Exercise training enhances glycolytic and oxidative enzymes in canine ventricular myocardium.

Aerobic exercise training evokes adaptations in the myocardial contractile machinery that enhance cardiac functional capacity; in comparison, the effects of training on the myocardium's energy generating pathways are less well characterized. This study tested the hypothesis that aerobic exercise training can increase the capacities of the major pathways of intermediary metabolism in canine myocardium. Mongrel dogs were conditioned by a 9-week treadmill running program or cage rested for 4 weeks. Exercise conditioning was evidenced by 26% and 22% decreases (P<0.05) in respective heart rates at rest and during submaximal exercise and by a 40% increase (P<0.05) in citrate synthase (CS) activity of the vastus lateralis. Glycolytic, TCA cycle, and beta-oxidative enzymes were assayed in myocardial extracts at 37 degrees C. Relative to sedentary controls, training increased glyceraldehyde 3-phosphate dehydrogenase (GAPDH) activity by 49% in left and 33% in right ventricle, and pyruvate kinase, CS, and 3-hydroxyacyl CoA dehydrogenase (HADH) activities by 74%, 91%, and 77%, respectively, in left ventricle (P<0.05). Immunoblotting further confirmed that training increased left ventricular contents of CS and GAPDH. Other measured enzymes (hexokinase, phosphofructokinase, lactate dehydrogenase, alpha-ketoglutarate dehydrogenase, malate dehydrogenase) were not altered by training in either ventricle. Kinetic analyses revealed increased maximum rates but unaltered substrate affinities of GAPDH, CS and HADH following training. Thus, aerobic exercise training augments the intermediary metabolic capacity of canine myocardium by selectively increasing the concentrations of regulatory enzymes of glycolysis and oxidative metabolism.