Abstract
A growing number of studies have shown that obesity induces airway hyperresponsiveness (AHR). AHR is a hallmark of asthma and several studies show a relation between obesity and development of asthmatic phenotype. Moderate intensity aerobic training (AT) inhibits asthma phenotype in experimental models of asthma, but the effects of AT on pulmonary response in a model of diet-induced obesity are unknown. Thus, 80 C57Bl/6 male mice were distributed in Control Lean (CL), Exercise Lean (EL), Obese (O) and Obese+Exercise (OE) groups (n=20). Obesity was induced by a classical model of diet-induced obesity (DIO) using high fat and hypercaloric diet. Treadmill aerobic training was performed for 4 weeks after the establishment of obesity and DIO remained during the whole protocol. The results demonstrated that AT reduced DIO-induced AHR for 25mg/mL (p<0.05) and 50mg/mL (p<0.05) of methacholine. AT also reduced DIO-induce pulmonary inflammation, as noted by reduced number of macrophages in bronchoalveolar lavage (BAL) (p<0.01), as well as by reduced levels of IL-1beta (p<0.01), IL-12p40 (p<0.01), IL-17 (p<0.01) and TNF-alpha (p<0.01) in BAL, while increased the levels of anti-inflammatory cytokine IL-10 (p<0.01). AT also reduced DIO-induced increases in leptin levels in blood (p<0.01) and in BAL (p<0.01). Parenchymal macrophages were also reduced in mice from OE group. Therefore, this study showed for the first time that AT reduces lung inflammation and AHR in a model of DIO-induced obesity and that anti-inflammatory IL-10 and leptin may be involved in these beneficial effects.
- Copyright ©the authors 2016