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In an elaborate manuscript, Noakes and Speedy argue that exercise-associated hyponatraemia (EAH) is due to overhydration and that the usual sodium deficit incurred during exercise plays an insignificant role.1,2 Furthermore, these researchers claim that the reluctance to accept their evidence may be because it conflicts with the prevalent message of the sports drink industry. This approach is, however, oversimplification of the situation and at best singlesided. Noakes and Speedy in actuality prove the obvious. Overhydration will dilute body fluid, and thus plasma sodium concentration, as the primary extracellular electrolyte, will consequently be reduced. However, because hyponatraemia can be observed in the presence of a normal, depleted or expanded plasma volume, the issue of hyponatraemia should be approached from a broader perspective. We emphasise that the inability to replace cumulative sodium losses in sweat during long physical exertions is not less important as the background for EAH, whereas hyperhydration is only a marginal, although vastly reported, condition associated with EAH.
Body fluid homoeostasis is a primary variable, which is important in the stability of the “inner environment”. Therefore, total body water and the proportion of extracellular to intracellular volumes should be maintained very delicately. Dehydration during exercise results in graded physiological responses, including a decrease in cardiac output despite an increase in heart rate, an increase in core temperature and a decrease in peripheral blood flow, which ultimately affects performance. Eichna et …
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