Cellular events

Dense granules seen in the mitochondria following heat exposure appear to be heat shock proteins which enhance thermotolerance ( Welch 1993).

The resemblance between the effects of antimuscarinic drugs (e.g. atropine), which produce a central anticholinergic syndrome, and heat illness is impressive. Heat-producing reactions, which occur at neuromuscular junctions (voluntary contractions, shivering), and sweat glands, which are both muscarinic, are under cholinergic nerve control.

Heat fatigue may be a manifestation of ATP depletion, in part secondary to sodium influx into the cells. This occurs when a high temperature increases membrane permeability to sodium, thereby dramatically stimulating the energy-consuming Na +K+-ATPase enzyme activity. The propagation of nerve impulses normally requires a Na+ and K+ gradient, which is constantly maintained by Na+,K+-ATPase. This enzyme is also responsible for maintaining cell volume by osmotically drawing water out of the cell in the direction of the net positive charges. When ATP is depleted, the activity of Na +,K+-ATPase is curtailed. This results in tissue edema and neural membrane depolarization, leading to the convulsions seen with heatstroke. In addition to the heat-induced energy depletion, high temperature is known to cause loss of cellular ATP synthesis. Thus, in the search for a primary lesion of heat injury, energy seems to be a focal point. Membrane destruction and protein denaturation have also been proposed, but with fewer advocates.

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