Effects of Exercise in the Heat on Predisposition to Heatstroke.

摘要

The concept that hard work in a hot environment can predispose to a serious deficit of effective arterial volume and shock (11, 13, 29) combined with both human and rat experimental data that indicates that working to exhaustion results in an increased rate of cellular injury and heatstroke mortality at low thermal loads appears to lend renewed support for a cardiovascular origin of heatstroke pathophysiology. These results appear to confirm that strenuous physical effort, even when the external heat load is moderate, can contribute more to the pathophysiology of heatstroke than an increased metabolic heat load. Taken in the general context of a model for heatstroke shock, these results would predict certain anomolous physiological and metabolic events in susceptible individuals such as: inappropriate increases in serum lactate, normal arterial PO2 and at some point, decreased total body oxygen consumption during progressive exertion-induced hyperthermia. At least two experimental approaches can be tested to explain the basis for this pathophysiological process: (1) the development of relative ischemia progressing to stagnant anoxia in the viscera due to inappropriate shifts in cardiac output and fluid volume or (2) a disruption in the steady state flux of energy transduction mechanisms such that the loss of function, as in sweat glands, might be seen as the effect of an underlying cellular disorder as well as a contributor to the pan-systemic failure in heatstroke.