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Approximately 80% of the athletes who collapse in marathon and other long distance sporting events do so only after they have crossed the finish line.1 Although it is usually taught that “dehydration” explains this phenomenon, logic suggests this to be unlikely because any dehydration induced hypovolaemia should cause cardiovascular failure when cardiac stress is highest—that is, during rather than after exercise when cardiovascular function is returning to the resting state. Instead it is clearly the act of stopping exercise that is the consequent, albeit paradoxical, cause of post-exercise collapse.
We have previously proposed that this form of exercise associated collapse is caused by the persistence into recovery of a state of low peripheral vascular resistance, compounded by removal of the skeletal muscle pump that maintains the right atrial filling pressure during exercise.1 According to this theory, the combination of a low peripheral vascular resistance and a sudden reduction in venous return would reduce stroke volume and cardiac output acutely, causing hypotension. Indeed this mechanism was used to explain the development of postural hypotension due to “dehydration exhaustion” in military personnel exposed to eight or more hours of exercise in desert heat without fluid replacement, in the classic studies of Adolph.2
Thus Adolph2 wrote that “the ultimate failure of the circulation (in dehydration exhaustion) is of a peripheral type . . . Dilated blood vessels of the skin require additional blood to fill them; correspondingly, …
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