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The mechanisms responsible for driving endogenous airway hyperresponsiveness (AHR) in the form of exercise-induced bronchoconstriction (EIB) are not fully understood. We examined alterations in airway phospholipid hydrolysis, surfactant degradation, and lipid mediator release in relation to AHR severity and changes induced by exercise challenge. Paired induced sputum ( n = 18) and bronchoalveolar lavage (BAL) fluid ( n = 11) were obtained before and after exercise challenge in asthmatic subjects. Samples were analyzed for phospholipid structure, surfactant function, and levels of eicosanoids and secreted phospholipase A 2 group 10 (sPLA 2 -X). A primary epithelial cell culture model was used to model effects of osmotic stress on sPLA 2 -X. Exercise challenge resulted in increased surfactant degradation, phospholipase activity, and eicosanoid production in sputum samples of all patients. Subjects with EIB had higher levels of surfactant degradation and phospholipase activity in BAL fluid. Higher basal sputum levels of cysteinyl leukotrienes (CysLTs) and prostaglandin D 2 (PGD 2 ) were associated with direct AHR, and both the postexercise and absolute change in CysLTs and PGD 2 levels were associated with EIB severity. Surfactant function either was abnormal at baseline or became abnormal after exercise challenge. Baseline levels of sPLA 2 -X in sputum and the absolute change in amount of sPLA 2 -X with exercise were positively correlated with EIB severity. Osmotic stress ex vivo resulted in movement of water and release of sPLA 2 -X to the apical surface. In summary, exercise challenge promotes changes in phospholipid structure and eicosanoid release in asthma, providing two mechanisms that promote bronchoconstriction, particularly in individuals with EIB who have higher basal levels of phospholipid turnover.

Exercise is a common trigger of bronchoconstriction. In recent years, there has been increased understanding of the pathophysiology of exercise-induced bronchoconstriction. Although evaporative water loss and thermal changes have been recognized stimuli for exercise-induced bronchoconstriction, accumulating evidence points toward a pivotal role for the airway epithelium in orchestrating the inflammatory response linked to exercise-induced bronchoconstriction. Overproduction of inflammatory mediators, underproduction of protective lipid mediators, and infiltration of the airways with eosinophils and mast cells are all established contributors to exercise-induced bronchoconstriction. Sensory nerve activation and release of neuropeptides maybe important in exercise-induced bronchoconstriction, but further research is warranted., (Copyright © 2018 Elsevier Inc. All rights reserved.)

This article summarizes the findings of an expert panel of nationally recognized allergists and pulmonologists who met to discuss how to improve detection and diagnosis of exercise-induced bronchoconstriction (EIB), a transient airway narrowing that occurs during and most often after exercise in people with and without underlying asthma. EIB is both commonly underdiagnosed and overdiagnosed. EIB underdiagnosis may result in habitual avoidance of sports and physical activity, chronic deconditioning, weight gain, poor asthma control, low self-esteem, and reduced quality of life. Routine use of a reliable and valid self-administered EIB screening questionnaire by professionals best positioned to screen large numbers of people could substantially improve the detection of EIB. The authors conducted a systematic review of the literature that evaluated the accuracy of EIB screening questionnaires that might be adopted for widespread EIB screening in the general population. Results of this review indicated that no existing EIB screening questionnaire had adequate sensitivity and specificity for this purpose. The authors present a call to action to develop a new EIB screening questionnaire, and discuss the rigorous qualitative and quantitative research necessary to develop and validate such an instrument, including key methodological pitfalls that must be avoided., (Copyright © 2014 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Rationale: Exercise-induced bronchoconstriction (EIB) is a highly prevalent condition with unclear pathogenesis. Two competing theories of the pathogenesis of EIB differ regarding the inflammatory basis of this condition., Objectives: Our goals were to establish whether epithelial cell and mast cell activation with release of inflammatory mediators occurs during EIB and how histamine and cysteinyl leukotriene antagonists alter the airway events occurring during EIB., Methods: Induced sputum was used to measure mast cell mediators and eicosanoids at baseline and 30 minutes after exercise challenge in 25 individuals with asthma with EIB. In a randomized, double-blind crossover study, the cysteinyl leukotriene antagonist montelukast and antihistamine loratadine or two matched placebos were administered for two doses before exercise challenge., Main Results: The percentage of columnar epithelial cells in induced sputum at baseline was associated with the severity of EIB. After exercise challenge, histamine, tryptase, and cysteinyl leukotrienes significantly increased and prostaglandin E(2) and thromboxane B(2) significantly decreased in the airways, and there was an increase in columnar epithelial cells in the airways. The concentration of columnar epithelial cells was associated with the levels of histamine and cysteinyl leukotrienes in the airways. Treatment with montelukast and loratadine inhibited the release of cysteinyl leukotrienes and histamine into the airways, but did not inhibit the release of columnar epithelial cells into the airways., Conclusions: These data indicate that epithelial cells, mast cell mediators, and eicosanoids are released into the airways during EIB, supporting an inflammatory basis for EIB.

Study Objective: To determine the effect of an aerobic conditioning program on fitness, respiratory physiology, and resting lung function in patients with mild asthma., Design: Prospective cohort study., Setting: Outpatient rehabilitation facility., Methods: Five patients with mild intermittent asthma and five normal control subjects completed a 10-week aerobic conditioning program. Pulmonary function studies and noninvasive cardiopulmonary exercise tests were performed before and after the conditioning program., Results: After aerobic conditioning, there were significant gains in maximum oxygen consumption (VO(2)max; 22.73 mL/kg/min vs 25.29 mL/kg/min, p = 0.01, asthma; 22.94 mL/kg/min vs 27.85 mL/kg/min, p = 0.03, control) and anaerobic threshold (0.99 L/min vs 1.09 L/min, p = 0.03, asthma; 0.89 L/min vs 1.13 L/min, p = 0.01, control) in both groups. Although FEV(1) was unchanged, the maximum voluntary ventilation (MVV) improved in the asthma group (96.0 L/min vs 108.2 L/min, p = 0.08, asthma; 134.0 L/min vs 131.2 L/min, p = 0.35, control). During exercise, minute ventilation (VE) for each level of work was decreased in the asthma group after conditioning, while little change occurred in the control group (68. 48 L/min vs 51.70 L/min at initial VO(2)max, p = 0. 02, asthma; 65.82 L/min vs 63.12 L/min at initial VO(2)max, p = 0.60, control). A significant decrease in the ventilatory equivalent (VE/oxygen consumption, 40.8 vs 30.4 at VO(2)max, p = 0.02, asthma; 37.2 vs 35.8 4 at VO(2)max, p = 0.02, control) and the dyspnea index (VE/MVV) at submaximal (0.44 vs 0.38, p = 0.05, asthma; 0.32 vs 0.38, p < 0.01, control) and maximal exercise (0.72 vs 0.63, p = 0.03, asthma; 0.49 vs 0.62, p = 0.02, control) occurred in the asthma group., Conclusions: Exercise rehabilitation improves aerobic fitness in both asthmatic and nonasthmatic participants of a 10-week aerobic fitness program. Additional benefits of improved ventilatory capacity and decreased hyperpnea of exercise occurred in patients with mild asthma.