Abstract: Objective To observe the effects of fenofibrate,peroxisome proliferator-activated receptors α（PPARα）activators,on myocardial energy metabolism in the rat model of heart failure post myocardial infarction（MI）.Methods The model of MI was established by ligation of left anterior descending artery.Twenty surviving rats were divided randomly into untreated myocardial ischemic group（MI group,n =10）and fenofibrate intervention groupF group,n =10,fenofibrate 30 mg/（kg·d）orally,sham-operated group（SH group,n =10）served as control.Hemodynamics were measured after 8 weeks treatment.PPARα,α/β-MHC（myosin heavy chain）mRNA expressions were examined by RT-PCR.Mitochondrial respiratory function were measured by Clark oxygen electrodes.The size of adenine acid pool（ATP,ADP,AMP）and phosphocreatine（Pcr）in mitochondria were measured by high performance liquid chromatography（HPLC）.The adenine nucleotide translocator（ANT）activity was detected by the atractyloside-inhibitor stop technique.Results Compared with the sham group,mRNA expression of PPARα and α/β-MHC mRNA were significantly decreased in MI group（P ＜0.01）,mitochondrial respiratory activity,transport activity of ANT and the high-energy phosphate content of mitochondria all exhibited a significant decrease（P ＜0.01）,the hemodynamic parameters was aggravated（P ＜0.01）,Compared with the MI group,fenofibrate intervention significantly increases the mRNA expression of PPARα and α/β-MHC（P ＜0.05）,improved mitochondrial respiratory activity and transport activity of ANT（P ＜0.05）,the hemodynamic parameters were ameliorated（P ＜0.05）,but the high-energy phosphate content of mitochondria did not change significantly（P ＞0.05）.Conclusion Heart failure after myocardial infarction was associated with recapitulation of myocardial fetal energy metabolism,fenofibrate could improve myocardia energy metabolism and delay the development of heart failure.