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Effect of Sodium Cromoglycate on Mast Cell Mediators during Hyperpnea in Athletes

KIPPELEN, PASCALE1,2; LARSSON, JOHAN3,4; ANDERSON, SANDRA D.1; BRANNAN, JOHN D.1; DAHLÉN, BARBRO4,5; DAHLÉN, SVEN ERIK3,4

Medicine & Science in Sports & Exercise: October 2010 - Volume 42 - Issue 10 - pp 1853-1860
doi: 10.1249/MSS.0b013e3181da4f7d
Basic Sciences

Introduction: The role of mast cells in the airway response to exercise and the benefit of sodium cromoglycate (SCG) in athletes are unclear.

Purpose: The purpose of this study was to clarify the role of mast cell mediators in the airway response to exercise in athletes and to investigate the effect of SCG.

Methods: Eleven athletes with exercise-induced bronchoconstriction (EIB+) and 11 without (EIB) performed a eucapnic voluntary hyperpnea (EVH) test (a surrogate for exercise) 10 min after inhalation of a placebo or 40 mg of the mast cell stabilizing agent sodium cromoglycate. The urinary concentrations of 9a,11β-PGF2 (a metabolite of PGD2 and a marker of mast cell activation) and leukotriene E4 (LTE4) were measured by enzyme immunoassay 60 min before and for 90 min after the challenge.

Results: In the EIB+ group, the maximum fall in forced expiratory volume in 1 s (FEV1) of 20.3% ± 3% on placebo was reduced to 11.5% ± 1.9% after SCG (P = 0.003). There was an increase in the urinary excretion of 9α,11β-PGF2 on the placebo day after EVH in both groups (P < 0.05) that was abolished by SCG. In the EIB+ group, there was also an increase of urinary LTE4 on the placebo day that was abolished by SCG, whereas the urinary excretion of LTE4 was inconsistent in the EIB group.

Conclusions: The results support mast cell activation with release of bronchoconstrictive mediators after hyperpnea in athletes with and without EIB and inhibition by SCG. The degree of airway responsiveness to the specific mediator released is likely to determine whether or not bronchoconstriction will occur after EVH.

1Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, AUSTRALIA; 2Centre for Sports Medicine and Human Performance, Brunel University, West London, UNITED KINDOM; 3Division of Physiology, The National Institute of Environmental Medicine at Karolinska Institutet, Stockholm, SWEDEN; 4Centre for Allergy Research at Karolinska Institutet, Stockholm, SWEDEN; and 5Division of Respiratory Medicine and Allergy, Department of Medicine at Karolinska University Hospital Huddinge, Stockholm, SWEDEN

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

Submitted for publication December 2009.

Accepted for publication February 2010.

©2010The American College of Sports Medicine