Airway hyperresponsiveness in elite swimmers: Is it a transient phenomenon? - 11/08/11
, Julie Turmel, MSc a, Louis-Philippe Boulet, MD a
Reprint requests: Valérie Bougault, PhD, Université du droit et de la santé Lille 2, FSSEP, 9 rue de l’université, 59790 Ronchin, France.Abstract |
Background |
Airway hyperresponsiveness is highly prevalent in competitive swimmers, but it is unknown whether this is transient or persistent.
Objectives |
To document changes in airway responsiveness and airway inflammation in elite swimmers during intense training and rest.
Methods |
Nineteen swimmers and 16 healthy controls completed a standardized questionnaire, allergy skin prick tests, exhaled nitric oxide measurement, eucapnic voluntary hyperpnea testing, methacholine challenge, and induced sputum analysis. Testing was performed during intense swimming and after at least 2 weeks of rest.
Results |
Sixteen swimmers and 13 controls were atopic. Airway responsiveness to methacholine and eucapnic voluntary hyperpnea was significantly higher in swimmers than in controls (P < .0001). A significant decrease in airway responsiveness was observed from training to rest in swimmers only (P < .005). This occurred with both methacholine challenge—with PC20 values of 6.0 mg/mL and 12.8 mg/mL, respectively—and eucapnic voluntary hyperpnea testing—with a maximum fall in FEV1 after voluntary testing of 14.1 L and 10.1 L, respectively. Eight of 12 swimmers with airway hyperresponsiveness during intense training had normal airway responsiveness during rest. No airway inflammation occurred, and no significant change in this parameter was observed from training to rest.
Conclusion |
Training may contribute to the development of airway hyperresponsiveness in elite swimmers, but this seems reversible in many athletes after training cessation for at least 2 weeks.
El texto completo de este artículo está disponible en PDF.Key words : Methacholine challenge, eucapnic voluntary hyperpnea, airway inflammation, athletes, asthma, follow-up
Abbreviations used : AHR, EVH, EVHf, FeNO, FVC, MCh, V1, V2
Esquema
| V.B. was supported in part by a grant from the Groupe de recherche en santé respiratoire from Université Laval (GESER), Quebec City, Quebec, Canada. |
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| Disclosure of potential conflict of interest: L.-P. Boulet is on the advisory board for AstraZeneca, Altana, GlaxoSmithKline, Merck Frosst, and Novartis; is an advisor for the Conseil du Médicament du Québec; is a Member of the Quebec Workmen Compensation Board Respiratory Committee; has received lecture fees from 3M, Altana, AstraZeneca, GlaxoSmithKline, Merck Frosst, and Novartis; has received research support from AstraZeneca, 3M, Altana, AsthmaTx, Boehringer-Ingelheim, Dynavax, Genentech, GlaxoSmithKline, IVAX, MedImmune, Merck Frosst, Novartis, Roche, Schering, Topigen, and Wyeth; has received support for the production of educational materials from AstraZeneca, GlaxoSmithKline, and Merck Frosst; is chair of the Canadian Thoracic Society Guidelines Dissemination and Implementation Committee; is co-leader of the Therapeutics Theme of the Canadian AllerGen Network of Centers of Excellence; holds the Laval University Chair on Knowledge Transfer, Prevention, and Education in Respiratory and Cardiovascular Health; and is a member of the Asthma Committee of the World Allergy Organization. The rest of the authors have declared that they have no conflict of interest. |
Vol 127 - N° 4
P. 892-898 - avril 2011 Regresar al número
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