Central integration of mechanisms in exercise hyperpnea.

Abstract

Many hypotheses have been advanced to explain the hyperpnea of exercise and its close relations to the level of metabolic work, expressed as oxygen uptake (VO2) and carbon dioxide production (VCO2). Evidence is presented that a neural central command mechanism from the hypothalamus is important in the driving of both respiration and circulatory adjustments during locomotion or exercise, and that short-term potentiation of neurons in the medulla makes an important contribution. Both are probably augmented by receptors in working muscle and by the effects of increased [K+] acting on the carotid bodies. Feedback from "respiratory" mechanisms, including CO2 and O2 mediated mechanisms and inputs from the lungs, are important in stabilizing ventilation at the level primarily dictated by the major neural mechanisms.