Three independent biological mechanisms cause exercise-associated hyponatremia: Evidence from 2,135 weighed competitive athletic performances

Abstract

To evaluate the role of fluid and Na + balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na + concentrations ([Na + ]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na + ]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na + ] between 129-135 mmol/liter, and 11% a serum [Na + ] of <129 mmol/liter. Serum [Na + ] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na + ] in a subset of 18 subjects was predicted from the amount of Na + that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na + ] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na + ], requiring the addition of significant amounts of Na + (>500 mmol) into an expanded volume of total body water. This Na + likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who ( i ) drink to excess during exercise, ( ii ) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and ( iii ) osmotically inactivate circulating Na + or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985.