Background: Right ventricular dysfunction in COPD is common, even in the absence of pulmonary hypertension.\nThe aim of the present study was to examine the effects of high intensity interval training (HIIT) on right ventricular\n(RV) function, as well as pulmonary blood vessel remodeling in a mouse model of COPD.\nMethods: 42 female A/JOlaHsd mice were randomized to exposure to either cigarette smoke or air for 6 hours/day,\n5 days/week for 14 weeks. Mice from both groups were further randomized to sedentariness or HIIT for 4 weeks.\nCardiac function was evaluated by echo cardiography and muscularization of pulmonary vessel walls by\nimmunohistochemistry.\nResults: Smoke exposure induced RV systolic dysfunction demonstrated by reduced tricuspid annular plane systolic\nexcursion. HIIT in smoke-exposed mice reversed RV dysfunction. There were no significant effects on the left\nventricle of neither smoke exposure nor HIIT. Muscularization of the pulmonary vessels was reduced after exercise\nintervention, but no significant effects on muscularization were observed from smoke exposure.\nConclusions: RV function was reduced in mice exposed to cigarette smoke. No Increase in pulmonary vessel\nmuscularization was observed in these mice, implying that other mechanisms caused the RV dysfunction. HIIT\nattenuated the RV dysfunction in the smoke exposed mice. Reduced muscularization of the pulmonary vessels due\nto HIIT suggests that exercise training not only affects the heart muscle, but also has important effects on the\npulmonary vasculature.
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