Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.
JACC Heart Fail. 2020 Feb;8(2):111-121. doi: 10.1016/j.jchf.2019.08.020. Epub 2019 Nov 6.
The aim of this study was to evaluate the association between age and invasive cardiovascular hemodynamics during upright exercise among healthy adults.
The marked age-related decline in maximal exercise oxygen uptake (peak VO) may contribute to the high burden of heart failure among older individuals and their greater severity of exertional symptoms. However, the mechanisms underlying this decline are not well understood.
A total of 104 healthy community-dwelling volunteers age 20 to 76 years well screened for cardiovascular disease underwent exhaustive upright exercise with brachial and pulmonary artery catheters; radionuclide ventriculography; and expired gas analysis for the measurement of peak VO, cardiac output, left ventricular stroke volume, end-diastolic volume, end-systolic volume, ejection fraction, pulmonary capillary wedge pressure, and arteriovenous oxygen difference.
Over a 5.5-decade age range, there was a 40% decline in peak VO due primarily to reduced peak exercise cardiac output; peak arteriovenous oxygen difference was unaffected by age. The lower age-related exercise cardiac output was related to lower peak exercise heart rate and stroke volume. Aging was also associated with lower peak exercise ejection fraction, indicating reduced inotropic reserve. Peak exercise end-diastolic volume was lower with aging despite similar left ventricular filling pressure, suggesting age-related reduced diastolic compliance limiting the use of the Frank-Starling mechanism to compensate for reduced chronotropic and inotropic reserves. These age relationships were unaffected by sex.
The age-related decline in exercise capacity among healthy persons is due predominantly to cardiac mechanisms, including reduced chronotropic and inotropic reserve and possibly reduced Frank-Starling reserve. Peak exercise left ventricular filling pressure and arteriovenous oxygen difference are unchanged with healthy aging.
本研究旨在评估健康成年人直立运动期间年龄与心血管侵入性血流动力学之间的关系。
最大运动摄氧量(峰值 VO)随年龄的显著下降可能导致心力衰竭在老年人中的负担加重,以及他们的运动症状更为严重。然而,这种下降的机制尚不清楚。
总共 104 名年龄在 20 至 76 岁之间、经过心血管疾病全面筛查的健康社区居住志愿者进行了全面的直立运动,使用肱动脉和肺动脉导管;放射性核素心室造影术;以及呼气分析,以测量峰值 VO、心输出量、左心室每搏量、舒张末期容积、收缩末期容积、射血分数、肺毛细血管楔压和动静脉血氧差。
在 5.5 个十年的年龄范围内,峰值 VO 下降了 40%,主要是由于峰值运动心输出量降低所致;峰值动静脉血氧差不受年龄影响。与年龄相关的较低运动心输出量与较低的峰值运动心率和每搏量有关。衰老也与较低的峰值运动射血分数有关,表明心肌收缩力储备降低。尽管左心室充盈压相似,但随着年龄的增长,峰值运动舒张末期容积降低,表明与年龄相关的舒张顺应性降低限制了 Frank-Starling 机制的使用,以补偿变时性和心肌收缩力储备的降低。这些年龄相关性不受性别影响。
健康人运动能力的年龄相关性下降主要归因于心脏机制,包括变时性和心肌收缩力储备降低,以及可能的 Frank-Starling 储备降低。健康衰老时,峰值运动左心室充盈压和动静脉血氧差不变。