Expression of MHC- and MCT1 in cardiac muscle after exercise training in myocardial-infarcted rats

Hashimoto, Takeshi, Naoshige Kambara, Ryuji Nohara, Masayuki Yazawa, and Sadayoshi Taguchi. Expression of MHCand MCT1 in cardiac muscle after exercise training in myocardial-infarcted rats. J Appl Physiol 97: 843–851, 2004. First published May 7, 2004; 10.1152/japplphysiol.01193.2003.—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 carbohydrate-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 min. After the rats performed 6 wk 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; noninfarcted region). MI impaired citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities in the AW (P 0.01) but not in the noninfarcted PW. No differences in the expression of MCT1 were found in either tissues of AW and PW after 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 MHCwas significantly increased in the AW and PW in MI rats compared with sham rats. However, exercise training resulted in a significant increase of MHCexpression 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, ensuring a beneficial role in the remodeling of the heart.