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运动和久坐大鼠心脏对压力超负荷的功能反应。

Heart functional responses to pressure overload in exercised and sedentary rats.

作者信息

Dowell R T, Cutilletta A F, Rudnik M A, Sodt P C

出版信息

Am J Physiol. 1976 Jan;230(1):199-204. doi: 10.1152/ajplegacy.1976.230.1.199.

Abstract

Female rats that had been subjected to a moderate treadmill running program were compared with sedentary animals on the basis of heart weight, selected biochemical measurements, and heart function. Exercised animals maintained normal growth rate, and cardiac hypertrophy was not present. Left ventricular RNA, DNA, and cytochrome c levels were unchanged. Heart functional measurements obtained in situ were similar in sedentary and exercised animals under control conditions. When subjected to sustained (1-3 days) aortic constriction pressure overload, exercised animals maintained or increased myocardial contractility. Contractility was depressed in sedentary animals. Both sedentary and exercised animals increased left ventricular end diastolic pressure without changing contractility during acute (1-3 min) pressure overload. However, exercised animals were able to fully regain normal cardiac output when the acute overload was relieved. Cardiac output remained approximately 10% below control in sedentary animals. The improved ability of previously exercised animals to withstand pressure overload appears to be due to alterations in adaptation rather than preliminary augmentation of metabolism or function.

摘要

将接受适度跑步机跑步训练的雌性大鼠与久坐不动的动物在心脏重量、选定的生化指标和心脏功能方面进行了比较。运动的动物保持正常生长速度,未出现心脏肥大。左心室RNA、DNA和细胞色素c水平未发生变化。在对照条件下,久坐和运动的动物原位获得的心脏功能测量结果相似。当受到持续(1 - 3天)的主动脉缩窄压力过载时,运动的动物维持或增强了心肌收缩力。久坐动物的收缩力降低。在急性(1 - 3分钟)压力过载期间,久坐和运动的动物左心室舒张末期压力均升高,但收缩力未改变。然而,当急性过载解除时,运动的动物能够完全恢复正常心输出量。久坐动物的心输出量仍比对照低约10%。先前运动的动物承受压力过载能力的提高似乎是由于适应性改变,而非代谢或功能的初步增强。

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