EXERCISE TRAINING ENHANCES GLYCOLYTIC AND OXIDATIVE ENZYMES IN CANINE MYOCARDIUM 362

Abstract

Epidemiological evidence indicates that endurance exercise training renders the myocardium resistant to ischemic injury. However, the mechanisms for exercise-induced cardioprotection are unknown. Exercise training increases activities of glycolytic and oxidative enzymes in skeletal muscle. The goal of this study was to determine whether training can also enhance the metabolic capabilities of cardiac muscle. Mongrel canines were subjected to 9 wk treadmill training; sedentary dogs were cage-rested for 4 wk. Stop-frozen samples of left (LV) and right (RV) ventricular myocardium were obtained from pentobarbital-anesthetized trained (Trn) and sedentary (Sed) dogs. Enzymes(HK: hexokinase; PFK; phosphofructokinase; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; PK: pyruvate kinase; LDH: lactate dehydrogenase; CS: citrate synthase; α-KGDH: α-ketoglutarate dehydrogenase; MDH: malate dehydrogenase) were extracted in phosphate buffer and assayed at 38°C. Thetable reports enzyme activities (U · mg protein-1); data are means ± SE, n = 4 (*: P< 0.05 vs. sedentary). Exercise training increased GAPDH activity in both ventricles. During ischemia, GAPDH is the primary rate controlling glycolytic reaction. Thus, increased GAPDH activity could support enhanced glycolysis in trained myocardium. Citrate synthase, which catalyzes carbon entry into the TCA cycle, was also increased in trained LV; thus, training enhances myocardial oxidative capacity.