Effects of β₁- and β₁ + β₂-antagonists on training-induced myocardial hypertrophy and enzyme adaptation

The effects of β₁- and β₁ + β₂-antagonists on the myocardial adaptation to exercise training were investigated in male Sprague-Dawley rats randomly divided into. trained (treadmill, 1 hr/day, 5 days/week for 10 weeks at 27 m/min, 15% grade) without drug (TC), sedentary without drug (SC), trained treated with atenolol (TA) (10 mg/kg body wt, i.p.), trained treated with propranolol (TP, 30 mg/kg body wt, i.p.), and sedentary propranolol. Doses of both β-antagonists were titrated to decrease the exercise heart rate by 25% compared to the controls. The heart weight and heart/body weight ratio were significantly greater in TC (1.28 ± 0.07 g (P < 0.01); 296 ± 12 mg/100 g body wt (P < 0.05) respectively) than in SC (1.09 ± 0.04 g and 268 ± 11 mg/100 g body wt), or in TP and TA. Myocardial mitochondrial protein was unchanged by training or β-blockade. Citrate synthase and /gb-hydroxyacyl CoA dehydrogenase activities were not altered. Carnitine palmitoyltransferase activity was increased in SP compared to SC. Training increased hexokinase activity only in TC (5.22 ± 0.12 vs 4.26 ± 0.23 μmol/min/g wet wt, P < 0.01). Lactate dehydrogenase activity increased significantly (P < 0.01) in both TC (383 ± 14 μmol/min/g wet wt) and TA (372 ± 14 μmol/min/g wet wt) compared to SC (276 ± 14 μmol/min/g wet wt), but not in TP versus SP. These data indicate that (1) β-adrenergic blockade prevents training-induced cardiac hypertrophy; (2) β-antagonists have little effect on the myocardial oxidative capacity; and (3) while the training induction of myocardial hexokinase is inhibited by both β₁ and β₁ + β₂-antagonists, myocardium may increase its ability to utilize lactate during exercise with training despite β₁-blockade.