AbstractBackground Repeated and prolonged inhalation of cold air is believed to be the cause of the high incidence and prevalence of exercise-induced bronchoconstriction and asthma in winter endurance athletes. There is strong evidence that the sustained bronchoconstriction after exercise and dry air hyperpnea challenges is due to the release of leukocyte-derived inflammatory mediators in the airways.Objective To examine whether a heat- and moisture-exchanging breathing device (HME) attenuates release of Type-2 inflammatory biomarkers into the airways following an exercise challenge in sub-zero temperatures among individuals without asthma.Design Randomized, cross-over design.Setting Laboratory test in environmental chamber (−15°C, 1.3 g/m2 absolute humidity, and 70% relative humidity). Participants 23 healthy, recreational-competitive athletes from a range of endurance sports, aged 18–53 years, completed the study. Exclusion criteria included current use of prescription medication (except hormonal contraceptives), recent respiratory illness, physician-diagnosed asthma, or symptoms of airborne allergies.Interventions Participants performed a 30-min warm-up followed by a 4-min maximal, self-paced running time trial, with and without HME. Main Outcome Measurements Concentrations of the acute inflammatory mediators Leukotriene E4 (LTE4) and 11β-Prostaglandin F2α (11β-PGF2α) were measured in urine pre- and 60 min post-exercise using enzyme immunoassay.Results Data were log-transformed and analyzed using repeated-measures ANOVA. LTE4 decreased from pre- to post-exercise (p < 0.001). Although there was no significant time × trial interaction, Bonferroni post-hoc tests indicated a significant post-exercise decrease in LTE4 in the HME trial only (p = 0.042). There was no effect of exercise alone nor HME on 11β-PGF2α responses to exercise.Conclusions Urinary LTE4 and 11β-PGF2α levels did not increase after an exercise challenge in participants without asthma, although LTE4 levels were nevertheless mildly attenuated by HME use, indicative of a mild protective effect of HME, in line with previous findings from this project.¹Referencehttps://doi.org/10.1007/s00421–022–04939-x
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