Frontiers of hormone research | 2019
Exercise-associated hyponatremia (EAH) refers to below-normal serum sodium concentrations [Na+] that develop during exercise. The pathogenesis of EAH is best described as a spectrum ranging between profound polydipsia to modest sweat sodium losses with hypovolemia and relative dilution. Non-osmotic arginine vasopressin (AVP) remains the unifying pathogenic stimulus to abnormal renal water retention in acute symptomatic EAH. Cases of hyponatremia are mostly reported after endurance sports, but are also observed after shorter duration events and in team sport athletes. The signs and symptoms of EAH are vague, and include bloating, vomiting, headache, and altered mental status. A diagnosis of EAH can only be confirmed by a blood test, whereas signs/symptoms guide the most appropriate treatment strategy. Mild-to-moderate EAH (without encephalopathy) can be treated with either fluid restriction or an oral bolus of a hypertonic saline solution. Severe EAH (with encephalopathy) is a life-threatening emergency and should be urgently treated with intravenous 100 mL boluses of 3% saline until the resolution of encephalopathy symptoms. The prevention of EAH is evolutionarily rooted in preventing overdrinking during exercise. Drinking according to the dictates of thirst is the most individualized strategy to prevent life-threatening dysnatremia during exercise, regardless of sport.