title: Effects of exercise training on pulmonary vessel muscularization and right ventricular function in an animal model of COPD.
abstract: BACKGROUND
  Right ventricular dysfunction in COPD is common, even in the absence of pulmonary hypertension. The aim of the present study was to examine the effects of high intensity interval training (HIIT) on right ventricular (RV) function, as well as pulmonary blood vessel remodeling in a mouse model of COPD.
  
  
  METHODS
  42 female A/JOlaHsd mice were randomized to exposure to either cigarette smoke or air for 6 hours/day, 5 days/week for 14 weeks. Mice from both groups were further randomized to sedentariness or HIIT for 4 weeks. Cardiac function was evaluated by echocardiography and muscularization of pulmonary vessel walls by immunohistochemistry.
  
  
  RESULTS
  Smoke exposure induced RV systolic dysfunction demonstrated by reduced tricuspid annular plane systolic excursion. HIIT in smoke-exposed mice reversed RV dysfunction. There were no significant effects on the left ventricle of neither smoke exposure nor HIIT. Muscularization of the pulmonary vessels was reduced after exercise intervention, but no significant effects on muscularization were observed from smoke exposure.
  
  
  CONCLUSIONS
  RV function was reduced in mice exposed to cigarette smoke. No Increase in pulmonary vessel muscularization was observed in these mice, implying that other mechanisms caused the RV dysfunction. HIIT attenuated the RV dysfunction in the smoke exposed mice. Reduced muscularization of the pulmonary vessels due to HIIT suggests that exercise training not only affects the heart muscle, but also has important effects on the pulmonary vasculature.
authors.forename: Erlend
authors.initials: E
authors.lastname: Hassel
authors.forename: Anne Marie
authors.initials: AM
authors.lastname: Berre
authors.forename: Anne Jarstein
authors.initials: AJ
authors.lastname: Skjulsvik
authors.forename: Sigurd
authors.initials: S
authors.lastname: Steinshamn
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005081:Exercise Therapy; D005260:Female; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000503:physiopathology*; D011651:Pulmonary Artery / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D011656:Pulmonary Emphysema / Q000503:physiopathology / Q000628:therapy; D020127:Recovery of Function; D012906:Smoke; D013997:Time Factors; D066253:Vascular Remodeling; D018497:Ventricular Dysfunction, Right / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D016278:Ventricular Function, Right
chemical_list: D012906:Smoke