Asthma and lower airway diseaseAirway remodeling and inflammation in competitive swimmers training in indoor chlorinated swimming pools
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Subjects
Twenty-three competitive swimmers age 17 years and older were recruited. They were nonsmokers, nonobese, and free of any other disease. All gave written informed consent.
Bronchial biopsies and the associated clinical data from 10 age-matched mild-asthmatic and 10 healthy nonallergic subjects were obtained from the Québec Respiratory Health Network Tissue Bank at the Institut Universitaire de Cardiologie et de Pneumologie de Québec. These subjects had given their consent for clinical evaluation,
Subjects
Subjects’ characteristics are presented in Table I. Swimmers competed at the provincial (n = 11) or national level (n = 12). The mean rest period since the last strenuous training or competition was 45 ± 55 days.
Twelve swimmers (52%) had a PC20 FEV1 of less than 16 mg/mL, and 5 of them (22%) had a PC20 FEV1 of less than 4 mg/mL. The FEV1 and forced vital capacity were higher in swimmers than in asthmatic and control groups (P < .05). Three swimmers had a previous physician-diagnosed asthma but
Discussion
We observed inflammatory and remodeling changes in bronchial biopsies of competing swimmers, with or without AHR, similar to nonathletes with mild asthma. Interestingly, swimmers showed greater goblet cell hyperplasia and increased mucin expression than did asthmatic subjects. Therefore, our results suggest that swimming training in chlorinated pools affects the structure of the airway in elite swimmers.
In our study, a majority of swimmers had atopy (18 of 23), which may have contributed to the
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2022, Science of the Total EnvironmentCitation Excerpt :Therefore, we performed the swimming protocol in Cpa3cre/+ mice (mast-cell deficient mice), but AHR was still present in Cpa3cre/+ mice swimming in chlorinated water. This suggest that there is no crucial role of mast cells in the induction of AHR in this EIB model, which is in contrast with previous studies where mast cells were described to be increased in the airway mucosa of swimmers compared to controls (Bougault et al., 2012). To conclude, in our 3-week swimming murine model, mimicking intensive swimming in chlorinated water, to study EIB in elite swimmers, we could confirm the presence of AHR in the mice intensively swimming in chlorinated water, in the absence of airway inflammation and airway epithelial damage.
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Valérie Bougault was supported in part by a grant from the Groupe de recherche en santé respiratoire from Université Laval (GESER), Québec, Quebec, Canada.
Disclosure of potential conflict of interest: L.-P. Boulet is on advisory boards for AstraZeneca, GlaxoSmithKline, MerckFrosst, and Novartis; receives lecture fees from 3M, AstraZeneca, GlaxoSmithKline, MerckFrosst, and Novartis; receives research support from AstraZeneca, GlaxoSmithKline, MerckFrosst, Schering, Altair, Asmacure, Boehringer-Ingelheim, Genentech, Pharmaxis, Wyeth; is an advisor for the Conseil du Medicament du Quebe and AETMIS and a member of the Quebec Workmen Compensation Board Respiratory Committee; is chair of the Canadian Thoracic Society Respiratory Guidelines Committee and chair of the GINA Guidelines Dissemination and Implementation Committee; is holder of the Laval University Chair on Knowledge Transfer, Prevention, and Education in Respiratory and Cardiovascular Health; and is a member of the Knowledge Translation (KT Canada) supported by the CIHR. The rest of the authors declare that they have no relevant conflicts of interest.