Abstract
Despite the well-known impact of exercise training in the prevention of cardiovascular diseases, few studies have been made to clarify the effects of exercise training in non-ischemic cardiomyopathies. In this study, we focused on the role of voluntary exercise training in a murine model of dilated cardiomyopathy (αMHC-MerCreMer:Sf/Sf) induced by cardiac-specific and tamoxifen-inductible inactivation of the Serum Response Factor. Seven days after tamoxifen injection, twenty-two mice αMHC-MerCreMer:Sf/Sf mice were allocated to sham (n=8, sedentary) and treated (n=14, voluntary wheel running) groups. In addition, seven αMHCMerCreMer: Sf/Sf mice without tamoxifen treatment were used as control. Treated group underwent four weeks of voluntary exercise on wheel (run 1.65±0.25 km/d). Cardiac function, fibrosis content and energetic metabolism were then blindly assessed in all animals. In treated group, fractional shortening declined less compared to sedentary group. This correlated with a lesser degree of LV remodeling, as LV end-diastolic and end-systolic diameters increased less from baseline values in exercised group compared to sedentary animals. Exercised animals also displayed a reduced gene expression of the stress-induced atrial and brain natriuretic factors. These protective effects were accompanied by a reduction of myocardial fibrosis. Moreover, exercise induces Peroxisome proliferator-activated receptor ©coactivator 1-alpha and mitochondrial aconitase protein levels suggesting that enhancement of mitochondrial biogenesis and/or metabolism slow down the progression of dilated cardiomyopathy. These results strongly support the interest of voluntary exercise training to the non-ischemic heart failure outcome with potential for its clinical use in the future. The author hereby declares no conflict of interest
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have