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RationaleParticipation in high-intensity exercise in early life might act as stressor to the airway barrier.ObjectivesTo investigate the effect of intense exercise and associated exposure to air pollution on the airway barrier in adolescent elite athletes compared with healthy controls and to study exercise-induced bronchoconstriction (EIB) in this population.MethodsEarly-career elite athletes attending ‘Flemish-Elite-Sports-Schools’ (12–18 years) of 4 different sport disciplines (n=90) and control subjects (n=25) were recruited. Presence of EIB was tested by the eucapnic voluntary hyperventilation (EVH) test. Markers at mRNA and protein level; RNA-sequencing; carbon load in airway macrophages were studied on induced sputum samples.Results444 genes were differentially expressed in sputum from athletes compared with controls, which were related to inflammation and epithelial cell damage and sputum samples of athletes contained significantly more carbon loaded airway macrophages compared with controls (24%, 95% CI 20% to 36%, p10and PM2.5exposure.ConclusionEarly-career elite athletes showed increased markers of air pollution exposure, epithelial damage and airway inflammation compared with controls. Acute exposure to increased air pollution PM10levels was linked to increased airway hyper-reactivity.Trial registration numberNCT03587675.

Several studies have already identified atopy as a risk factor for the development of exercise-induced bronchoconstriction (EIB) in adult elite athletes (1-3). Skin prick test or serum specific IgE to common aero-allergens is used to determine the patient's atopy status (4). In 2009, Bonini M et al. introduced a screening tool to predict atopy in elite adult athletes, namely the Allergy Questionnaire for Athletes or short the AQUA© questionnaire (5). This article is protected by copyright. All rights reserved. ispartof: PEDIATRIC ALLERGY AND IMMUNOLOGY vol:29 issue:6 pages:648-650 ispartof: location:England status: published

Introduction: Exercise-induced bronchoconstriction (EIB) is more common in athletes compared to the general population. The eucapnic voluntary hyperventilation test is used to detect EIB in adult athletes. It is however unclear whether this technique is also applicable to young athletes. Methods Young athletes (basketball (n = 13), football (n = 19), swimming (n = 12)) were recruited at the start of their elite sports career (12–14 years). Eight age-matched controls were also recruited. Eucapnic voluntary hyperventilation test was performed according to ATS guidelines in all subjects. A second (after 1 year, n = 32) and third (after 2 years, n = 39) measurement was performed in a subgroup of athletes and controls. Results At time of first evaluation, 3/13 basketball players, 4/19 football players, 5/11 swimmers and 1/8 controls met criteria for EIB (fall in FEV 1 ≥10% after EVH). A ventilation rate of >85% of the maximal voluntary ventilation (MVV) is recommended by current guidelines (for adults) but was only achieved by a low number of individuals (first occasion: 27%, third occasion: 45%) However, MVV in young athletes corresponds to 30 times FEV 1 , which is equivalent to 85% of MVV in adults. A threshold of 70% of MVV (21 times FEV 1 ) is feasible in the majority of young athletes. Conclusion EIB is present in a substantial number of individuals at the age of 12–14 years, especially in swimmers. This underscores the importance of screening for EIB at this age. EVH is feasible in young elite athletes, however target ventilation needs to be adjusted accordingly.

Background Daily intensive exercise by elite athletes can result in exercise-induced asthma especially in elite swimmers and this may be linked to epithelial damage. Objective To study airway epithelial damage and release of damage-associated molecular patterns (DAMPs) after intensive exercise in elite athletes and controls. Methods We recruited competitive swimmers (n = 26), competitive indoor athletes (n = 13) and controls (n = 15) without any history of asthma. Lung function was measured before, immediately after and 24 h after a 90-min intensive exercise protocol. Sputum induction was performed at baseline and 24 h after exercise. Exercise-induced bronchoconstriction (EIB) was assessed by the eucapnic voluntary hyperventilation test. Results Baseline sputum uric acid, high mobility group box-1, CXCL8 mRNA, sputum neutrophils and serum Clara cell protein-16 (CC-16) were significantly higher in competitive swimmers compared with controls. Intensive swimming for 90 min resulted in an increase of sputum IL-1β, IL-6 and TNF mRNA in competitive swimmers, and of sputum IL-6 mRNA and sputum neutrophils in controls. Although all participants were asymptomatic, seven competitive swimmers, one indoor athlete and one control met the criteria for EIB. Conclusion Our findings show that the intensive training combined with exposure to by-products of chlorination induces airway epithelial damage in competitive swimmers. This is associated with increased damage-associated molecular patterns, innate cytokine release and neutrophilic airway inflammation.