Effect Of Moderate-Intensity Endurance Exercise On The Cardiac Hypertrophy Signaling Pathway

In recent years, using the physical activity to prevent and heal the cardiovascular disease becomes a research hotspot. It is reported although there are many positive factors of the cardiac hypertrophy induced by the moderate-intensity endurance exercise; the athlete will still be arrhythmia, cardiac conduction disorders and so on. So the cardiac hypertrophy induced by the moderate-intensity endurance exercise should be physiological cardiac hypertrophy or pathological cardiac hypertrophy; the expression of the representative signaling pathway of physiological cardiac hypertrophy:PI3K/Akt/mTOR signaling pathway, Angâ…¡and AT1R signaling pathway and other related signaling molecules also has not been reported systematically and clearly.Objective:Using the 8 weeks of moderate-intensity treadmill endurance training, to build a cardiac hypertrophy model of rats. On this basis:According to the expression change of cardiac injury markers (cardiac troponin T, cardiac troponin I and BNP), combined with the histological phenotype, to determine the character of the cardiac hypertrophy induced by moderate-intensity endurance exercise. By the mRNA expression changes of the heart local Angâ…¡and AT1R, combined with our previous study, to determine whether this representative signaling pathway of pathological cardiac hypertrophy be activated, and the effect of this signaling pathway in cardiac hypertrophy at this time. We want to discuss the effect of moderate-intensity endurance exercise on the expression of cardiac PI3K/Akt/mTOR signaling pathway, clarify the mechanism of the signaling pathway specific changes. So we can determine the character of the cardiac hypertrophy induced by moderate-intensity endurance and provide the morphology and biochemistry theory for the athlete's heart endocrine and signaling pathway research. Also, we can provide the newer theory and experiment foundation for optimal sports program, effective prevention of cardiac injury, heart health promotion, and exercise prescription for cardiovascular disease. Methods:(1) Using the 8 weeks of moderate-intensity treadmill endurance training, to build a cardiac hypertrophy model of rats. Endurance training programs is accordant with Fenning, combined with the maximum oxygen uptake control method of Wisl?ff, and the relative intensity remain at about 60%-65% VO 2max.(2) Using the real-time quantitative PCR method to test the mRNA expression of PI3K, PDK1, Akt, mTOR, p70S6K, eIF4E, AMPK, Angâ…¡and AT1R.(3) After anesthetized, removed the blood and heart, testing the levels of serum cardiac troponin T, cardiac troponin I, BNP, cardiac Akt and mTOR by ELISA method. (4) Using the immunohistochemistry combined with computer image processing technology measured the immune response positive area and optical density of Akt, mTOR, p70S6K and eIF4E. (5) Using the HE stain to observe the cardiac morphology.Results:After the cardiac hypertrophy induced by the moderate-intensity endurance exercise, heart function was significantly improved, the levels of serum cardiac troponin T, cardiac troponin I and BNP had not changed significantly; After the moderate-intensity endurance exercise, the mRNA expression of heart local Angâ…¡was significantly increased, while AT1R was significantly reduced; After the moderate-intensity endurance exercise, the mRNA expression of PI3K, PDK1, Akt and AMPK were not significantly increased, by using immunohistochemistry combined with computer image processing technology, Akt immune-positive area and optical density were not significantly enhanced, and the immune response did not occur in the cell membrane, the Akt protein content was not significantly increased by ELISA testing. After the moderate-intensity endurance exercise, the mRNA expression of mTOR, p70S6K and eIF4E was increased significantly; by using immunohistochemistry combined with computer image processing technology, the mTOR, p70S6K and eIF4E immune-positive area and optical density were significantly enhanced; the mTOR protein content was significantly increased by ELISA testing. Conclusion:The 8 weeks moderate-intensity treadmill endurance exercise can build an animal cardiac hypertrophy model to provide an experimental basis for studying the athlete's heart; After the moderate-intensity treadmill endurance training, the serum cardiac troponin slightly elevated, but this could not show the myocardial cell necrosis, and the reason of the routine increase release after exercise may be:after cardiac hypertrophy, cardiac troponin synthesis increased, and cardiac function demand increased. BNP level did not change prompted that the cardiac function did not deteriorating, did not trend to pathological cardiac hypertrophy even the chronic heart failure and other cardiac disease; After the 8 weeks of moderate-intensity treadmill endurance training, the expression of AT1R decreased, so weakened the effect of promoting cell growth by local Angâ…¡, then it started the regulation mechanism to prevent cardiac hypertrophy trend to pathological changes. This results suggested that the receptor level and (or) affinity changes was the key factor in the tendency of physiological cardiac hypertrophy to pathological cardiac hypertrophy. The Angâ…¡level and (or) affinity changes did not reflect the character of cardiac hypertrophy. It also shows that the Angâ…¡/AT1R signaling pathway is not the key role in the physiological cardiac hypertrophy signaling network, which is induced by endurance training, the key signaling pathway is mTOR signaling pathway. Different With pure physiological cardiac hypertrophy, the PI3K/Akt signaling pathway was not activated, suggested that there are differences between exercise-induced "physiological hypertrophy" and simple "physiological hypertrophy".