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.
D000328:Adult; D000818:Animals; D001833:Body Temperature Regulation; D004285:Dogs; D005260:Female; D006359:Heat Exhaustion / Q000209:etiology* / Q000401:mortality; D006358:Hot Temperature / Q000009:adverse effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D005082:Physical Exertion; D051381:Rats; D000637:Transaminases / Q000097:blood
D000637:Transaminases