【作者】 张军；

【导师】 曾凡星；

【作者基本信息】 北京体育大学 ， 运动人体科学， 2014， 博士

【摘要】 本研究从分子生物学水平深入分析大运动量和减量训练后,心肌哺乳动物雷帕霉素靶蛋白(mTOR)信号通路和钙调神经磷酸酶(CaN)/活化T细胞核因子(NFAT)信号的变化特点,并阐明对心肌影响的机理。分析大运动量和减量训练的合理性,为科学训练提供理论依据。研究方法：雄性SD大鼠随机分为8组,即3周大运动量训练组、3天、6天和2周减量训练组及其相应的对照组。3周大运动量训练后进行减量训练。取各组左心室肌组织,采用Western blotting方法测定PI3K p85、PI3K p110α、PI3K p110γ、Akt、mTOR, p70S6K.4E-BP1、CaN和NFAT等蛋白和磷酸化。心肌组织形态学采用HE染色在光镜下观察。研究结果：3周大运动量训练和2周减量训练后,心肌组织形态没有显著变化,未发现心肌组织损伤的形态学改变。6天减量训练后,心肌PI3K p110α蛋白表达显著增加(P<0.05)。3周大运动量训练和减量训练后,心肌PI3K p110γ蛋白表达无显著变化(P>0.05)。3天减量训练后,心肌Akt(Ser473)磷酸化/Akt显著降低(P<0.05)。3天减量训练后,心肌mTOR(Ser2448)磷酸化显著增加(P<0.05),mTOR(Ser2448)磷酸化/mTOR显著增加(P<0.05)。3周大运动量训练后,心肌p70S6K(Thr389)磷酸化显著增加(P<0.05)。减量训练后,心肌p70S6K显著减少(P<0.05)。3周大运动量训练后,心肌mTOR(Ser2448)磷酸化/mTOR和CaN显著减少(P<0.05)。3周大运动量训练和减量训练后,心肌NFAT c3(Ser265)磷酸化无显著改变(P>0.05)。结论：本研究制定的大运动量和减量训练方案未引起大鼠心肌组织形态的显著改变,适度的大运动量训练和减量训练是合理的。减量训练能引起心肌PI3K p110α和mTOR激活,对心脏有利。信号蛋白在运动训练的短期内即发生变化,而心肌组织结构的适应性变化需要更长时间。减量训练能引起mTOR信号通路中的PI3K和mTOR(Ser2448)磷酸化增加,但是增加的时间和幅度上有差异。心肌PI3K-Akt-mTOR信号通路在减量训练过程中的变化总体上是一致的。更多还原

【Abstract】 The change characteristics of mTOR pathway and CaN/NFAT in cardiac muscles were analyzed in molecule biology level after heavy stress training and tapering. The mechanism of the effects on cardiac muscles was illuminated. The rationality of heavy stress training and tapering was analyzed and the theory basis was provided for scientific training. Methods:Male SD rats were divided in8groups in the research, including the group of3weeks of heavy stress training, the group of3days of tapering, the group of6days of tapering, the group of2weeks of tapering and the corresponding control groups. They were tapered after3weeks of heavy stress training. The cardiac muscles of left ventricles were taken as samples. The signal proteins and phosphorylation were tested by the method of Western Blotting, including PI3K p110α, PI3K p110γ, Akt, mTOR, p70S6K,4E-BP1, CaN, NFAT, and so on. The conformations of cardiac muscles organizations were observed by HE coloration in the light mirror. Results:The conformations of cardiac muscles organizations weren’t changed significantly after3weeks of heavy stress training and2weeks of tapering. There were not any injuries on the cardiac muscles. PI3K p110α protein expressions were increased significantly in cardiac muscles after6days of tapering (P<0.05). PI3K p110γ wasn’t changed significantly after3weeks of heavy stress training and tapering (P>0.05). The ratio of Akt(Ser473) phosphorylation and Akt was decreased significantly in cardiac muscles after3days of tapering (P<0.05). MTOR(Ser2448) phosphorylation and the ratio of mTOR(Ser2448) phosphorylation and mTOR were increased significantly in cardiac muscles after3days of tapering (P<0.05). P70S6K(Thr389) phosphorylation was increased significantly in cardiac muscles after3weeks of heavy stress training (P<0.05). P70S6K was decreased significantly in cardiac muscles after tapering (P<0.05). The ratio of mTOR (Ser2448) phosphorylation and mTOR and CaN were decreased significantly in cardiac muscles after3weeks of heavy stress training (P<0.05). NFAT c3(Ser265) phosphorylation was not changed significantly in cardiac muscles after3weeks of heavy stress training and tapering (P>0.05). Conclusions:The project of training and tapering didn’t result in the significant changes of the cardiac muscles. Modest heavy stress training and tapering were reasonable. The activations of PI3K p110α and mTOR were brought by tapering in cardiac muscles, which was available for cardiac muscles. Signal proteins changed after short-term training. But it needed a long time for the adaptable changes of the cardiac muscles’structures. The increase of PI3K and mTOR(Ser2448) phosphorylation in mTOR pathway could be brought by tapering (P<0.05). But there were some differences in the time and range of the increase. It proved that the change of PI3K-Akt-mTOR pathway was consistent in cardiac muscles.更多还原