|（1.School of Physical Education，Chongqing Normal University，Chongqing 401331，China；2.Shandong Sport University，Jinan 250102，China)
Abstract: In order to probe into the effects of aerobic exercise on the pathological cardiac hypertrophy of rats suf-fering chronic heart failure and the possible mechanism, and to provide a theoretical criterion for exercise recovery from heart failure, the authors established a chronic heart failure model by ligating the coronary artery of Wistar rats, randomly divided the rats into a sham operation control group (SC), a sham operation exercise group (SE), a heart failure control group (HC) and a heart failure exercise group (HE) after operation, let the rats in groups SE and HE carry out 10-week treadmill training, let the rats in groups SC and HC maintain a calm condition, measured the rats’ exercise endurance (maximum running speed and time to exhaustion) by utilizing the experiment of exercise whose load was gradually increased via the treadmill, by means of echocardiogram, measured cardiac structure and function parameters, which included left ventricular internal diameter during diastole (LVIDd), left ventricular in-ternal diameter during systole (LVIDs), left ventricular anterior wall diameter during diastole (LVAWDd), left ven-tricular anterior wall diameter during systole (LVAWDs), left ventricular posterior wall diameter during diastole (LVPWDd), left ventricular posterior wall diameter during systole (LVPWDs), left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF), by means of pressure transducer inserted retrograde in left ventricle, measured hemodynamic parameters, which included left ventricular systolic pressure (LVSP), left ven-tricular end-diastolic pressure (LVEDP), maximal developing rate of left ventricular pressure (＋dp/dtmax) and maximal descending rate of left ventricular pressure (－dp/dtmax), weighed the rats, then took out their heat, meas-ured left ventricular weight (LVW) and right ventricular weight (RVW), calculated left ventricular mass index (LVMI), by means of histopathological detection (HE) and Masson staining, carried out histopathological observa-tion and acquired myocardial cross-sectional area (CSA) and collagen volume fraction (CVF), by means of real-time fluorescent quantitation PCR technique, measured mRNA expression level of myocardial α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC), atrial natriuretic factor (ANF), sarcoplasmic endoplasmic reticulum Ca2+-ATPase (SERCA2a), collagen type I (Col-I) and collagen type III (Col-III), by means of Western Blot tech-nique, measured protein expression level of myocardial cysteine aspartate protease-3 (Caspase-3), calcineurin (CaN) Aβ catalytic subunit (CaNAβ), nuclear factor of activation T cell 3 (NFAT3), phosphatidylinositol 3-kinase (PI3K) p110α catalytic subunit [PI3K(p110α)] and phospho-Akt (p-Akt). Results: (1) as compared with the rats in group SC, the BW and LVEDP of the rats in group SE decreased (P<0.05), their maximum running speed, time to exhaus-tion, LVW, LVMI, LVIDd, LVFS, LVEF, LVSP, ±dp/dtmax, CSA, mRNA of α-MHC and SERCA2a, protein of PI3K(p110α) and p-Akt increased (P<0.05); the maximum running speed, time ot exhaustion, BW, LVIDd, LVFS, LVEF, LVSP, ±dp/dtmax, mRNA of α-MHC and SERCA2a of the rats in group HC decreased (P<0.05), their LVW, LVMI, LVAWDd, LVAWDs, LVPWDd, LVPWDs, LVEDP, CSA, CVF, mRNA of ANF, β-MHC, Col-I and Col-III, protein of CaNAβ, NFAT3 and Caspase-3 increased (P<0.05); (2) as compared with the rats in group HC, the maximum running speed, time to exhaustion, LVW, LVMI, LVIDd, LVFS, LVEF, LVSP, ±dp/dtmax, CSA, mRNA of α-MHC and SERCA2a of the rats in group HE increased (P<0.05), their LVEDP, CVF, mRNA of ANF, β-MHC, Col-I and Col-III, protein of CaNAβ, NFAT3 and Caspase-3 decreased (P<0.05). The said results indicated the fol-lowings: long-term aerobic exercise promoted the changing of the heart of the rats suffering heart failure from pathological hypertrophy to physiological hypertrophy, restrained left ventricle remodeling, and improved cardiac functions and exercise endurance, whose mechanism was related to that exercise restrained CaN-NFAT signal path-way and activated PI3K-Akt signal pathway, and then down-regulated fetal gene expression, up-regulated contrac-tile protein, alleviated myocardial fibrosis and restrained cardiomyocyte apoptosis.
Key words: sports medicine；aerobic exercise；chronic heart failure cardiac hypertrophy；rat