Response to a fluid load in athletes with a history of exercise induced hyponatremia
Speedy DB, Noakes TD, Bowell T, Thompson JMD, Rerher N, Boswell DR Med. Sci. Sports Exercise 2001;33:1434-42


To determine whether athletes who had previously developed hyponatremia during an ultradistance triathlon show an impaired ability to excrete a large fluid load compared with athletes who had completed the same race without developing hyponatremia.


Six athletes who had developed hyponatremia ([Na] < 135 mmol x L(-1)) in the 1997 Ironman Triathlon (study cases) were compared with six athletes who completed the same race without hyponatremia (controls). All participants consumed 3.4 L of water over 2 h at rest. Weight, urine output, urine electrolytes, serum [Na(+)], hemoglobin, and hematocrit were measured every 30 min. Changes in plasma volume and residual fluid volume in the gut were estimated from these data.


There were no significant differences between cases and controls in any parameters measured. Maximal rates of urine production (+/- SD) (1043 +/- 331 mL x h(-1) for cases, 878 +/- 168 mL x h(-1) for controls) were substantially behind the rate of fluid intake (1500 mL x h(-1)). Consequent to fluid retention, serum [Na(+)] fell progressively in both groups. Five cases and four controls developed hyponatremia. There was an inverse correlation between change in body weight and change in [Na(+)] (r = -0.67). Estimated changes in the intra- and extra-cellular fluid volumes could account for all the retained fluid, and there was little evidence for fluid accumulation in the bowel.


When evaluated at rest, there does not appear to be any unique pathophysiological characteristic that explains why some athletes develop hyponatremia in response to fluid overload during prolonged exercise. Rather, hyponatremia was induced with equal effect in both cases and controls, consequent to progressive fluid overload of all the body fluid compartments and without evidence for fluid retention in the small bowel.

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