Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes
(2011) In Journal of Applied Physiology 111(4). p.1059-1065- Abstract
- Bolger C, Tufvesson E, Anderson SD, Devereux G, Ayres JG, Bjermer L, Sue-Chu M, Kippelen P. Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes. J Appl Physiol 111: 1059-1065, 2011. First published July 28, 2011; doi:10.1152/japplphysiol.00113.2011.-Injury to the airway epithelium has been proposed as a key susceptibility factor for exercise-induced bronchoconstriction (EIB). Our goals were to establish whether airway epithelial cell injury occurs during EIB in athletes and whether inhalation of warm humid air inhibits this injury. Twenty-one young male athletes (10 with a history of EIB) performed two 8-min exercise tests near maximal aerobic capacity in cold dry (4 degrees C, 37%... (More)
- Bolger C, Tufvesson E, Anderson SD, Devereux G, Ayres JG, Bjermer L, Sue-Chu M, Kippelen P. Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes. J Appl Physiol 111: 1059-1065, 2011. First published July 28, 2011; doi:10.1152/japplphysiol.00113.2011.-Injury to the airway epithelium has been proposed as a key susceptibility factor for exercise-induced bronchoconstriction (EIB). Our goals were to establish whether airway epithelial cell injury occurs during EIB in athletes and whether inhalation of warm humid air inhibits this injury. Twenty-one young male athletes (10 with a history of EIB) performed two 8-min exercise tests near maximal aerobic capacity in cold dry (4 degrees C, 37% relative humidity) and warm humid (25 degrees C, 94% relative humidity) air on separate days. Postexercise changes in urinary CC16 were used as a biomarker of airway epithelial cell perturbation and injury. Bronchoconstriction occurred in eight athletes in the cold dry environment and was completely blocked by inhalation of warm humid air [maximal fall in forced expiratory volume in 1 s = 18.1 +/- 2.1% (SD) in cold dry air and 1.7 +/- 0.8% in warm humid air, P < 0.01]. Exercise caused an increase in urinary excretion of CC16 in all subjects (P < 0.001), but this rise in CC16 was blunted following inhalation of warm humid air [median CC16 increase pre- to postchallenge = 1.91 and 0.35 ng/mu mol in cold dry and warm humid air, respectively, in athletes with EIB (P = 0.017) and 1.68 and 0.48 ng/mu mol in cold dry and warm humid air, respectively, in athletes without EIB (P = 0.002)]. The results indicate that exercise hyperpnea transiently disrupts the airway epithelium of all athletes (not only in those with EIB) and that inhalation of warm moist air limits airway epithelial cell perturbation and injury. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2208252
- author
- Bolger, C. ; Tufvesson, Ellen LU ; Anderson, S. D. ; Devereux, G. ; Ayres, J. G. ; Bjermer, Leif LU ; Sue-Chu, M. and Kippelen, P.
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- asthma, airway epithelial injury, Clara cell
- in
- Journal of Applied Physiology
- volume
- 111
- issue
- 4
- pages
- 1059 - 1065
- publisher
- American Physiological Society
- external identifiers
-
- wos:000295972000015
- scopus:80054679406
- pmid:21799131
- ISSN
- 1522-1601
- DOI
- 10.1152/japplphysiol.00113.2011
- language
- English
- LU publication?
- yes
- id
- 28f169c5-400a-4cc9-9a2c-87f0fdbfcdae (old id 2208252)
- date added to LUP
- 2016-04-01 10:40:44
- date last changed
- 2022-04-28 00:22:14
@article{28f169c5-400a-4cc9-9a2c-87f0fdbfcdae, abstract = {{Bolger C, Tufvesson E, Anderson SD, Devereux G, Ayres JG, Bjermer L, Sue-Chu M, Kippelen P. Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes. J Appl Physiol 111: 1059-1065, 2011. First published July 28, 2011; doi:10.1152/japplphysiol.00113.2011.-Injury to the airway epithelium has been proposed as a key susceptibility factor for exercise-induced bronchoconstriction (EIB). Our goals were to establish whether airway epithelial cell injury occurs during EIB in athletes and whether inhalation of warm humid air inhibits this injury. Twenty-one young male athletes (10 with a history of EIB) performed two 8-min exercise tests near maximal aerobic capacity in cold dry (4 degrees C, 37% relative humidity) and warm humid (25 degrees C, 94% relative humidity) air on separate days. Postexercise changes in urinary CC16 were used as a biomarker of airway epithelial cell perturbation and injury. Bronchoconstriction occurred in eight athletes in the cold dry environment and was completely blocked by inhalation of warm humid air [maximal fall in forced expiratory volume in 1 s = 18.1 +/- 2.1% (SD) in cold dry air and 1.7 +/- 0.8% in warm humid air, P < 0.01]. Exercise caused an increase in urinary excretion of CC16 in all subjects (P < 0.001), but this rise in CC16 was blunted following inhalation of warm humid air [median CC16 increase pre- to postchallenge = 1.91 and 0.35 ng/mu mol in cold dry and warm humid air, respectively, in athletes with EIB (P = 0.017) and 1.68 and 0.48 ng/mu mol in cold dry and warm humid air, respectively, in athletes without EIB (P = 0.002)]. The results indicate that exercise hyperpnea transiently disrupts the airway epithelium of all athletes (not only in those with EIB) and that inhalation of warm moist air limits airway epithelial cell perturbation and injury.}}, author = {{Bolger, C. and Tufvesson, Ellen and Anderson, S. D. and Devereux, G. and Ayres, J. G. and Bjermer, Leif and Sue-Chu, M. and Kippelen, P.}}, issn = {{1522-1601}}, keywords = {{asthma; airway epithelial injury; Clara cell}}, language = {{eng}}, number = {{4}}, pages = {{1059--1065}}, publisher = {{American Physiological Society}}, series = {{Journal of Applied Physiology}}, title = {{Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes}}, url = {{http://dx.doi.org/10.1152/japplphysiol.00113.2011}}, doi = {{10.1152/japplphysiol.00113.2011}}, volume = {{111}}, year = {{2011}}, }