Abstract

Background: Exercise-induced bronchoconstriction (EIB) is a transient airway narrowing, occurring during or shortly after intensive exercise in non-asthmatic elite athletes. Often, these athletes are also exposed to harmful environmental conditions such as diesel exhaust particles (DEP) at high ventilation rates during intensive training. Objective: To develop a mouse model of EIB and to investigate the influence of DEP-induced exacerbations on acute respiratory responses, lung inflammation and lung physiology in this model. Methods: Balb/c mice were intranasally challenged 5 days a week for 3 weeks long with saline or 0.2 mg/ml DEP, prior to an incremental running protocol or resting period. Once a week, early respiratory responses were measured using a double chamber plethysmograph. At day 24, mice were sacrificed to determine lung function, such as airway resistance, FEV0.1 and FVC. Broncho-alveolar lavage was performed to determine airway inflammation and involvement of cytokines and DAMPS. Results: Submaximal exercise resulted in a decreased peak inspiratory flow (immediately after exercise) and an improved FEV0.1, which were both not influenced by DEP exposure. Yet, DEP induced neutrophilic airway inflammation but it was not enhanced when combining with exercise. However, DEP uptake in lung macrophages appears to be higher in combination with exercise. Conclusion: Changes in acute respiratory responses, such as PIF, indicate that submaximal exercise results in EIB, independently from DEP exposure. Moreover, exercising mice did not show an exacerbation response upon DEP exposure. However, more research is needed to identify underlying mechanisms of exercise-induced acute responses.

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