• Courtney Kipps, Sanjay Sharma, and Dan Tunstall Pedoe.
• Charing Cross Hospital and Queen Mary, University of London, UK. courtneykipps@yahoo.co.uk
• Br J Sports Med. 2011 Jan 1;45(1):14-9.

BackgroundExercise-associated hyponatraemia (EAH) is a potentially fatal cause of collapse in endurance exercise. It is understood to be a dilutional hyponatraemia caused by an increase of total body water relative to the amount of exchangeable sodium stores. Fourteen runners presented to one London hospital with symptomatic EAH several hours after finishing the 2003 London Marathon, and more recently, a young male runner died from the complications of severe EAH after crossing the finish line of the London Marathon.ObjectivesTo determine the incidence of EAH in runners in the London Marathon.MethodsVolunteers were recruited at race registration where they were weighed, had blood tests and completed a demographic and experience questionnaire. Weights, blood tests and a fluid intake questionnaire were repeated after the finish. Blood was analysed on-site using hand-held i-STAT blood analysers.ResultsOf the 88 volunteers, 11 (12.5%) developed asymptomatic hyponatraemia (serum sodium 128-134 mmol/l). They consumed more fluid (p<0.001) and gained more weight (p<0.001) than did those without hyponatraemia.ConclusionsA significant proportion (12.5%) of healthy volunteers developed asymptomatic hyponatraemia running a marathon in cool conditions. On average, these runners consumed more fluid and gained more weight than did non-hyponatraemic runners, although fluid intake was not related to weight gain in this study. Four of the 11 hyponatraemic runners lost weight over the course of the marathon, strengthening the case for an additional factor, such as inappropriate antidiuretic hormone release during exercise, in the development of EAH.

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