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In 1991, we provided definitive evidence that exercise-associated hyponatraemia (EAH) is caused by abnormal fluid retention in those who overdrink during prolonged exercise, but this finding was ignored. Instead, in 1996, influential guidelines of the American College of Sports Medicine (ACSM) promoted the concept that athletes should drink ‘as much as tolerable’ during exercise. What followed was an epidemic of cases of EAH and its associated encephalopathy (EAHE). A recent study funded by the sports drink industry confirms our 1991 finding by showing that 95% of the variance in the serum sodium concentration during exercise can be explained by changes in body mass alone. The possibility is that commercial influence delayed the acceptance of our findings for two decades.
Describing the first reported cases of EAH and its EAHE in 1985, we postulated that: ‘The aetiology of this condition appears to be voluntary hyperhydration with hypotonic solutions combined with moderate sweat sodium chloride losses…advice (on fluid replacement) should be tempered with the proviso that the intake of hypotonic fluids in excess of that required to balance sweat and urine losses may be hazardous in some individuals.’1
A study of fluid and sodium balance in eight ultramarathon runners with EAHE published in 19912 showed that normalisation of their serum sodium concentrations ([Na+]) occurred only after all had excreted a fluid excess ranging from 2 to 6 l. None had developed a larger sodium deficit than did a control group of runners without EAH or EAHE. We concluded that: ‘This study conclusively resolves this issue (of what causes EAHE). It shows that each of eight subjects who collapsed with the hyponatremia of exercise (mean plasma sodium concentration 122.4±2.2 mM) were fluid overloaded by an amount ranging from 1.22 to 5.92 liters.’ As a result, ‘the hyponatremia of exercise …
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