Cardioprotective Effect and Its Mechanism of Exercise Training Up-Regulating the Expression of M₃ Receptor on Myocardial Infarction in Rats

objective:Cardioprotective effect and mechanism of exercise training up-regulating the expression of M3 receptor on myocardial infarction.Methods:48 male Sprague-Dawley rats were randomly assigned to four groups(n=12,per group):control group(C),myocardial infarction group(MI),moderate-intensity aerobic exercise with myocardial infarction group(ME1)and high-intensity aerobic interval exercise with myocardial infarction group(ME2),Rats in C group are breed normally.MI was induced by ligation of the left anterior descending(LAD)coronary artery in MI group。Rats in ME1 and ME2group take treadmill exercise for8 wk after 1wk post-operation.ME1 group running began at the speed of 10m/min for 5min,then accelerate from 3m/min to 16m/min.ME2 group running began at the speed of 10m/min for 10 min,then the speed increases to 25 m/min,after 7min,slow down at the speed of15m/min for 3min.Take the process alternatively.The total exercise time of ME1 and ME2are both 60 min,5d/1wk×8wk.LVSP,LVEDP,±dp/dtmax and the cardiac function changes are measured after training.Myocardial collagen fibers were observed by histological section and Masson staining.The expression of myocardial M3 R was observed and analyzed by immunoflourecence.The myocardial protein content of M3 R,MEK1/2,P-ERK1/2,ERK1/2 and apopto-sis related Bcl-2and Bax were assayed by Western Blot.Results:MI increased CVF and LVEDP(P<0.01),but decreased LVSP and-dp/dtmax(P<0.01).After MI myocardial M3 positive staining,after MI M3 protein expression significantly higher(P<0.01),MEK1/2,PERK1/2/ERK1/2 protein expression were significantly increased(P<0.01,P<0.01),after the MI the Bcl-2/Bax expression significantly reduced(P <0.01).ME1 and ME2 group CVF%,LVEDP significantly reduced(P<0.01),ME1-dp/dtmaxsignificantly increased(P<0.01),ME2 LVSP increased significantly(P<0.01).ME1 and ME2groups were identified myocardial M3,ME1 and ME2 M3 protein expression significantly increased(P<0.01,P<0.01).ME1 and ME2group Bcl-2/Bax expression significantly reduced in the MI group(P<0.01,P<0.01).ME1 and ME2index had no significant difference.Conclusions:Moderate-intensity aerobic exercise and high-intensity aerobic interval exercise can upregulate the M3R-MEK1/2-ERK1/2signaling pathway,thus inhibit the apoptosis of myocardial cells,reduce myocardial interstitial fibrosis and promote cardiac function after MI.