Canan Benjamin D, Haizlip Kaylan M, Xu Ying, Monasky Michelle M, Hiranandani Nitisha, Milani-Nejad Nima, Varian Kenneth D, Slabaugh Jessica L, Schultz Eric J, Fedorov Vadim V, Billman George E, Janssen Paul M L
Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio; and.
Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio; and Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio.
J Appl Physiol (1985). 2016 Apr 15;120(8):817-24. doi: 10.1152/japplphysiol.00775.2015. Epub 2016 Jan 28.
It is well known that moderate exercise training elicits a small increase in ventricular mass (i.e., a physiological hypertrophy) that has many beneficial effects on overall cardiac health. It is also well known that, when a myocardial infarction damages part of the heart, the remaining myocardium remodels to compensate for the loss of viable functioning myocardium. The effects of exercise training, myocardial infarction (MI), and their interaction on the contractile performance of the myocardium itself remain largely to be determined. The present study investigated the contractile properties and kinetics of right ventricular myocardium isolated from sedentary and exercise trained (10-12 wk progressively increasing treadmill running, begun 4 wk after MI induction) dogs with and without a left ventricular myocardial infarction. Exercise training increased force development, whereas MI decreased force development that was not improved by exercise training. Contractile kinetics were significantly slower in the trained dogs, whereas this impact of training was less or no longer present after MI. Length-dependent activation, both evaluated on contractile force and kinetics, was similar in all four groups. The control exercise-trained group exhibited a more positive force-frequency relationship compared with the sedentary control group while both sedentary and trained post-MI dogs had a more negative relationship. Last, the impact of the β-adrenergic receptor agonist isoproterenol resulted in a similar increase in force and acceleration of contractile kinetics in all groups. Thus, exercise training increased developed force but slowed contractile kinetics in control (noninfarcted animals), actions that were attenuated or completely absent in post-MI dogs.
众所周知，适度的运动训练会使心室质量略有增加（即生理性肥大），这对心脏整体健康有许多有益影响。同样众所周知的是，当心肌梗死损害心脏的一部分时，剩余的心肌会发生重塑，以补偿有功能的存活心肌的损失。运动训练、心肌梗死（MI）及其相互作用对心肌自身收缩性能的影响在很大程度上仍有待确定。本研究调查了从久坐不动和经过运动训练（在心肌梗死诱导后4周开始，进行10 - 12周逐渐增加强度的跑步机跑步训练）的犬类中分离出的右心室心肌的收缩特性和动力学，这些犬类有无左心室心肌梗死。运动训练增加了力量发展，而心肌梗死则降低了力量发展，运动训练并未改善这种情况。训练有素的犬类的收缩动力学明显较慢，而在心肌梗死后，训练的这种影响较小或不再存在。在收缩力和动力学方面评估的长度依赖性激活在所有四组中相似。与久坐不动的对照组相比，运动训练的对照组表现出更积极的力 - 频率关系，而久坐不动和心肌梗死后训练的犬类都有更消极的关系。最后，β - 肾上腺素能受体激动剂异丙肾上腺素的影响导致所有组的力量增加和收缩动力学加速相似。因此，运动训练增加了对照组（未梗死动物）的发展力量，但减慢了收缩动力学，而在心肌梗死后的犬类中，这些作用减弱或完全不存在。
