Abstract

At onset of exercise, signals from the central nervous system result in immediate vagal withdrawal and resulting increases in heart rate and blood pressure. From the second heart beat peripheral nerve (reflex) influence from exercising muscle can be detected. With continued exertion this influence becomes increasingly important. Sympathetic nerve signals to resting muscle are dominated by influence from metaboreceptors in exercising muscle, while sympathetic nerve signals to skin are more influenced by the central nervous system. Cardiovascular responses to static contractions increase with contraction intensity as well as with the muscle mass. Plasma catecholamines rise in proportion to increases in cardiovascular variables and are influenced by a central nervous mechanism early in the contraction. Furthermore, during static contractions the increase in plasma adrenaline (epinephrine) is larger relative to that of noradrenaline than during dynamic exercise. Both catecholamine responses and responses of pituitary hormones depend on the active muscle mass, but are small compared to those during dynamic exercise. Experiments designed to enhance central command, resulting in increased cardiovascular and endocrine responses and experiments in which an attenuation of peripheral nerve influence resulted in reduced changes in these variables during exercise, contrast with the notion that the 2 neural control mechanisms are redundant. Rather, the 2 neural influences on the autonomic nervous system work in concert in static work. Verf.-Ref.