Figure 30a summarizes important cardiovascular adaptations that occur at increasing levels of dynamic (rhythmic) exercise, thereby allowing working muscles to be supplied with the increased amount of O2 they require. By far the most important of these adaptations is an increase in cardiac output (CO), which rises almost linearly with the rate of muscle O2 consumption (level of work) as a result of increases in both heart rate and to a lesser extent stroke volume. The heart rate is accelerated by a reduction in vagal tone, and by increases in sympathetic nerve firing and circulating catecholamines. The resulting stimulation of cardiac β-adrenoceptors increases stroke volume by increasing myocardial contractility and enabling more complete systolic emptying of the ventricles. CO is the limiting factor determining the maximum exercise capacity.
Table 30.1 shows that the increased CO is channelled mainly to the active muscles, which may receive 85% of CO against about 15–20% at rest, and to the heart. This is caused by a profound arteriolar vasodilatation in these organs. Dilatation of terminal arterioles causes capillary recruitment, a large increase in the number of open capillaries, which shortens the diffusion distance between capillaries and muscle fibres. This, combined with increases in PCO2, temperature and acidity, promotes the release of O2 from haemoglobin, allowing skeletal muscle to increase its O2 extraction from the basal level of 25–30% to about 90% during maximal exercise.
Increased firing of sympathetic nerves and levels of circulating catecholamines constrict arterioles in the splanchnic and renal vascular beds, and in non-exercising muscle, reducing the blood flow to these organs. Cutaneous blood flow is also initially reduced. As core body temperature rises, however, cutaneous blood flow increases as autonomically mediated vasodilatation occurs to promote cooling (see Chapter 25). With very strenuous exercise, cutaneous perfusion again falls as vasoconstriction diverts blood to the muscles. Blood flow to the crucial cerebral vasculature remains constant.