Hyperpnoea-Induced Bronchoconstriction and Urinary CC16 Levels in Athletes.

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 hyperpnoea 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 hyperpnoea 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 minutes after an 8 minutes eucapnic voluntary hyperpnoea (EVH) test in fifty female individuals (28 athletes and 22 untrained). RESULTS:: Nineteen subjects (10 athletes) demonstrated a sustained bronchoconstriction after EVH (mean ± SE FEV1 fall from baseline: 23.5 ± 2.6%). The remaining subjects had a negative challenge result with a 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 pre- to post-challenge: athletes EVH- 0.083 ng.μmol, athletes EVH 0.223 ng.μmol, untrained EVH- 0.074 ng.μmol, untrained EVH 0.571 ng.μmol; P > 0.05). CONCLUSION:: Urinary levels of Clara cell protein CC16 are increased after eucapnic voluntary hyperpnoea in all individuals (trained and untrained, with and without EIB) suggestive of dehydration-induced perturbation of the distal respiratory epithelium during episodes of hyperventilation.