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The authors’ conclusion that the aetiology of exercise-associated hyponatraemia (EAH) is more complex than our “oversimplified” explanation stems from their misunderstanding of how fluid balance is regulated during and after exercise and their ignorance of the conclusions of our most recent publication.1
In contrast with their assertion that “body fluid homeostasis is a primary variable which is important in the stability of the ‘internal environment’”, the accepted reality (in all physiological disciplines other than the exercise sciences) is that the plasma osmolality is the internal variable that is homoeostatically regulated during exercise2 as it is at rest. The point is that the human body is not designed to regulate its body weight during exercise. Thus, if subjects ingest sufficient fluid to match their sweat or weight losses during exercise, their plasma osmolality and sodium concentrations ([Na+]) will fall to an extent that depends on the precision with which they follow those instructions.
This is precisely shown by the authors’ own data. Thus, when their soldiers ingested enough fluid to replace their sweat losses during 10 h of exercise, their serum [Na+] fell regardless of whether or not they ingested additional sodium. This has been repeatedly shown.3–6
But, as argued elsewhere,7 it is not certain of what relevance this finding is to athletes who drink according to their normal biological controls—that is, according to thirst2 and who therefore lose weight during exercise, while maintaining or increasing their serum [Na+]. To conclude on the basis of this fallacious argument that all athletes must ingest sodium if they are to prevent EAH during exercise is illogical.7 Rather, athletes should simply be encouraged to avoid the …
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