Physiol Rep. 2026 Aug;14(16):e71071. doi: 10.14814/phy2.71071.
ABSTRACT
Ozone (O) is a photochemical air pollutant known to reduce lung function and induce respiratory symptoms. This study aimed to determine whether breathing route influences O-induced lung function changes during exercise. Thirteen recreationally active participants (6 females, V̇Opeak = 45.8 ± 5.3 mL/kg/min), with no history of cardiovascular or pulmonary disease or exercise-induced bronchoconstriction, completed a double-blind crossover study with four experimental visits. Participants performed 30 min of low-intensity cycling (90% of power at the first ventilatory threshold) while breathing exclusively nasally or orally under room air or 0.40 ppm O. Spirometry was assessed before and after each trial, and dyspnea (Multidimensional Dyspnea Profile) every 5 min during exercise. O exposure impaired pulmonary function, reducing FEV, FVC, PEF, FEF25-75, and FEV/FVC (all p < 0.05). Regardless of environmental condition, oral breathing produced modestly greater post-exercise reductions in FEV, PEF, FEF25-75, and FEV/FVC than nasal breathing, but no breathing route × environment interaction was observed. Nasal breathing was associated with greater breathing effort and air hunger (p < 0.05). Thus, O exposure impaired pulmonary function and increased dyspnea regardless of breathing route. Although nasal breathing slightly attenuated overall post-exercise lung function decline, it did not protect against O-induced pulmonary impairment and increased breathing discomfort during exercise.
PMID:42638389 | DOI:10.14814/phy2.71071