BRONCHOCONSTRICTION OCCURS IN PRACTICE SESSIONS IN SWIMMERS

Luke-Zeitoun, M., Wildman-Tobriner, B., Ghio, E., Hatamiya, N., Luke, A., Nielson, D., Lazarus, S., & Gold, W. (2012). Post-exercise airway response to atropine in healthy elite swimmers. Presentation 2237 at the 59th Annual Meeting of the American College of Sports Medicine, San Francisco, California; May 29-June 2, 2012.

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"There is a high prevalence of airway hyperresponsiveness (AHR) in endurance athletes, particularly in elite swimmers. Athletes develop exercise-induced bronchoconstriction at a higher rate than the general population. Vagal activity has been shown to be increased in high level athletes and is known to promote bronchoconstriction. The goal of this study was to determine the direct effects of parasympathetic tone on airway responsiveness in healthy elite swimmers."

Bronchial response to exercise was measured in healthy NCAA Division 1 University swimmer (M = 4; F = 3) on two occasions. To provoke exercise-induced bronchoconstriction, Ss exercised for eight minutes on a cycle ergometer at 90% of their maximal heart rate while breathing dry air. In one of the visits, the athletes received intravenous saline (placebo). In the other visit, they received intravenous atropine (0.04 mg/kg), given in divided doses (0.01 mg/kg every 30 seconds) between minutes eight and ten of exercise to selectively achieve parasympathetic blockade by the end of the exercise challenge. Airway conductance was measured by body plethysmography before and 3, 6, 10, 15, 20 and 30 minutes after the exercise challenge.

Postexercise airway conductance as percent of pre-exercise values showed significant changes over time, significant differences between the experimental conditions, and a significant condition x time interaction. Airway conductance was significantly lower for placebo, as compared with atropine at 6, 10, and 30 minutes post-exercise. The lowest values for airway conductance occurred during the placebo trial at three minutes post-exercise (88% pre-exercise). The highest values for airway conductance occurred during the atropine trial at 30 minutes post-exercise (173% pre-exercise).

Implication. Parasympathetic blockade results in airway dilation in healthy elite swimmers. These data suggest that vagal mechanisms play a major role in post-exercise airway response and possibly the development of exercise-induced bronchoconstriction in competitive swimmers.

[Editor's Note: The implication here is that bronchoconstriction is a natural phenomenon from swimming training. Elsewhere on the Swimming Science Journal, this response has been suggested as stemming from swimming in chlorinated pools, where in some cases it reaches such proportions as to be diagnosed as exercise-induced asthma, and in extreme cases has warranted the cessation of participation in chlorine environments. Some non-chlorine competitive swimming pool environments do not provoke bronchoconstriction and so the implications of this study were perhaps too sweeping because the nature of the chemicals in the environment was not controlled.]

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