The sympathetic nervous system plays a role in changing vascular resistance in the periphery when there is cardiac stimulation. Vasoconstriction, which is mediated by the sympathetic nervous system, increases vascular resistance, causing blood to be redirected away from the skin, kidneys, splanchnic regions, and inactive muscles. During exercise, there is an increase in cardiac output and blood flow to active muscles. The myocardium receives increased blood flow, while blood flow to the brain remains unchanged. Initially, blood flow in the skin decreases during exercise but then increases as body temperature rises. However, as total body oxygen consumption reaches its maximum, the skin vessels constrict, leading to a decrease in blood flow. The most significant circulatory adjustment during prolonged exercise occurs in the vasculature of the active muscles. The release of vasoactive metabolites in the contracting muscles causes dilation of the resistance vessels. This dilation intensifies as the intensity of exercise increases. The vasodilator substances released by the contracting muscles include potassium, adenosine, and a decrease in tissue pH. These substances cause the terminal arterioles to relax, resulting in a significant increase in blood flow through the muscles. This metabolic vasodilation in active muscles happens shortly after the start of exercise. The decrease in total peripheral resistance allows the heart to pump more blood with less effort and higher efficiency. The capillary circulation also undergoes marked changes during exercise. In resting state, only a small percentage of the capillaries are perfused, but in actively contracting muscle, nearly all the capillaries contain flowing blood due to capillary recruitment. This recruitment leads to an increased surface area available for gas, water, and solute exchange. Additionally, hydrostatic pressure in the capillaries increases as a result of resistance vessel relaxation. Consequently, water and solutes move into the muscle tissue. Tissue pressure rises during exercise as fluid continues to exit the capillaries, and this fluid is carried away by the lymphatic vessels. The lymph flow increases due to the rise in capillary hydrostatic pressure and the massaging effect of the contracting muscles on the lymphatic vessels containing valves. Contracting muscles actively extract oxygen from the perfusing blood, which leads to an increase in the arteriovenous oxygen difference.
When cardiac stimulation occurs, the sympathetic nervous system also changes vascular resistance in the periphery. Sympathetic nervous system–mediated vasoconstriction increases vascular resistance and thereby diverts blood away from the skin, kidneys, splanchnic regions, and inactive
Cardiac output (L/min) 22 18 14 10 6 2 0.25 1 2 3 4 O2 uptake (L/min) Skin Heart and brain Viscera Muscle Maximum Vo2 .
•Fig. 19.16 ApproximatedistributionofcardiacoutputatrestandatdifferentlevelsofexerciseuptothemaximalO2consumption(V˜O2)in 0 0 5 10 15 800 1600 0.006 0.010 0.014 60 100 140 180 5 10 15 90 100 110 60 100 140 180 Mean Systolic pressure Diastolic pressure anormalyoungman.(RedrawnfromRuchHP,PattonTC.Physiology and Biophysics. 12thed.Philadelphia:Saunders;1974.)
Fig. 19.16 ). This increase in vascular resistance persists throughout the period of exercise.
Cardiac output and blood flow to active muscles increase as the intensity of exercise increases. Blood flow to the myocardium increases, whereas flow to the brain is unchanged. Blood flow in the skin initially decreases during exercise, then increases as body temperature rises with increments in the duration and intensity of exercise, and finally decreases when the skin vessels constrict as total body O2 consumption nears its maximal value (see
Fig. 19.16
The major circulatory adjustment to prolonged exercise occurs in the vasculature of the active muscles. Local formation of vasoactive metabolites causes marked dilation of the resistance vessels. This dilation progresses with increases in the intensity of exercise. Potassium is one of the vasodilator substances released by the contracting muscle, and this ion may be partly responsible for the initial decrease in vascular resistance in the active muscles. Other contributing factors may be the release of adenosine and a decrease in tissue pH during sustained exercise. The local accumulation of metabolites causes the terminal arterioles to relax, and blood flow through the muscle may increase 15to 20-fold above the resting level. This metabolic vasodilation of the precapillary vessels in active muscles occurs very soon after the onset of exercise. The decrease in TPR enables the heart to pump more blood at a lesser load, and it pumps more efficiently than if TPR were unchanged (see •Fig. 19.17 Effectsofdifferentlevelsofexercise(i.e.,work)onseveralcardiovascularvariables.(DatafromCarlstenA,GrimbyG.The Circulatory Response to Muscular Exercise in Man. Springfield,
IL:CharlesCThomas;1966.)
Marked changes in the capillary circulation also occur during exercise. At rest, only a small percentage of the capillaries are perfused, whereas in actively contracting muscle, all or nearly all of the capillaries contain flowing blood (capillary recruitment). The surface area available for exchange of gases, water, and solutes is increased many times. Furthermore, hydrostatic pressure in the capillaries is increased because of relaxation of the resistance vessels. Hence, water and solutes move into the muscle tissue. Tissue pressure rises and remains elevated during exercise as fluid continues to move out of the capillaries; this tissue fluid is carried away by the lymphatic vessels. Lymph flow is increased as a result of the rise in capillary hydrostatic pressure and the massaging effect of the contracting muscles on the valve-containing lymphatic vessels (see
Contracting muscle avidly extracts O2 from the perfusing blood and thereby increases the arteriovenous O2 difference (