PDF(Pubmed)
Abstract：
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.
摘要：
锻炼不容忍，通过峰值耗氧量（VO2）测量，是心力衰竭（HF）的标志性特征。在老年HF患者中，由于与衰老相关的变化，例如瘦肌肉量减少，肥胖的增加，运动时最大心率和外周血流量降低。随着年龄的增长，峰值V²O2呈非线性降低，在生命的后几十年中加速。由于HF引起的中枢和外周适应不良，峰值V²O2进一步降低。中枢机制包括峰值心率受损，每搏输出量,收缩性，增加的填充压力，和迟钝的血管舒张反应.外周机制包括内皮功能障碍，减少流向肌肉的血液，骨骼肌氧化能力受损。这篇综述集中介绍了导致老年HF患者有氧能力受损的机制。
