Hyperpnea-Induced Bronchoconstriction and Urinary CC16 Levels in Athletes

BOLGER, CLAIRE1; TUFVESSON, ELLEN2; SUE-CHU, MALCOLM3,4; DEVEREUX, GRAHAM5; AYRES, JON G.5,6; BJERMER, LEIF2; KIPPELEN, PASCALE1,7

Medicine & Science in Sports & Exercise: July 2011 - Volume 43 - Issue 7 - pp 1207-1213
doi: 10.1249/MSS.0b013e31820750d8
Basic Sciences

Purpose: Exercise-induced bronchoconstriction (EIB) is a common condition in both individuals with asthma and otherwise healthy elite athletes. Although excessive water loss by peripheral airways during hyperpnea is regarded as the initial trigger for EIB, the cascade of events that follows remains unclear. Our goal was to establish whether transient disruption of the airway epithelial barrier occurs after a short period of hyperpnea of dry air in athletes with EIB.

Methods: Urinary concentration of the pneumoprotein Clara cell (CC16) was used as an assumed biomarker of lung epithelial cell damage or dysfunction. Samples were collected at baseline and for 90 min after an 8-min eucapnic voluntary hyperpnea (EVH) test in 50 female individuals (28 athletes and 22 untrained).

Results: Nineteen subjects (10 athletes) demonstrated a sustained bronchoconstriction after EVH (mean ± SE forced expiratory volume in the first second (FEV1) fall from baseline = 23.4% ± 2.6%). The remaining subjects had a negative challenge result with an FEV1 fall of 5.9% ± 0.6%. An increase (P < 0.001) in urinary CC16 concentration was noticed after EVH in all but one subject, with no group difference (median CC16 increase before to after challenge: athletes EVH 0.083 ng·μmol−1, athletes EVH+ 0.223 ng·μmol−1, untrained EVH 0.074 ng·μmol−1, untrained EVH+ 0.571 ng·μmol−1; P > 0.05).

Conclusions: Urinary levels of CC16 are increased after EVH in all individuals (trained and untrained, with and without EIB) suggestive of dehydration-induced perturbation of the distal respiratory epithelium during episodes of hyperventilation.

1School of Medical Sciences, University of Aberdeen, Aberdeen, UNITED KINGDOM; 2Department of Respiratory Medicine & Allergology, Lund University Hospital, Lund, SWEDEN; 3Department of Lung Medicine, St. Olavs Hospital, University Hospital of Trondheim, Trondheim, NORWAY; 4Department of Circulation and Imaging, Norwegian University of Science and Technology, Trondheim, NORWAY; 5Department of Occupational Medicine, University of Aberdeen, Aberdeen, UNITED KINGDOM; 6Institute of Occupational and Environmental Medicine, University of Birmingham, Birmingham, UNITED KINGDOM; and 7Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge, UNITED KINGDOM

Address for correspondence: Pascale Kippelen, Ph.D., Centre for Sports Medicine & Human Performance, School of Sport & Education, Brunel University, Uxbridge, Middlesex, UB8 3PH, United Kingdom; E-mail: pascale.kippelen@brunel.ac.uk.

Submitted for publication June 2010.

Accepted for publication November 2010.

© 2011 American College of Sports Medicine