The Effects Of Heavy Stress Training And Tapering On MTOR Pathway And CaN/NFAT In Cardiac Muscles

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.