|（1.School of Physical Education，Weifang University，Weifang 261061，China；2.School of Physical Education，Luoyang Nomal College，Luoyang 471022，China）
Abstract: In order to probe into regulation made by long-term aerobic exercising on the myocardial energy metabo-lism of rats suffering a chronic heart failure and any possible mechanism, the authors established a post myocardial infarction heart failure model after having ligated the coronary artery of the rats, let the rats rest for 4 weeks, then divided them randomly into a sham operation sedentary group (Sham), a myocardial infarction sedentary group (MI-Sed) and a myocardial infarction exercising group (MI-Ex). The rats in the MI-Ex group exercised on a tread-mill for 8 weeks, while the rats in the Sham and MI-Sed groups maintained a sedentary condition. After the experi-ment was completed, by using the left ventricle tube method the authors measured hemodynamic parameters, which include left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal devel-oping rate of left ventricular pressure (＋(dp/dt)max) and maximal descending rate of left ventricular pressure (－(dp/dt)max); by means of Masson dyeing the authors carried out histopathological observation; by using the colorimetric method the authors measured myocardial glycogen, fat acid (FA) and lactic acid content; by using real-time fluorescent quantitation PCR the authors determined myocardial peroxisome proliferator-activated receptor α (PPARα) and car-nitine palmitoyl transferase-1 (CPT-1) mRNA level; by using the Western blot method, the authors measured AMPK, glucose transporter (GLUT4), peroxisome proliferator-activated receptor γ coactivator lα (PGC-1α) protein of myocar-dium. The authors revealed the following findings: as compared with the rats in the Sham group, the LVSP and ±(dp/dt)max of the rats in the MI-Sed group decreased significantly (P<0.01), their LVEDP increased significantly (P<0.01); their myocardial glycogen content decreased (P<0.01), their FA and lactic acid content increased (P<0.01); their PPARα, CPT-1 mRNA decreased (P<0.01); their phosphorylated AMPKα (p-AMPKα) protein level increased (P<0.05), their GLUT4 and PGC-1α decreased (P<0.01); as compared with the rats in the MI-Sed group, the LVEDP and ±(dp/dt)max of the rats in the MI-Ex group increased (P<0.01), their LVEDP decreased significantly (P<0.01); their myocardial glycogen content increased (P<0.05), their FA and lactic acid content decreased (P<0.01); their PPARα, CPT-1 mRNA and p-AMPKα, GLUT4 and PGC-1α protein level of myocardium increased significantly (P<0.01). The findings indicate that long-term aerobic exercising improves the metabolic remodeling of a failing heart and enhances cardiac functions by activating AMPK and its downstream signal pathways.
Key words: sports biochemistry；adenosine monophosphate-activated protein kinase；heart failure；energy me-tabolism；aerobic exercising；metabolic remodeling；rat