Tucker Wesley J, Haykowsky Mark J, Seo Yaewon, Stehling Elisa, Forman Daniel E
The University of Texas at Arlington, Arlington, TX, USA.
Department of Medicine, Section of Geriatric Cardiology, Veterans Affairs Geriatric Research Education, and Clinical Center, University of Pittsburgh, 3471 Fifth Avenue, Suite 500, Pittsburgh, PA, 15213, USA.
Curr Heart Fail Rep. 2018 Dec;15(6):323-331. doi: 10.1007/s11897-018-0408-6.
To discuss the impact of deleterious changes in skeletal muscle morphology and function on exercise intolerance in patients with heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF), as well as the utility of exercise training and the potential of novel treatment strategies to preserve or improve skeletal muscle morphology and function.
Both HFrEF and HFpEF patients exhibit a reduction in percent of type I (oxidative) muscle fibers and oxidative enzymes coupled with abnormal mitochondrial respiration. These skeletal muscle abnormalities contribute to impaired oxidative metabolism with an earlier shift towards glycolytic metabolism during exercise that is strongly associated with exercise intolerance. In both HFrEF and HFpEF patients, peripheral "non-cardiac" factors are important determinants of the improvement in exercise tolerance following aerobic exercise training. Adjunctive strategies that include nutritional supplementation with amino acids and/or anabolic drugs to stimulate anabolic molecular pathways in skeletal muscle show great promise for improving exercise tolerance and treating heart failure-associated sarcopenia, but these efforts remain early in their evolution, with no immediate clinical applications. There is consistent evidence that heart failure is associated with multiple skeletal muscle abnormalities which impair oxygen uptake and utilization and contribute greatly to exercise intolerance. Exercise training induces favorable adaptations in skeletal muscle morphology and function that contribute to improvements in exercise tolerance in patients with HFrEF. The contribution of skeletal muscle adaptations to improved exercise tolerance following exercise training in HFpEF remains unknown and warrants further investigation.
探讨射血分数降低的心力衰竭（HFrEF）和射血分数保留的心力衰竭（HFpEF）患者骨骼肌形态和功能的有害变化对运动不耐受的影响，以及运动训练的效用和新型治疗策略在保留或改善骨骼肌形态和功能方面的潜力。
HFrEF和HFpEF患者均表现出I型（氧化型）肌纤维百分比和氧化酶减少，同时伴有线粒体呼吸异常。这些骨骼肌异常导致氧化代谢受损，运动期间更早地转向糖酵解代谢，这与运动不耐受密切相关。在HFrEF和HFpEF患者中，外周“非心脏”因素都是有氧运动训练后运动耐量改善的重要决定因素。包括补充氨基酸和/或合成代谢药物以刺激骨骼肌合成代谢分子途径的辅助策略，在改善运动耐量和治疗心力衰竭相关的肌肉减少症方面显示出巨大前景，但这些努力仍处于早期阶段，尚无直接临床应用。有一致证据表明，心力衰竭与多种骨骼肌异常有关，这些异常会损害氧气摄取和利用，并极大地导致运动不耐受。运动训练可诱导骨骼肌形态和功能产生有利的适应性变化，有助于改善HFrEF患者的运动耐量。运动训练后骨骼肌适应性变化对HFpEF患者运动耐量改善的贡献尚不清楚，值得进一步研究。
