Exercise therapy (voluntary wheel running) rescued dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restored exercise capacity in mice with cardiometabolic HFpEF.
Does exercise therapy (voluntary wheel running) improve skeletal muscle dysfunction and exercise intolerance in mice with cardiometabolic HFpEF?
Exercise therapy restores exercise capacity and rescues skeletal muscle metabolic dysfunction in a murine model of cardiometabolic HFpEF.
Exercise intolerance, a hallmark of heart failure with preserved ejection fraction (HFpEF) exacerbated by obesity, involves unclear mechanisms related to skeletal muscle metabolism. In a "2-hit" model of HFpEF, we investigated the ability of exercise therapy (voluntary wheel running) to reverse skeletal muscle dysfunction and exercise intolerance. Using state-of-the-art metabolic cages and a multiomic approach, we demonstrate exercise can rescue dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restore exercise capacity in mice with cardiometabolic HFpEF. These results underscore the importance of skeletal muscle metabolism to improve exercise intolerance in HFpEF.
Quiriarte et al. (Wed,) conducted a other in Cardiometabolic HFpEF. Exercise therapy (voluntary wheel running) was evaluated on Skeletal muscle dysfunction and exercise intolerance. Exercise therapy (voluntary wheel running) rescued dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restored exercise capacity in mice with cardiometabolic HFpEF.