Objective:To explore any effect of aerobic exercise on cardiac energy metabolism and mitochondrial respiration after myocardial infarction.Methods:Forty-five Sprague-Dawley rats were randomly divided into a sham operation group, a heart failure control group and a heart failure exercise group. Myocardial infarction was induced in the heart failure groups using coronary artery ligation. Four weeks after the successful modeling, the heart failure exercise group underwent 8 weeks of aerobic treadmill exercise. The cardiac function and exercise ability of all of the rats were then observed using echocardiography and the incremental treadmill exercise test. Myocardial creatine phosphate (PCr) and adenosine triphosphate (ATP) were measured by magnetic resonance spectroscopy, and the respiratory function of the myocardial mitochondria was evaluated by using cell respirometry.Results:Compared with the sham operation group, the average PCr content, PCr/ATP ratio, oxygen consumption of mitochondrial respiratory chain complexes I and II, left ventricular shortening fraction (FS) and ejection fraction (EF), maximum running speed, exhaustion distance and exhaustion time in the incremental treadmill exercise test were all significantly worse in the heart failure control group. Moreover, the average ATP content, complex I oxygen consumption, left ventricular FS and EF, and the maximum running speed, exhaustion distance and exhaustion time in incremental treadmill exercise of the heart failure exercise group were all superior to those of the heart failure control group.However, no significant differences were observed in the average PCr/ATP ratio between the heart failure exercise and control groups.Conclusions:Regular aerobic exercise can improve cardiac performance after chronic heart failure, at least in rats. The mechanism may be related to increased levels of myocardial ATP and better mitochondrial complex I functioning. The PCr/ATP ratio may not be a suitable biomarker for evaluating the benefits of exercise for the heart.