Effects of exercise in the heat on predisposition to heatstroke.

This article reviews briefly the historical origins for both the cardiovascular and neural-anhidrotic concepts of heatstroke pathophysiology. It describes how deemphasis of the role of anhidrosis as the primary cause of heatstroke has resulted in: (a) an increased acceptance of animal models for heatstroke research; (b) further evidence that rigid reliance on the classic heatstroke symptoms (coma, anhidrosis, and a fever over 106 degrees F) can result in underdiagnosis; and (c) new research consistant with the hypothesis that exhaustive physical effort, by worsening circulatory collapse and metabolic acidosis predisposes tissue to hyperthermic injury and, as a result, substantially lowers the threshold for heatstroke injury and mortality. Thus, a new hypothesis combining the essential features of both direct thermal injury and cardiovascular origins of heatstroke pathophysiology may be necessary.