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Exhaled breath temperature in elite swimmers: The effects of a training session in adolescents with or without asthma.
Pediatric Allergy and Immunology 2015 September
BACKGROUND: Cooling of the airways and inflammation have been pointed as possible mechanisms for exercise-induced asthma (EIA). We aimed to investigate the effect of training and asthma on exhaled breath temperature (EBT) of elite swimmers.
METHODS: Elite swimmers annually screened (skin prick tests, spirometry before and after salbutamol inhalation, induced sputum cell counts, and methacholine bronchial challenge) at our department (n = 27) were invited to this prospective study. Swimmers who agreed to participate in the present study (n = 22, 10 with asthma) had axillary temperature and EBT measured (X-halo(®) ) before and after a swimming training session (aerobic/non-aerobic). Linear regression models were used to assess the effect of asthma and other possible explanatory variables (demographics, PD20 , baseline EBT, training intensity, axillary temperature, and the number of hours trained in that week) on EBT change.
RESULTS: EBT significantly increased after training independently of lung function, airway responsiveness, and inflammation in all swimmers (mean ± SD: 0.32 ± 0.57; p = 0.016). No differences were observed between asthmatic swimmers and others. A significant correlation was observed between baseline and post-exercise EBTs (r = 0.827, p < 0.001). Asthma was not a predictor of ΔEBT after adjusting for confounders; baseline EBT was the variable most strongly associated with ΔEBT, explaining by itself alone 46% of the outcome (r(2) = 0.464).
CONCLUSION: Although these are preliminary data, a relationship between airway's inflammation and respiratory heat loss during exercise could not be confirmed, suggesting that the increase in exhaled breath temperature is a physiologic rather than a pathological response to exercise.
METHODS: Elite swimmers annually screened (skin prick tests, spirometry before and after salbutamol inhalation, induced sputum cell counts, and methacholine bronchial challenge) at our department (n = 27) were invited to this prospective study. Swimmers who agreed to participate in the present study (n = 22, 10 with asthma) had axillary temperature and EBT measured (X-halo(®) ) before and after a swimming training session (aerobic/non-aerobic). Linear regression models were used to assess the effect of asthma and other possible explanatory variables (demographics, PD20 , baseline EBT, training intensity, axillary temperature, and the number of hours trained in that week) on EBT change.
RESULTS: EBT significantly increased after training independently of lung function, airway responsiveness, and inflammation in all swimmers (mean ± SD: 0.32 ± 0.57; p = 0.016). No differences were observed between asthmatic swimmers and others. A significant correlation was observed between baseline and post-exercise EBTs (r = 0.827, p < 0.001). Asthma was not a predictor of ΔEBT after adjusting for confounders; baseline EBT was the variable most strongly associated with ΔEBT, explaining by itself alone 46% of the outcome (r(2) = 0.464).
CONCLUSION: Although these are preliminary data, a relationship between airway's inflammation and respiratory heat loss during exercise could not be confirmed, suggesting that the increase in exhaled breath temperature is a physiologic rather than a pathological response to exercise.
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