中文摘要：

超载锻练(OE ) 通过导致 autophagy 和 apoptosis 引起心肌的损害。在这研究，我们检验了 autophagy 禁止者 3-methyladenine (3 麻省) 是否能减轻导致 OE 的心脏的损害。老鼠与 3 麻省被注射(15 mg/kg， iv ) 或在前盐使遭到了到 OE 的各种各样的紧张包括没有游泳(控制) ， 2 h 游泳(温和紧张的锻练， MIE ) ，有 2.5% 身体重量超载的 2 h 游泳(中等 OE；MOE ) ， 5% 超载(集中的 OE；IOE ) 或 2.5% 过载直到用尽(彻底的 OE；EOE ) 。在 OE 以后，心被收获为词法并且 biochemiacal 分析。心脏的形态学， autophagosomes 和 apoptosis 与 H&E 染色，传播电子显微镜学和 TUNEL 分析被检验分别地。Autophagy 相关的蛋白质到(LC3-II/I 和 Beclin-1 ) 并且 apoptosis 相关的蛋白质(Bcl-2/Bax ) 用西方的弄污被估计。我们的结果证明与控制相比， MIE 没改变展出了未经触动的心肌的纤维并且干净地安排了 cardiomyocytes 的心纸巾的词法结构。然而， IOE 导致了 cardiomyocytes 的不规则的安排并且显著地增加了 cardiomyocytes 的宽度，而 EOE 引起了更肿、平的破坏 cardiomyocytes。与增加的 OE 紧张同时(MOE， IOE， EOE ) ， cardiomyocyte autophagy 和 apoptosis 变得越来越突出，象增加的 apoptotic 房间和减少的 Bcl-2/Bax 比率一样由 autophagosomes 的增加的数字和 LC3-II/I 和 Beclin-1 的表示层次证实了。3 麻省管理显著地在 MOE， IOE 和 EOE 老鼠稀释了 cardiomyocytes 以及所有 autophagy 相关、 apoptosis 相关的畸形的导致 OE 的词法变化。因此， autophagy 禁止者 3 麻省能在老鼠减轻导致 OE 的心损害。

英文摘要：

Overload-exercise （OE） causes myocardial injury through inducing autophagy and apoptosis. In this study we examined whether an autophagy inhibitor 3-methyladenine （3-MA） could alleviate OE-induced cardiac injury. Rats were injected with 3-MA （15 mg/kg, iv） or saline before subjected to various intensities of OE, including no swim （control）, 2 h swim （mild-intensity exercise, MIE）, 2 h swim with 2.5% body weight overload （moderate OE; MOE）, 5% overload （intensive OE; IOE） or 2.5% overload until exhausted （exhaustive OE; EOE）. After OE, the hearts were harvested for morphological and biochemiacal analysis. The cardiac morphology, autophagosomes and apoptosis were examined with H＆E staining, transmission electron microscopy and TUNEL analysis, respectively. Autophagyrelated proteins to （LC3-Ⅱ/Ⅰ and Beclin-1） and apoptosis-related proteins （Bci-2/Bax） were assessed using Western blotting. Our results showed that compared with the control, MIE did not change the morphological structures of the heart tissues that exhibited intact myocardial fibers and neatly arranged cardiomyocytes. However, IOE resulted in irregular arrangement of cardiomyocytes and significantly increased width of cardiomyocytes, whereas EOE caused more swollen and even disrupted cardiomyocytes. In parallel with the increased OE intensity （MOE, IOE, EOE）, cardiomyocyte autophagy and apoptosis became more and more prominent, evidenced by the increasing number of autophagosomes and expression levels of LC3-Ⅱ/Ⅰ and Beclin-1 as well as the increasing apoptotic cells and decreasing Bcl-2/Bax ratio. 3-MA administration significantly attenuated OE-induced morphological changes of cardiomyocytes as well as all the autophagy- and apoptosis-related abnormalities in MOE, IOE and EOE rats. Thus, the autophagy inhibitor 3-MA could alleviate OE-induced heart injury in rats.