Exercise-Associated Hyponatremia: 2017 Update

Abstract

Exercise-associated hyponatremia (EAH) was initially described in the 1980s in endurance athletes, and work done since then has conclusively identified that overdrinking beyond thirst and non-osmotic arginine vasopressin release are the most common etiologic factors. In recent years, EAH has been described in a broader variety of athletic events and also has been linked to the development of rhabdomyolysis. The potential role of volume and sodium depletion in a subset of athletes has also been described. This review focuses on the most recent literature in the field of EAH and summarizes key new findings in the epidemiology, pathophysiology, treatment, and prevention of this condition.

Keywords: exercise; hyponatremia; pathogenesis; rhabdomyolysis; water.

Figure 1

Reported cases of exercise-associated hyponatremia (EAH) along the spectrum of pathophysiology. Cases of EAH per sport are superimposed upon the broad spectrum of volemic pathophysiology: (1) hypervolemia—overzealous drinking with arginine vasopressin (AVP) stimulated fluid retention and minimal sodium losses or sodium over-correction (black triangle); (2) euvolemia—moderate drinking with AVP stimulated fluid retention and mild (compensable) sodium losses (gold triangle); and (3) hypovolemia—moderate drinking (volemic thirst) with AVP stimulated fluid retention, and under-replaced sodium losses (red triangle).

Figure 2

Pathogenic factors involved in the development of exercise-associated hyponatremia (EAH). EAH develops from multiple mechanisms and can occur in both states of volume excess and depletion with AVP secretion occurring in both cases. It is important to note that none of these mechanisms occur in isolation, and they can overlap in any given patients (for example, sodium loss and excess water intake can occur in the same patient) Abbreviations: Na, sodium; AVP, arginine vasopressin; GI, gastrointestinal; CNS, central nervous system; RAAS, renin–angiotensin–aldosterone system.

Figure 3

Putative bidirectional relationship between exercise-associated hyponatremia (EAH) and rhabdomyolysis. EAH may lead to rhabdomyolysis through changes in the skeletal muscle membrane (osmotic shock) and activation of reactive oxygen species (ROS) along with increases in intracellular calcium (Ca) that activate intracellular proteases and lead to cellular breakdown. Rhabdomyolysis either through this mechanism or by other means leads to local and systemic inflammation and release of interleukin-6 (IL-6), which may increase arginine vasopressin (AVP) levels further lowering serum sodium. Non-steroidal anti-inflammatory drug use may also contribute to excess AVP release.

Figure 4

Treatment of exercise-associated hyponatremia (EAH) according to signs and symptoms. Evidenced-base treatment options for EAH associated with mild (yellow), moderate (orange), or severe clinical signs and symptoms.