Obesity results in decreased lung function and increased inflammation. Moderate aerobic exercise (AE) reduced lung inflammation and remodeling in a variety of respiratory disease models. Therefore, this study investigated whether AE can attenuate a diet-induced obesity respiratory phenotype; including airway hyper-responsiveness (AHR), remodeling and inflammation.Methods:
Sixty C57Bl/6 male mice were distributed into four groups: control lean (CL), exercise lean (EL), obese (O) and obese exercise (OE) groups (2 sets of 7 and 8 mice per group; n=15). A classical model of diet-induced obesity (DIO) over 12weeks was used. AE was performed 60min/day, 5days/week for 5weeks. Airway hyperresponsiveness (AHR), lung inflammation and remodeling, adipokines and cytokines in bronchoalveolar lavage (BAL) was determined.Results:
A high fat diet over 18weeks significantly increased body weight (p<.0001). Five weeks of AE significantly reduced both AHR and pulmonary inflammation. AHR in obese mice that exercised was reduced at the basal level (p<.05), vehicle (PBS) (p<.05), 6.25 MCh mg/mL (p<.05), 12.5 MCh mg/mL (p<.01), 25 MCh mg/mL (p<.01) and 50 MCh mg/mL (p<.05). Collagen (p<.001) and elastic (p<.001) fiber deposition in airway wall and also smooth muscle thickness (p<.001) were reduced. The number of neutrophils (p<.001), macrophages (p<.001) and lymphocytes (p<.01) were reduced in the peribronchial space as well as in the BAL: lymphocytes (p<.01), macrophages (p<.01), neutrophils (p<.001). AE reduced obesity markers leptin (p<.001), IGF-1 (p<.01) and VEGF (p<.001), while increased adiponectin (p<.01) in BAL. AE also reduced pro-inflammatory cytokines in the BAL: IL-1β (p<.001), IL-12p40 (p<.001), IL-13 (p<.01), IL-17 (p<.001, IL-23 (p<.05) and TNF-alpha (p<.05), and increased anti-inflammatory cytokine IL-10 (p<.05).Conclusions:
Aerobic exercise reduces high fat diet-induced obese lung phenotype (AHR, pulmonary remodeling and inflammation), involving anti-inflammatory cytokine IL-10 and adiponectin.