Exercise-associated hyponatremia

Last weekend I participated in a mountain 50-mile ultramarathon race. Although my own performance was less than I had anticipated, I enjoyed listening to the other runners. As a fellow participant, I appreciate hearing their experiences. As an endocrinologist, however, I am fascinated by the physiology of extreme endurance activity.

Death during such events is extremely rare. However, one cause of fatalities is exercise-associated hyponatremia. First described in the mid-1980s, hyponatremia has been found to be more common in endurance athletes than previously thought. Before that time, runners were advised to not drink fluids during their races. Since then, they were recommended to consume as much fluid is possible to avoid dehydration. Many races provide sports beverages with the intent of maintaining hydration and normal electrolyte status. Now with the popularity increasing of marathon races and beyond, hyponatremia is becoming more common. Some studies have shown an incidence as high as 13% to 18% after some races.

Exercise-associated hyponatremia is defined as serum sodium <135 mmol/L during or after prolonged endurance exercise. Exercise-associated hyponatremic encephalopathy is low serum sodium along with symptoms such as confusion, seizures and altered mental status. If not treated properly, exercise-associated hyponatremic encephalopathy can result in death.

There are several factors that increase the risk of exercise-associated hyponatremia. The most important factor is the excessive intake of fluids. Consuming sports beverages marketed as providing adequate electrolyte replacement instead of plain water has not been shown to prevent hyponatremia.

Gender is another important risk factor. Of 26 cases of hyponatremia reported in the San Diego Marathon, 23 were women. Longer race times, lower BMI, fewer previous marathons and slower training paces also are associated with increased risk. The use of nonsteroidal anti-inflammatory drugs have also been found to be associated with hyponatremia in some athletes.

Excessive consumption of fluids is most certainly a precipitating factor. However, an inability to suppress arginine vasopressin during exercise may also contribute. Even despite unchanged serum sodium, in one study plasma arginine vasopressin was found to remain markedly elevated during a 56-kilometer ultramarathon. The authors postulate that this was due to non-osmotic stimulation from decreased plasma volume along with possible additional effects from brain natriuretic peptide, oxytocin and corticosterone.

Emergency medical personnel must be cautious when treating runners during or after endurance races. There have been cases of death or worsening symptoms after treatment with intravenous 0.9% sodium chloride. Treatment of symptomatic exercise-associated hyponatremia with 3% sodium chloride is now advised. The Second International Exercise-Associated Hyponatrmia Consensus Panel in New Zealand in 2007, along with others, suggest giving a single 100 cc bolus of 3% sodium chloride, repeated up to two times if symptoms persist. The advantage of this approach is that symptoms may be reversed dramatically, an infusion pump is not required and the risks of overcorrection are minimized compared to prolonged infusion.