Airway hyperresponsiveness (AHR) and exercise-induced bronchoconstriction (EIB) are conditions commonly affecting high-intensity athletes such as competitive swimmers.1 Due to the nature of their work, they sustain increased ventilation rates and recurring exposure to and inhalation of chlorine by-products often leading to asthma and respiratory symptoms throughout their careers.2 AHR and EIB in athletes have been well defined, however, studies focusing on immunological relevance in symptom onset may prove useful in developing preventative measures.3
Decaesteker T, et al. from KU Leuven established a 3-week swimmers EIB murine model and investigated the effects of chlorine exposure during swimming sessions. Using the flexiVent, they assessed lung function in mice three hours post-session. Airway hyperreactivity (AHR), permeability, integrity and inflammation parameters were defined in each subject.4
They found a significant increase in airway resistance from mice swimming in chlorinated water compared to controls in tap water. However, both experimental and control groups did not present cellular inflammation, difference in lung immune populations or lung tight junction mRNA expression.4 Swimming sessions with SCID and Rag2−/−γc−/− mice did not show significant differences in AHR compared to controls suggesting limited involvement of the innate and adaptive immune systems.4
Overall, this study evaluates the effects of chlorine exposure during intensive swimming in a murine model mimicking EIB in athletic swimmers. Their findings support pronounced AHR with limited immunological involvement. Further investigation is required to elucidate neurogenic pathway and/or monocyte involvement in AHR onset.
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