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Title: A standard, single dose of inhaled terbutaline attenuates hyperpnoea-induced bronchoconstriction and mast cell activation in athletes
Authors: Simpson, AJ
Bood, JR
Anderson, SD
Romer, LM
Dahlén, B
Dahlén, S-E
Kippelen, P
Keywords: inhaled β2-agonist;exercise-induced bronchoconstriction;eucapnic voluntary hyperpnoea;prostaglandin D2
Issue Date: 1-May-2016
Publisher: American Physiological Society
Citation: Journal of Applied Physiology, 120(9): pp. 1011 - 1017, (2016)
Abstract: Release of broncho-active mediators from mast cells during exercise hyperpnoea is a key factor in the pathophysiology of exercise-induced bronchoconstriction (EIB). Our aim was to investigate the effect of a standard, single dose of an inhaled β2-adrenoceptor agonist on mast cell activation in response to dry air hyperpnoea in athletes with EIB. Twenty-seven athletes with EIB completed a randomised, double blind, placebo-controlled, crossover study. Terbutaline (0.5 mg) or placebo was inhaled15 min prior to 8 min of eucapnic voluntary hyperpnoea (EVH) with dry air. Pre- and post-bronchial challenge, urine samples were analysed by enzyme immunoassay for 11β-prostaglandin(PG)F2α. The maximum fall in forced expiratory volume in 1 sec(FEV1) of 14 (12-20)% (median and interquartile range) following placebo was attenuated to 7 (5-9)% with the administration of terbutaline (P<0.001). EVH caused a significant increase in 11β-PGF2α from (27-57) ng·mmol creatinine-1 at baseline to (43-72) ng·mmol creatinine-1 at its peak post-EVH following placebo (P=0.002). The rise in 11β-PGF2α was inhibited with administration of terbutaline: 39 (28-44) ng·mmol creatinine-1 at baseline vs. 40 (33-58) ng·mmol creatinine-1 at its peak post-EVH (P=0.118). These data provide novel in vivo evidence of mast cell stabilisation following inhalation of a standard dose of terbutaline prior to bronchial provocation with EVH in athletes with EIB.
ISSN: 8750-7587
Appears in Collections:Dept of Life Sciences Research Papers

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