Stratton J R, Levy W C, Cerqueira M D, Schwartz R S, Abrass I B
Division of Cardiology, Seattle VA Medical Center, WA 98108.
Circulation. 1994 Apr;89(4):1648-55. doi: 10.1161/01.cir.89.4.1648.
Cardiac aging alters many of the acute responses to exercise stress, but the extent to which chronic exercise (ie, training) can alter or improve the effects of aging in humans is largely unknown.
Cardiovascular responses to graded supine exercise stress (beginning at 200 kpm and increasing by 200 kpm every 3 minutes till exhaustion) were assessed using radionuclide ventriculography in 13 older (age, 60 to 82 years) and 11 young (age, 24 to 32 years) rigorously screened healthy men before and after 6 months of endurance training. Repeated-measures ANOVA was used to test significance. During exercise, the old group had a lesser increase in heart rate (+105% old versus +166% young), a greater increase in mean blood pressure (+35% old versus +22% young), lesser increases in ejection fraction (+3 ejection fraction units old versus +11 units young) and peak ejection rate (+62% old versus +119% young), a greater increase in end-diastolic volume index (+8% old versus -10% young), a lesser fall in end-systolic volume index (-0% old versus -32% young), and a lesser increase in cardiac index (+135% old versus +189% young) (all P < .01 young/old versus exercise stage). Stroke volume index response to exercise was not different with aging (+14% old versus +6% young, P = NS). Exercise training increased maximal oxygen intake by 21% in the older group (28.9 +/- 4.6 to 35.1 +/- 3.8 mL.kg-1.min-1, P < .001) and by 17% in the young (44.5 +/- 5.1 to 52.1 +/- 6.3 mL.kg-1.min-1, P < .001) and increased peak workload by 24% in the old and 28% in the young. Exercise training had no differential effects on old versus young men. Among all subjects, training significantly reduced the resting heart rate by 12% (-8 beats per minute) and increased resting end-diastolic volume index by 13% (+9 mL/M2) and resting stroke volume index by 18% (+7 mL/M2) (all P < .01). At peak exercise, cardiac index increased by 16% (+1.07 L.M-2.min-1) compared with before training, which was the result of an increase in stroke volume of 18% (+7 mL/M2) (P < .001); peak heart rate was unchanged. The increase in stroke volume index at peak exercise was the result of both a 12% increase in end-diastolic volume index (+8 mL/M2) (P < .01) and an increase in ejection fraction (+3 ejection fraction units) (P < .05) at peak exercise. The increased ejection fraction at peak exercise occurred despite a 9% increase in systolic blood pressure (+18 mm Hg) (P < .01), suggesting an increase in contractility. Thus, both the young and old increased peak exercise cardiac output by use of the Frank-Starling mechanism (ie, cardiac dilatation) as well as an increase in ejection fraction.
We conclude that there is an age-associated decline in heart rate, ejection fraction, and cardiac output responses to supine exercise in healthy men. Although the stroke volume responses of the young and old are similar, the old tend to augment stroke volume during exercise more through cardiac dilatation, with an increase in end-diastolic volume (+8%) but without much change in ejection fraction (+3 ejection fraction units), whereas the young rely more on an increase in the ejection fraction (+11 ejection fraction units) with no cardiac dilatation (-10%). Despite the significant cardiovascular changes that occur in the response to a single bout of exercise with aging, adaptations to chronic exercise training were not different with aging and included improvements in maximal workload and increases in ejection fraction, stroke volume index, and cardiac index at peak exercise.
心脏衰老会改变许多对运动应激的急性反应,但长期运动(即训练)在多大程度上能够改变或改善人类衰老的影响,目前很大程度上尚不清楚。
使用放射性核素心室造影术,对13名年龄较大(60至82岁)和11名年龄较小(24至32岁)且经过严格筛选的健康男性,在耐力训练6个月前后,评估其对分级仰卧运动应激(从200千帕米开始,每3分钟增加200千帕米直至力竭)的心血管反应。采用重复测量方差分析来检验显著性。运动期间,老年组心率增加较少(老年组增加105%,年轻组增加166%),平均血压升高较多(老年组升高35%,年轻组升高22%),射血分数增加较少(老年组增加3个射血分数单位,年轻组增加11个单位),峰值射血率增加较少(老年组增加62%,年轻组增加119%),舒张末期容积指数增加较多(老年组增加8%,年轻组减少10%),收缩末期容积指数下降较少(老年组下降0%,年轻组下降32%),心脏指数增加较少(老年组增加135%,年轻组增加189%)(所有P值均小于0.01,年轻组/老年组与运动阶段相比)。老年与年轻男性的每搏输出量指数对运动的反应无差异(老年组增加14%,年轻组增加6%,P值无统计学意义)。运动训练使老年组的最大摄氧量增加21%(从28.9±4.6增至35.1±3.8毫升·千克⁻¹·分钟⁻¹,P值小于0.001),年轻组增加17%(从44.5±5.1增至52.1±6.3毫升·千克⁻¹·分钟⁻¹,P值小于0.001),并使老年组的峰值工作量增加24%,年轻组增加28%。运动训练对老年男性和年轻男性没有差异影响。在所有受试者中,训练使静息心率显著降低12%(每分钟降低8次),静息舒张末期容积指数增加13%(增加9毫升/平方米),静息每搏输出量指数增加18%(增加7毫升/平方米)(所有P值均小于0.01)。在运动峰值时,与训练前相比,心脏指数增加16%(增加1.07升·平方米⁻¹·分钟⁻¹),这是每搏输出量增加18%(增加7毫升/平方米)的结果(P值小于0.001);峰值心率未改变。运动峰值时每搏输出量指数的增加是舒张末期容积指数增加12%(增加8毫升/平方米)(P值小于0.01)和运动峰值时射血分数增加(增加3个射血分数单位)(P值小于0.05)共同作用的结果。尽管收缩压增加了9%(增加18毫米汞柱)(P值小于0.01),运动峰值时射血分数仍增加,提示心肌收缩力增加。因此,年轻组和老年组均通过Frank-Starling机制(即心脏扩张)以及射血分数增加来提高运动峰值时的心输出量。
我们得出结论,健康男性对仰卧运动的心率、射血分数和心输出量反应存在与年龄相关的下降。尽管年轻组和老年组的每搏输出量反应相似,但老年组在运动期间往往更多地通过心脏扩张来增加每搏输出量,舒张末期容积增加(8%),但射血分数变化不大(增加3个射血分数单位),而年轻组更多地依赖射血分数增加(增加11个射血分数单位)且无心脏扩张(减少10%)。尽管随着年龄增长,单次运动反应中会发生显著的心血管变化,但对长期运动训练的适应性在年龄方面并无差异,包括最大工作量的改善以及运动峰值时射血分数、每搏输出量指数和心脏指数的增加。