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Hyperpnea-induced bronchoconstriction and urinary CC16 levels in athletes
Claire Bolger1, Ellen Tufvesson, Malcolm Sue-Chu
1School of Medical Sciences, Department of Occupational Medicine, University of Aberdeen, Aberdeen, United Kingdom.
Medicine and Science in Sports and Exercise
|December 7, 2010
Summary
Elite athletes and individuals with asthma experience exercise-induced bronchoconstriction (EIB). A study found increased urinary Clara cell protein 16 (CC16) after hyperpnea, suggesting airway epithelial disruption due to dehydration.
Area of Science:
- Respiratory Medicine
- Exercise Physiology
- Biomarker Research
Background:
- Exercise-induced bronchoconstriction (EIB) affects athletes and asthmatics.
- The exact mechanism triggering EIB post-hyperpnea remains unclear.
- Airway epithelial barrier disruption is a potential factor.
Purpose of the Study:
- To investigate transient airway epithelial barrier disruption after hyperpnea in athletes with EIB.
- To assess if airway epithelial damage occurs following a short period of dry air hyperpnea.
Main Methods:
- Measured urinary Clara cell protein 16 (CC16) as a biomarker for lung epithelial damage.
- Collected samples from 50 female participants (28 athletes, 22 untrained) at baseline and post-EVH test.
- Utilized an 8-minute eucapnic voluntary hyperpnea (EVH) test.
Main Results:
- Nineteen subjects (10 athletes) showed significant bronchoconstriction post-EVH (FEV1 fall >20%).
- Urinary CC16 concentration increased significantly (P<0.001) in nearly all subjects after EVH.
- No significant difference in CC16 increase was observed between athletes and untrained individuals.
Conclusions:
- Increased urinary CC16 levels post-EVH suggest dehydration-induced perturbation of the respiratory epithelium.
- This occurs in both trained and untrained individuals, irrespective of EIB presence.
- Hyperpnea may transiently disrupt the airway epithelial barrier through dehydration.
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