercise thus represents a balance between cardiac output and TPR (see ). Systolic pressure usually increases more than diastolic pressure, which results in an increase in pulse pressure (see
Fig. 19.17 ). The larger pulse pressure is primarily attributable to a greater stroke volume, but also to more rapid ejection of blood by the left ventricle and diminished peripheral runoff during the brief ventricular ejection period (see also
During exhaustive exercise, the compensatory mechanisms begin to fail. The heart rate attains a maximal level of approximately 180 beats per minute, and stroke volume reaches a plateau. The heart rate may then decrease, which results in a fall in blood pressure. The exercising individual also frequently becomes dehydrated. Sympathetic vasoconstrictor activity supersedes the vasodilator influence on vessels of the skin so that the rate of heat loss is decreased. Body temperature is normally elevated during exercise. A reduction in heat loss through cutaneous vasoconstriction can lead to very high body temperatures and to acute distress during severe exercise. Tissue pH and blood pH decrease as a result of increased production of lactic acid and CO2. The reduced pH may be a key factor that determines •Fig. 19.19 Cardiovascularadjustmentsinexercise.Plus signs indicateincreasedactivity,andminus signs indicatedecreasedactivity.C,vasoconstrictoractivity;D,vasodilatoractivity;IX,glossopharyngeal nerve;VR,vasomotorregion;X,vagusnerve.
the maximal amount of exercise that a given individual can tolerate. Muscle pain, a subjective feeling of exhaustion, and loss of the will to continue determine exercise tolerance. A summary of the neural and local effects of exercise on the cardiovascular system is diagrammed in
Fig. 19.19
When exercise stops, the heart rate and cardiac output quickly decrease: The sympathetic drive to the heart is essentially removed. In contrast, TPR remains low for some time after the exercise is stopped, presumably because vasodilator metabolites have accumulated in the muscles during the exercise period. As a result of the reduced cardiac output and persistence of vasodilation in the muscles, arterial pressure falls, often below preexercise levels, for brief periods. Blood pressure is then stabilized at normal levels by the baroreceptor reflexes.