The Trails

Shape 5 Live Search

The systemic cardiovascular response to exercise that provides for the additional blood flow to contracting muscle depends on whether the muscle contractions are primarily isometric or primarily isotonic with the performance of external work. With the start of an isometric muscle contraction, the heart rate rises, probably as a result of psychic stimuli acting on the medulla oblongata. The increase is largely due to decreased vagal tone, although increased discharge of the cardiac sympathetic nerves plays some role. 

 
The blood flow of resting skeletal muscle is low (2–4 mL/100 g/min). When a muscle contracts, it compresses the vessels in it if it develops more than 10% of its maximal tension; when it develops more than 70% of its maximal tension, blood flow is completely stopped. Between contractions, however, flow is so greatly increased that blood flow per unit of time in a rhythmically contracting muscle is increased as much as 30-fold. Local mechanisms maintaining a high blood flow in exercising muscle include a fall in tissue PO2, a rise in tissue PCO2, and accumulation of K+ and other vasodilator metabolites. The temperature rises in active muscle, and this further dilates the vessels.
 
Dilation of the arterioles and precapillary sphincters causes a 10- to 100-fold increase in the number of open capillaries. The average distance between the blood and the active cells—and the distance O2 and metabolic products must diffuse—is thus greatly decreased. The dilation increases the cross-sectional area of the vascular bed, and the velocity of flow therefore decreases
 
The systemic cardiovascular response to exercise that provides for the additional blood flow to contracting muscle depends on whether the muscle contractions are primarily isometric or primarily isotonic with the performance of external work. With the start of an isometric muscle contraction, the heart rate rises, probably as a result of psychic stimuli acting on the medulla oblongata. The increase is largely due to decreased vagal tone, although increased discharge of the cardiac sympathetic nerves plays some role. Within a few seconds of the onset of an isometric muscle contraction, systolic and diastolic blood pressures rise sharply. Stroke volume changes relatively little, and blood flow to the steadily contracting muscles is reduced as a result of compression of their blood vessels.
 
The response to exercise involving isotonic muscle contraction is similar in that there is a prompt increase in heart rate, but different in that a marked increase in stroke volume occurs. In addition, there is a net fall in total peripheral resistance due to vasodilation in exercising muscles. Consequently, systolic blood pressure rises only moderately, whereas diastolic pressure usually remains unchanged or falls.
 
The difference in response to isometric and isotonic exercise is explained in part by the fact that the active muscles are tonically contracted during isometric exercise and consequently contribute to increased total peripheral resistance.
 
Cardiac output is increased during isotonic exercise to values that may exceed 35 L/min, the amount being proportionate to the increase in O2 consumption. The maximal heart rate achieved during exercise decreases with age. In children, it rises to 200 or more beats/min; in adults it rarely exceeds 195 beats/min, and in elderly individuals the rise is even smaller.
Both at rest and at any given level of exercise, trained athletes have a larger stroke volume and lower heart rate than untrained individuals and they tend to have larger hearts.
Training increases the maximal oxygen consumption (VO2max) that can be produced by exercise in an individual. VO2max averages about 38 mL/kg/min in active healthy men and about 29 mL/kg/min in active healthy women. It is lower in sedentary individuals. VO2max is the product of maximal cardiac output and maximal O2 extraction by the tissues, and both increase with training.
 
A great increase in venous return also takes place with exercise, although the increase in venous return is not the primary cause of the increase in cardiac output. Venous return is increased by the activity of the muscle and thoracic pumps; by mobilization of blood from the viscera; by increased pressure transmitted through the dilated arterioles to the veins; and by noradrenergically mediated venoconstriction, which decreases the volume of blood in the veins. Blood mobilized from the splanchnic area and other reservoirs may increase the amount of blood in the arterial portion of the circulation by as much as 30% during strenuous exercise. After exercise, the blood pressure may transiently drop to subnormal levels, presumably because accumulated metabolites keep the muscle vessels dilated for a short period. However, the blood pressure soon returns to the pre-exercise level. The heart rate returns to normal more slowly.