Calcium levels in the brain underlie temperature control during exercise in the primate

Abstract

ALTHOUGH it is known that the hyperthermia in man accompanying steady-state submaximal exercise is a regulated rise which is virtually independent of the ambient temperature¹, a fundamental question persists. What are the neural mechanisms involved in this regulated rise and in the ensuing hyperthermia encountered during severe work in the heat? It has been proposed that the elevation in the temperature set-point associated with fever has as its basic component a change in the hypothalamic balance between the essential cations, Na and Ca² (refs 2, 3). Is it possible that such a mechanism could underlie the shift in temperature set-point which occurs during exercise? To explore this idea, we undertook two types of experiments. First, an artificial cerebrospinal fluid (CSF) containing excess Ca²⁺ ions was infused into the third ventricle. Secondly the kinetics of endogenous Ca², as reflected by its retention or release into the third ventricle, was analysed. We report here that Ca²⁺ ions, acting directly on the brain, can indeed attenuate or entirely block the hyperthermia of exercise without necessarily interfering with work output; further, the actual efflux of Ca²⁺ ions from the diencephalon increases markedly during the exercise-induced hyperthermia.