Regulation made by long-term aerobic exercising on the myocardial energy metabolism of rats suffering a chronic heart failure
In order to probe into regulation made by long-term aerobic exercising on the myocardial energy metabolism 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 treadmill for 8 weeks,while the rats in the Sham and MI-Sed groups maintained a sedentary condition.After the experiment 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 carnitine 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 myocardium.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(P0.01),their LVEDP increased significantly(P0.01);their myocardial glycogen content decreased(P0.01),their FA and lactic acid content increased(P0.01);their PPARα,CPT-1 mRNA decreased(P0.01);their phosphorylated AMPKα(p-AMPKα) protein level increased(P0.05),their GLUT4 and PGC-1α decreased(P0.01);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(P0.01),their LVEDP decreased significantly(P0.01);their myocardial glycogen content increased(P0.05),their FA and lactic acid content decreased(P0.01);their PPARα,CPT-1 mRNA and p-AMPKα,GLUT4 and PGC-1α protein level of myocardium increased significantly(P0.01).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.