Rajaie Cardiovascular Medical and Research Center, Fellowship in Heart Failure and Transplantation, Iran University of Medical Sciences, Tehran, Islamic Republic of Iran.
Department of Sport Science, Faculty of Education and Psychology, Shiraz University, Shiraz, Islamic Republic of Iran.
Life Sci. 2019 Mar 15;221:319-326. doi: 10.1016/j.lfs.2019.02.045. Epub 2019 Feb 22.
Myocardial infarction (MI), an important cause of morbidity and mortality, can be followed by left ventricular dysfunction and cardiomyocyte loss. Cardiac repair mechanisms may subsequently improve left ventricular function. Exercise training has been suggested to have cardioprotective effects against MI damage, but detailed knowledge is lacking on the effects of different types and intensities of exercise training on molecular targets of cardiomyocyte regeneration.
MI was induced in male Wistar rats by ligating the left anterior descending coronary artery. After MI induction, the rats were randomly assigned to one of five groups: sham operated, and experimental MI followed by no exercise, or low, moderate or high intensity exercise Cardiac function and infarct size were assessed by echocardiography and Evans blue/TTC staining, respectively. The expression of mRNA markers and proteins associated with myocardial regeneration was measured with RT-PCR and western blotting.
Exercise training at different intensities improved cardiac function and levels of stem cell and cardiomyocyte markers, and reduced infarct size. mRNA levels of GATA4, Nkx2.5 and c-Kit and protein expression of Nkx2.5 and c-Kit were significantly increased in all MI-exercise groups. The high-intensity exercise group had greater increases than the low and moderate intensity exercise groups. In the high-intensity exercise group, Sca-1 and CITED4 increased more than in the low-intensity exercise group. C/EBPβ mRNA and protein levels decreased after exercise training, with greater reductions in the high-intensity exercise group than the low- or moderate-intensity groups.
The findings suggest that by targeting cardiogenesis, high-intensity training can exert cardioprotective effects against cardiac dysfunction in an experimental model of MI.
心肌梗死(MI)是发病率和死亡率的重要原因,可导致左心室功能障碍和心肌细胞丧失。随后的心脏修复机制可能改善左心室功能。运动训练被认为对 MI 损伤具有心脏保护作用,但缺乏关于不同类型和强度的运动训练对心肌细胞再生的分子靶点的详细知识。
通过结扎左前降支冠状动脉在雄性 Wistar 大鼠中诱导 MI。MI 诱导后,大鼠被随机分为五组之一:假手术组和无运动、低强度、中强度或高强度运动的实验性 MI 组。通过超声心动图和 Evans 蓝/TTC 染色分别评估心脏功能和梗死面积。用 RT-PCR 和 Western blot 测量与心肌再生相关的 mRNA 标志物和蛋白的表达。
不同强度的运动训练改善了心脏功能和干细胞和心肌标志物的水平,并减少了梗死面积。所有 MI 运动组的 GATA4、Nkx2.5 和 c-Kit 的 mRNA 水平和 Nkx2.5 和 c-Kit 的蛋白表达均显著增加。高强度运动组的增加幅度大于低强度和中强度运动组。在高强度运动组中,Sca-1 和 CITED4 的增加高于低强度运动组。运动训练后 C/EBPβmRNA 和蛋白水平降低,高强度运动组比低强度或中强度组降低更明显。
这些发现表明,通过靶向心脏发生,高强度训练可以在 MI 的实验模型中对心脏功能障碍发挥心脏保护作用。