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Repeated injury of the airway epithelium caused by hyperpnoea of poorly conditioned air has been proposed as a key factor in the pathogenesis of exercise-induced bronchoconstriction (EIB) in athletes. In animals, the short-acting β2-agonist terbutaline has been shown to reduce dry airflow-induced bronchoconstriction and the associated shedding of airway epithelial cells. Our aim was to test the efficacy of inhaled terbutaline in attenuating hyperpnoea-induced bronchoconstriction and airway epithelial injury in athletes. Twenty-seven athletes with EIB participated in a randomized, double-blind, placebo-controlled, crossover study. Athletes completed an 8-min eucapnic voluntary hyperpnoea (EVH) test with dry air on two separate days 15 min after inhaling 0.5 mg terbutaline or a matching placebo. Forced expiratory volume in 1 s (FEV1) and urinary concentration of the club cell (Clara cell) protein 16 (CC16, a marker of airway epithelial perturbation) were measured before and up to 60 min after EVH. The maximum fall in FEV1 of 17 ± 8% (SD) on placebo was reduced to 8 ± 5% following terbutaline (P < 0.001). Terbutaline gave bronchoprotection (i.e., post-EVH FEV1 fall <10%) to 22 (81%) athletes. EVH caused an increase in urinary excretion of CC16 in both conditions (P < 0.001), and terbutaline significantly reduced this rise (pre- to postchallenge CC16 increase 416 ± 495 pg/μmol creatinine after placebo vs. 315 ± 523 pg/μmol creatinine after terbutaline, P = 0.016). These results suggest that the inhalation of a single therapeutic dose of terbutaline offers significant protection against hyperpnoea-induced bronchoconstriction and attenuates acute airway epithelial perturbation in athletes.

Background: cerebral autoregulation (CA) is the ability to control cerebral blood flow during fluctuations in arterial blood pressure (ABP). It is impaired in a number of conditions including acute stroke, though studies so far have not found a decline in CA with age. CA is very sensitive to changes in pCO₂., Objective: this study investigates the effect of ageing on CA using a moving-window autoregressive moving average (MW-ARMA) to calculate CA as autoregulatory index (ARMA-ARI) during hypercapnia and hypocapnia, to ascertain whether this method would detect age-related differences in CA due to change in pCO₂., Method: ECG was used to measure R-R interval, Finapres to measure ABP and capnography to measure end-tidal CO₂. Transcranial Doppler ultrasonography was used to measure left and right middle cerebral artery cerebral blood flow velocity (CBFV). Hypercapnia was induced by a breath-hold, hypocapnia by hyperventilation., Results: thirty volunteers of mean age 25 ± 6 years and 30 volunteers of mean age 64 ± 4 years were recruited. CBFV was higher and change in CBFV due to respiratory manoeuvre was significantly greater in the younger group compared with the older group. However, no difference in ARMA-ARI was found between the groups., Conclusion: these findings suggest that CA is not affected by healthy ageing.