Objectives:To examine evidence of exercise-induced bronchoconstriction (EIB) defined as ≥10% reduction in forced expiratory volume in one second (FEV 1 ) and exercise-induced arterial hypoxemia (EIAH) defined as ≥4% reduction in oxygen saturation (SpO 2 ) from before to after participation in the Norseman Xtreme Triathlon. Secondarily, to assess whether changes in FEV 1 and SpO 2 are related to respiratory symptoms, training volume, and race time. Methods: In this quasi-experimental non-controlled study, we included 63 triathletes (50♂/13♀) aged 40.3 (±9.0) years (mean ± SD). Fifty-seven (46♂/11♀) measured lung function and 54 (44♂/10♀) measured SpO 2 before the race, 8-10 minutes after the race (post-test 1) and the day after the race (post-test 2). Respiratory symptoms and training volume were recorded with modified AQUA questionnaire. ANOVA for repeated measures was used to detect differences in lung function and SpO 2 .Statistical significance was accepted at 0.05 level. Results: Twenty-six participants (46%) presented with EIB at post-test 1 and 16 (28%) at post-test 2. Lung function variables were significantly reduced from baseline to post-test 1 and 2. Thirty-five participants (65%) showed evidence of mild to moderate EIAH. No significant correlations were observed except a weak correlation between maximal reduction in FEV 1 and respiratory symptoms (r = 0.35, P = .016). Conclusion: Our results demonstrated that 46% of the participants presented with EIB and 65% showed evidence of EIAH after the Norseman Xtreme Triathlon. Changes in FEV 1 and SpO 2 were not correlated to weekly training hours or race time. We observed a weak correlation between maximal reduction in FEV 1 and respiratory symptoms. K E Y W O R D S exercise-induced arterial hypoxemia, exercise-induced bronchoconstriction, triathletes | 1009 STENSRUD ET al.

Regular physical activity decreases the risk of cardiovascular disease, type II diabetes, obesity, certain cancers, and all-cause mortality. Nevertheless, there is mounting evidence that extreme exercise behaviors may be detrimental to human health. This review collates several decades of literature on the physiology and pathophysiology of ultra-marathon running, with emphasis on the cardiorespiratory implications. Herein, we discuss the prevalence and clinical significance of postrace decreases in lung function and diffusing capacity, respiratory muscle fatigue, pulmonary edema, biomarkers of cardiac injury, left/right ventricular dysfunction, and chronic myocardial remodeling. The aim of this article is to inform risk stratification for ultra-marathon and to edify best practice for personnel overseeing the events (i.e., race directors and medics).

Respiratory function has become a global health priority. Not only is chronic respiratory disease a leading cause of worldwide morbidity and mortality, but the COVID-19 pandemic has heightened attention on respiratory health and the means of enhancing it. Subsequently, and inevitably, the respiratory system has become a target of the multi-trillion-dollar health and wellness industry. Numerous commercial, respiratory-related interventions are now coupled to therapeutic and/or ergogenic claims that vary in their plausibility: from the reasonable to the absurd. Moreover, legitimate and illegitimate claims are often conflated in a wellness space that lacks regulation. The abundance of interventions, the range of potential therapeutic targets in the respiratory system, and the wealth of research that varies in quality, all confound the ability for health and exercise professionals to make informed risk-to-benefit assessments with their patients and clients. This review focuses on numerous commercial interventions that purport to improve respiratory health, including nasal dilators, nasal breathing, and systematized breathing interventions (such as pursed-lips breathing), respiratory muscle training, canned oxygen, nutritional supplements, and inhaled l-menthol. For each intervention we describe the premise, examine the plausibility, and systematically contrast commercial claims against the published literature. The overarching aim is to assist health and exercise professionals to distinguish science from pseudoscience and make pragmatic and safe risk-to-benefit decisions.

Water transport and local (airway) hydration are critical for the normal functioning of lungs and airways. Currently, there is uncertainty regarding the effects of systemic dehydration on pulmonary function. Our aims were: i) to clarify the impact of exercise- or fluid restriction-induced dehydration on pulmonary function in healthy adults; and ii) to establish whether systemic or local rehydration can reverse dehydration-induced alterations in pulmonary function. Ten healthy participants performed four experimental trials in a randomized order (2 h exercise in the heat twice, and 28 h fluid restriction twice). Pulmonary function was assessed using spirometry and whole-body plethysmography in the euhydrated, dehydrated, and rehydrated states. Oral fluid consumption was used for systemic rehydration, and nebulized isotonic saline inhalation for local rehydration. Both exercise and fluid restriction induced mild dehydration (2.7±0.7% and 2.5±0.4% body mass loss, respectively; p<0.001) and elevated plasma osmolality (p<0.001). Dehydration across all four trials was accompanied by a reduction in forced vital capacity (152±143 mL, p<0.01) and concomitant increases in residual volume (216±177 mL, p<0.01) and functional residual capacity (130±144 mL, p<0.01), with no statistical differences between modes of dehydration. These changes were normalized by fluid consumption, but not nebulization. Our results suggest that, in healthy adults: i) mild systemic dehydration induced by exercise or fluid restriction leads to pulmonary function impairment, primarily localized to small airways; and ii) systemic, but not local, rehydration reverses these potentially deleterious alterations.