Authors: Timothy Allerton, Jake Doiron, Mahmoud Elbatreek, Zhen Li, James Stampley, Gregory Davis, Robert Noland, Brian Irving, Thomas Sharp, Huijing Xia, Sanjiv Shah, David Lefer
Published: 2024-10-09
DOI: 10.1161/res.135.suppl_1.tu104
Source: Full article
Introduction: Cardiometabolic heart failure with preserved ejection fraction (HFpEF) results in severe exercise intolerance. Dysregulated skeletal muscle metabolism and mitochondrial function are key drivers of exercise intolerance in cardiometabolic HFpEF. Mitochondrial hydrogen sulfide (H2S) generated by 3-mercaptopyruvate sulfur transferase (3-MST) exerts potent bioenergetic properties. We have recently shown that H2S bioavailability is significantly attenuated in HFpEF. The role of H2S in skeletal muscle metabolism and exercise tolerance in HFpEF is currently unknown.