The McGill Physiology Virtual Lab

Exercise Physiology Laboratory

Cardio/CNS contribution

Many factors contribute to the changes observed during and immediately after exercise. The following will be covered:

Cardio-CNS contribution
Respiratory contribution
Changes at the muscular level
Energy expenditure during exercise

Cardiac output may increase to 35L/min in well-trained athletes. In untrained individuals it can reach 20-25L/min. Most of the increase in cardiac output goes to the exercising muscles. There is an increase in blood flow to skin (dissipation of heat) and to the heart (increased work performed by the heart). Increased flows are the result of local arteriolar vasodilation. In both skeletal and cardiac muscles, vasodilation is mediated by local metabolic factors, and in the skin, it is achieved mainly by a decrease in the firing of sympathetic neurons supplying skin vessels. Simultaneously with vasodilation in these three regions, a vasoconstriction occurs in the kidneys and gastrointestinal organs, due to an increase in activity of sympathetic neurons supplying them.

Distribution of the systemic cardiac output at rest
and during strenuous exercise

Vasodilation of arterioles in the skeletal and heart muscles and skin causes a decrease in total peripheral resistance to blood flow. This decrease is partially offset by vasoconstriction of arterioles in other organs. But the vasodilation in muscle arterioles is not compensated, and the net result is a marked decrease in total peripheral resistance to blood flow.

The mean arterial pressure is the arithmetic product of the cardiac output and the total peripheral resistance (P=COxR). During exercise, the cardiac output increases more than the total resistance decreases, so the mean arterial pressure usually increases by a small amount. Pulse pressure, in contrast, markedly increases because of an increase in both stroke volume and the speed at which the stroke volume is ejected.

The cardiac output increase is due to a large increase in heart rate and a small increase in stroke volume.

The heart rate increases because of a decrease in parasympathetic activity of SA node combined with increased sympathetic activity.

The stroke volume increases because of increased ventricular contractility, manifested by an increased ejection fraction and mediated by sympathetic nerves to the ventricular myocardium.

End-diastolic volume increase slightly. Because of this increased filling, the Frank-Starling mechanism also contributes to the increased stroke volume (stroke volume increases when end-diastolic volume increases).

Cardiac output can be increased to high levels only if the peripheral processes favoring venous return to the heart are simultaneously activated to the same degree. Factor promoting venous return:

  1. increased activity of the skeletal-muscle pump.

  2. increased depth and frequency of respiration; respiratory pump.

  3. sympathetically mediated increase in venous tone

  4. greater ease of blood flow from arteries to veins.

Control of sympathetic outflow

One or more discrete control centers in the brain are activated by output from the cerebral cortex. Descending pathways from these centers transmit these centers’ activity to the appropriate autonomic preganglionic neurons eliciting the firing patterns typical for exercise. These centers become activated before the exercise started.

Once exercise is started, local chemical changes in the muscle can develop, particularly during high levels of exercise, because of imperfect matching between blood flow and metabolic demands. These changes activate chemoreceptors in the muscle. Afferent input from these receptors goes to the medullary cardiovascular centers. The result is a further increase in heart rate, myocardial contractility, and vasoconstriction in the nonactivated organs. Mechanoreceptors of the exercising muscle are also stimulated and provide an excitatory input to the medullary cardiovascular center.

The arterial baroreceptors

As mean and pulsatile pressure increase, baroreceptors should respond to increase parasympathetic and decrease sympathetic outflows, a pattern designed to counter the rise in arterial pressure. During exercise the exact opposite occurs: the arterial baroreceptors increase the arterial pressure during exercise. The reason is that one of neuronal component of the central command output goes to the arterial baroreceptors and ‘resets’ them upwards as exercise begins. The resetting causes a decrease firing frequency in the baroreceptors, signalling for decreased parasympathetic and increase in sympathetic outflow.

To continue with the next section: respiratory contribution, click here