n-3 PUFA-Enriched Diet Preserves Skeletal Muscle Mitochondrial Function and Redox State and Prevents Muscle Mass Loss in Mice with Chronic Heart Failure

Rationale and Methods: Skeletal muscle derangements, potentially including mitochondrial dysfunction with altered dynamics high reactive oxygen species (ROS) generation, may lead to protein catabolism wasting, resulting in low exercise capacity reduced survival chronic heart failure (CHF). We hypothesized that 8-week n-3-PUFA isocaloric partial dietary replacement (Fat = 5.5% total cal; EPA + DHA 27% fat) normalizes gastrocnemius (GM) regulators, tissue pro-oxidative changes, catabolic preserved GM mass rodent CHF [Myocardial infarction (MI)-induced by coronary artery ligation, left-ventricular ejection fraction <50%]. Results: Compared control animals (Sham), had a higher fission-fusion ratio, ATP ROS production, pro-inflammatory insulin signalling. normalized all derangements the state (oxidized glutathione ratio), associated cytokine profile, enhanced muscle-anabolic signalling prevention of CHF-induced weight loss (all p < 0.05 vs. NS S). Conclusions: for 8 weeks production function. effects result skeletal mass, potential improve major patient outcomes clinical settings.