Neural influence on cardiovascular and endocrine responses to static exercise in humans.

At the onset of exercise, signals from the central nervous system result in immediate vagal withdrawal and resulting increases in heart rate and arterial blood pressure. From the second heart beat peripheral nerve (reflex) influence from exercising muscle can be detected. With continued exertion, especially with large muscle groups, this influence becomes increasingly important. Sympathetic nerve signals to resting muscle can be influenced by the central nervous system, but 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 the percentage of maximum contraction intensity as well as with the muscle mass involved. 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 the responses of pituitary hormones depend on the active muscle mass, but are small compared to those established during dynamic exercise. Experiments designed to enhance central command, resulting in increased cardiovascular and endocrine responses compared to control experiments 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 eliciting the responses manifest during static exercise.