Researchers at McLean Hospital, in Belmont, Mass., have found that exercise-associated hyponatremia„in addition to being caused by the consumption of too much water or sports drink volume during a marathon, is also the result of a hormonal stress response, which decreases urine formation and prevents the excretion of excess water.
The researchers at McLean Hospitalƒan affiliate of„Harvard Medical School and„Massachusetts General Hospital, and one of the nation_s top psychiatric hospitalsƒreported their findings in the May 2007 issue (abstract) of the„American Journal of Medicine.„Arthur J. Siegel, MD, chief of the Department of Internal Medicine at McLean, says ˙This is a major paradigm shift for those who think that exercise-associated hyponatremia is due primarily to salt loss or over-consumption of fluids. It_s also an inside job. Avid drinking may be a precondition, but dysregulation of the anti-diuretic hormone or arginine vasopressin (AVP), which governs water balance, emerges as the root cause.Ó„
Secretion of AVP governs water balance and is normally suppressed when an excess is present in body fluids. However, failure of appropriate suppression prevents excretion of excess water, which then results in the rapid fall of blood sodium levels. According to Siegel, under such circumstances the continued ingestion of dilute fluids, including sports drinks, leads to potentially fatal acute cerebral edema.„
Siegel and his colleagues tested blood samples from asymptomatic and collapsed runners at the 2001, 2002, 2003 and 2004 Boston marathons, including investigation of two fatal cases in 2002 (with the permission of their families). The findings confirmed inappropriate secretion of AVP as the proximate cause, meeting criteria for a condition first described in the American Journal of Medicine in 1967. This connection pointed to using hypertonic solutions, such as 3% saline, as a treatment for life-threatening cases of EAH, as previously validated for this syndrome.„
Once exercise-associated hyponatremia is diagnosed in a runner, concentrated bouillon can be given orally for those who can drink, or 3% saline can be given intravenously for those experiencing seizures or coma.„
˙The message especially for slower runners, such as charity fundraisers, is awareness that over-hydration is more dangerous than dehydration,Ó says Siegel. ˙Such participants may need to decrease their drinking rate commensurate with their race pace.Ó Siegel also encourages runners to monitor changes in body weight to monitor fluid status during training, as advised in new American College of Sports Medicine guidelines. Scales for this purpose have been available in American Red Cross stations at the most recent Boston race to assist in early diagnosis before progression to collapse.
Seigel says, ˙Runners who gain weight [during training] are over-hydrating and need to restrict intake of both water and sports drinks.Ó He points out that symptomatic runners should be evaluated with blood tests, because early symptoms of EAH may be similar to those of dehydration. He adds that this strategy can differentiate these opposite disorders of hydration for triage to condition-specific treatment protocols.„
The cause of AVP dysregulaton during prolonged exercise was also addressed in the article. The cytokine interleukin (IL)-6 is released from skeletal muscle after ˙hitting the wall,Ó which triggers secretion of stress-response hormones, including cortisol, prolactin and AVPƒunder conditions in which the latter would normally be suppressed.„
Seigel says, ˙We were confronted with the conundrum of how a runner could succumb to fatal water intoxication during a marathon. Identifying the root cause pointed us to novel strategies for prevention and treatment.Ó