Gerstenblith G, Renlund D G, Lakatta E G
Fed Proc. 1987 Apr;46(5):1834-9.
Measurements of cardiac performance for humans at various ages is influenced by the variable examined, the population and techniques employed, and the factors that co-vary with age, including the presence of disease and physical conditioning. Interstudy differences in the extent to which occult coronary disease is present in older subjects and in the level of physical conditioning among subjects may underlie the variable perspectives contained in the literature of how aging affects cardiovascular function. In carefully screened, highly motivated but not athletically trained community-dwelling subjects, resting cardiovascular parameters are not age related except for systolic blood pressure, which increases with age. During vigorous exercise the mechanisms used to achieve a high level of cardiac output shift from a dependence on a catecholamine-mediated increase in heart rate and inotropy to a dependence on the Frank Starling mechanism. One reason for the age difference in cardiovascular response to exercise may be a diminished responsiveness to beta-adrenergic stimulation in these subjects. In other elderly subjects who cannot exercise to high work loads, a decline in stroke volume as well as heart rate at peak exercise has been observed. Whether the inability of these individuals to augment stroke volume is caused by a decrease in the ability of the heart to increase diastolic filling, by a decrease in systolic pump function caused by an increased afterload, by intrinsic myocardial contractile defects, or by a greater diminution of the cardiovascular response to beta-adrenergic stimuli is presently unknown.
对不同年龄段人类心脏功能的测量受到多种因素影响，包括所检测的变量、所采用的人群和技术，以及与年龄共同变化的因素，如疾病的存在和身体状况。老年受试者隐匿性冠状动脉疾病的存在程度以及受试者身体状况水平的研究间差异，可能是文献中关于衰老如何影响心血管功能的不同观点的潜在原因。在经过仔细筛选、积极性高但未经过运动训练的社区居住受试者中，除收缩压随年龄增加外，静息心血管参数与年龄无关。在剧烈运动期间，实现高水平心输出量的机制从依赖儿茶酚胺介导的心率和心肌收缩力增加转变为依赖Frank Starling机制。这些受试者心血管对运动反应存在年龄差异的一个原因可能是对β-肾上腺素能刺激的反应性降低。在其他无法进行高负荷运动的老年受试者中，观察到运动峰值时 stroke volume（搏出量）以及心率下降。目前尚不清楚这些个体无法增加搏出量是由于心脏增加舒张期充盈的能力下降、后负荷增加导致的收缩泵功能下降、内在心肌收缩缺陷，还是由于心血管对β-肾上腺素能刺激的反应性更大程度降低所致。
