In: Anatomy and Physiology
The formula for Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance. Please explain the normal responses of Cardiac Output during graded exercise (intensity increases) and total peripheral resistance.
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.
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.
he 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).