Singam Narayana Sarma V, Tabi Meir, Fleg Jerome L
Division of Critical Care Medicine, Mayo Clinic, Rochester, MN 55903, USA.
Department of Critical Care, Washington Hospital Center Washington DC, 20010, USA.
Rev Cardiovasc Med. 2022 Sep 13;23(9):313. doi: 10.31083/j.rcm2309313. eCollection 2022 Sep.
Exercise intolerance, measured by peak oxygen consumption (V̇O2), is a hallmark feature of heart failure (HF). The effect is compounded in the elderly HF patient by aging-associated changes such as a reduction in lean muscle mass, an increase in adiposity, and a reduction in maximal heart rate and peripheral blood flow with exercise. There is a non-linear reduction in peak V̇O2 with age that accelerates in the later decades of life. Peak V̇O2 is further reduced due to central and peripheral maladaptation from HF. Central mechanisms include impaired peak heart rate, stroke volume, contractility, increased filling pressures, and a blunted vasodilatory response. Peripheral mechanisms include endothelial dysfunction, reduced blood flow to muscles, and impaired skeletal muscle oxidative capacity. This review presents a focused update on mechanisms leading to impaired aerobic capacity in older HF patients.
通过峰值耗氧量（V̇O2）衡量的运动不耐受是心力衰竭（HF）的一个标志性特征。在老年HF患者中，衰老相关的变化会加剧这种影响，如瘦肌肉量减少、肥胖增加、运动时最大心率和外周血流量降低。随着年龄增长，峰值V̇O2呈非线性下降，在生命的后几十年加速下降。由于HF导致的中枢和外周适应不良，峰值V̇O2会进一步降低。中枢机制包括峰值心率受损、每搏输出量、收缩力、充盈压增加以及血管舒张反应减弱。外周机制包括内皮功能障碍、肌肉血流量减少和骨骼肌氧化能力受损。本综述重点介绍了导致老年HF患者有氧能力受损的机制的最新情况。
