Physiological adaptation to physical conditioning. Old problems revisited.

Abstract

Three classical problems in the field of man's adaptive response to exercise are reviewed. A case is made for the pump capacity of the heart limiting maximal oxygen uptake in man. This conclusion is based on findings that the capacity of skeletal muscle of man markedly surpasses that of the heart supplying it with a flow and thereby oxygen. It is suggested that only one third of the muscle mass of man can fully tax the capacity of the heart and consume the oxygen delivered by the heart. If a larger muscle mass is intensely engaged in the exercise, vasoconstriction must occur in the arterioles of the exercising limbs to avoid a reduction in blood pressure. Evidence is presented that a decrease in heart rate at submaximal exercise-observed after a period of physical conditioning, is caused by an altered autonomic chronotropic activity to heart, which most likely is due to a less potent feed back reflex from exercising muscles. The enlarged stroke volume is secondary to a larger diastolic filling, which via a Frank-Starling mechanism results in an elevation in the stroke volume. Last, it is argued that the altered metabolic response to exercise after physical conditioning, i.e. the larger lipid oxidation and reduced lactate production, results from local regulatory mechanisms rather than from changes in supply of oxygen, substrates, or hormones. Further, the muscle metabolic response to exercise is thought to play a major role in modulating systemic cardiovascular regulation in exercise.