A previous study by our group showed that regular exercise training (ET) attenuated pulmonary injury in an experimental model of chronic exposure to cigarette smoke (CS) in mice, but the time-course effects of the mechanisms involved in this protection remain poorly understood. We evaluated the temporal effects of regular ET in an experimental model of chronic CS exposure. MaleC57BL/6 mice were divided into four groups: Control (sedentary+air), Exercise (aerobic training+air), Smoke (sedentary+smoke) and Smoke+Exercise (aerobic training+smoke). Mice were exposed to CS and ET for 4, 8 or 12 weeks. Exercise protected mice exposed to CS from emphysema and reductions in tissue damping and tissue elastance after 12 weeks (P<0.01). The total number of inflammatory cells in the BAL increased in the Smoke group, mainly due to the recruitment of macrophages after 4 weeks, neutrophils and lymphocytes after 8 weeks and lymphocytes and macrophages after 12 weeks (P<0.01). Exercise attenuated this increase in mice exposed to CS. The protection conferred by exercise was mainly observed after exercise adaptation. Exercise increased IL-6 and IL-10 in the quadriceps and lungs (P<0.05) after 12 weeks. Total antioxidant capacity and SOD was increased and TNF-α and oxidants decreased in lungs of mice exposed to CS after 12 weeks (P<0.05). The protective effects of exercise against lung injury induced by cigarette smoke exposure suggests that anti-inflammatory mediators and anti-oxidant enzymes play important roles in COPD development mainly after the exercise adaptation.
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