年轻人和老年人对运动的心血管反应。

Federation proceedings Pub Date : 1987-04-01
G Gerstenblith, D G Renlund, E G Lakatta
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摘要

不同年龄的人的心脏性能测量受所检查的变量、所采用的人口和技术以及与年龄共同变化的因素(包括疾病的存在和身体状况)的影响。在老年受试者中隐匿性冠状动脉疾病的存在程度和受试者之间身体调节水平的研究间差异,可能是关于衰老如何影响心血管功能的文献中包含的不同观点的基础。在精心筛选的、积极性高但没有运动训练的社区居民中,静息心血管参数与年龄无关,只有收缩压随年龄增长而增加。在剧烈运动期间,用于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肌力增强转变为依赖Frank Starling机制。心血管对运动反应的年龄差异的一个原因可能是这些受试者对-肾上腺素能刺激的反应减弱。在其他不能进行高负荷运动的老年受试者中,已观察到峰值运动时中风量和心率的下降。目前尚不清楚这些个体无法增加卒中容量是由于心脏增加舒张充盈的能力下降、后负荷增加引起的收缩泵功能下降、内在心肌收缩缺陷还是由于心血管对β -肾上腺素能刺激反应的更大减弱。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cardiovascular response to exercise in younger and older men.

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.

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