To evaluate the hypothesis that increasing the potential for glycolytic metabolism would benefit the functioning of infarcted myocardium we investigated whether mild exercise training would increase the activities of oxidative enzymes, expression of carbohydrates-related transport proteins (monocarboxylate transporter MCT1 and glucose transporter GLUT4), and myosin heavy chain (MHC) isoforms. Myocardial infarction (MI) was produced by occluding the proximal left coronary artery in rat hearts for 30 minutes. After 6 weeks of run training on a treadmill, the wall of the left ventricle was dissected and divided into the anterior wall (AW, infarcted region) and posterior wall (PW, non-infarcted region). MI impaired citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD) activities in the AW (p<0.01), but not in the non-infarcted PW. No differences in the expression of MCT1 were found in either tissues of AW and PW following MI, whereas exercise training significantly increased the MCT1 expression in all conditions, except AW in the MI rats. Exercise training resulted in an increased expression of GLUT4 protein in the AW in the Sham rats and in the PW in the MI rats. The relative amount of MHC- was significantly increased in the AW and PW in MI rats as compared to Sham rats. However, exercise training resulted in a significant increase of MHC- expression in both AW and PW in both Sham and MI rats (p<0.01). These findings suggest that mild exercise training enhanced the potential for glycolytic metabolism and ATPase activity of the myocardium, even in the MI rats, assuring a beneficial role in the remodeling of the heart.