Tate C A, Hyek M F, Taffet G E
Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX 77204-5515.
Med Sci Sports Exerc. 1994 May;26(5):561-7.
The decline of maximal cardiac output (Qmax) is a major factor responsible for the lower maximal oxygen consumption of elderly mammals. The lower Qmax is associated with aging-related decreases in maximal heart rate (HR-max) and maximal stroke volume (SVmax). The mechanism(s) for the slower HRmax, unchanged by exercise training, is unknown. The decrement in SVmax, however, can be improved, as shown by the enhanced systolic and diastolic properties of the elderly heart after exercise training. One major problem is diastolic dysfunction observed in the absence of disease. Diastolic dysfunction (a decrease in peak ventricular filling after systole or a prolonged relaxation of contracted muscle) results from in part a downregulation of the sarcoplasmic reticulum's (SR) calcium ATPase that sequesters cytosolic calcium via the hydrolysis of ATP. Exercise training of sedentary old mammals produces a faster relaxation and an upregulation of the SR calcium ATPase. Yet the characteristic shift of myosin toward the slower isoform is unaltered by exercise training. The molecular signals and mechanisms underlying these aging-related alterations in sedentary and physically active individuals are unknown. An enhancement of cardiac function by exercise training, though, is preserved in advanced age.
最大心输出量（Qmax）的下降是导致老年哺乳动物最大耗氧量降低的主要因素。较低的Qmax与最大心率（HR-max）和最大心搏量（SVmax）随年龄增长而下降有关。运动训练无法改变HRmax变慢的机制尚不清楚。然而，SVmax的下降可以得到改善，运动训练后老年心脏收缩和舒张特性增强就证明了这一点。一个主要问题是在无疾病情况下出现的舒张功能障碍。舒张功能障碍（收缩期后心室充盈峰值降低或收缩肌肉舒张时间延长）部分是由于肌浆网（SR）钙ATP酶下调所致，该酶通过ATP水解来隔离胞质钙。对久坐不动的老年哺乳动物进行运动训练可使其舒张更快，并上调SR钙ATP酶。然而，肌球蛋白向较慢亚型的特征性转变并未因运动训练而改变。久坐不动和积极运动个体中这些与衰老相关的变化背后的分子信号和机制尚不清楚。不过，运动训练对心脏功能的增强作用在高龄时依然存在。
