PT  - JOURNAL ARTICLE
AU  - Erlend Hassel
AU  - Anne Marie Ormbostad Berre
AU  - Anne Jarstein Skjulsvik
AU  - Ulrik Wisløff
AU  - Sigurd Loe Steinshamn
TI  - Cardiovascular effects of exercise training in an animal model of COPD
DP  - 2014 Sep 01
TA  - European Respiratory Journal
PG  - P601
VI  - 44
IP  - Suppl 58
4099  - http://erj.ersjournals.com/content/44/Suppl_58/P601.short
4100  - http://erj.ersjournals.com/content/44/Suppl_58/P601.full
SO  - Eur Respir J2014 Sep 01; 44
AB  - Exercise has been shown to improve cardiac function in COPD, but little is known about mechanisms involved.Aim:Study the effects of exercise on the cardiovascular system in a mouse model of COPD.Methods:42 female A/JOlaHsd mice were randomized to exposure to either cigarette smoke (CS) or air (FA) for 6 h/day, 5 d/w for 14 weeks. The mice were then kept sedentary (Sed) or put through treadmill interval training (IT) for 4 weeks. Echocardiography was performed and the mice were then killed and the lungs were histomorphometrically analyzed. Airspace enlargement was assessed by mean linear intercept (MLI) and sections stained with antibodies to smooth muscle actin/vonWillenbrand were used to quantify degree of pulmonary artery remodeling.Results:View this table:CS exposure led to significant airspace enlargement (P=.026). IT led to increased VO2peak (p<0.001). TAPSE was decreased by CS exposure (p=0.008), and attenuated by interval training (p<0.001). Pulmonary vessel muscularization was reduced by IT (p=0.04). There were no significant effects on left ventricle.Conclusions:In this COPD model we found that smoke exposure led to significant reduction in right ventricular function, and this reduction was attenuated by treadmill running. A reduction of pulmonary vessel muscularization due to exercise training may contribute to this improvement in right ventricular function.