Renal function and vasopressin during marathon running

Abstract

Over the past 2 decades, exercise-associated hyponatraemia (EAH) has emerged as an important complication of prolonged endurance physical activities. Data collected since the first reports of EAH have strongly implicated a dilutional hyponatraemia from inappropriate retention of body water as the primary cause of EAH. Although high rates of fluid consumption clearly contribute to the pathogenesis of EAH, a review of the available data does not support the view that EAH can be ascribed solely to excess drinking. Because the kidney is exquisitely sensitive to low plasma levels of the antidiuretic hormone arginine vasopressin (AVP) and because many non-osmotic stimuli to AVP secretion normally occur during prolonged endurance exercise activity, it is more likely that a combination of higher than normal fluid intakes in the setting of modest elevations of plasma AVP levels from a variety of potential stimuli during prolonged physical activity accounts for the majority of cases of EAH. In any individual, the degree to which AVP secretion is stimulated and whether it can be suppressed with sufficient fluid ingestion, will determine their susceptibility to EAH as a result of fluid ingestion both before and after physical activity, accounting for the high degree of individual variability in the occurrence of this potentially life-threatening metabolic disorder.