Highlights
Patients with heart failure with reduced ejection fraction (HFrEF) showed higher resting skeletal muscle myosin ATP consumption than matched controls, supporting the concept that peripheral muscle energetics are intrinsically abnormal in this syndrome.
Proteomics identified distinct regulation of acetyl-lysine sites in HFrEF skeletal muscle, suggesting that post-translational remodeling may contribute to altered contractile protein behavior and inefficient energy use.
