Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonselective and beta 1-selective adrenergic antagonists were tested for their effects on enzymatic adaptation to exercise training in rats as follows: trained + placebo (TC); trained + propranolol (TP); trained + atenolol (TA); and corresponding sedentary groups, SC and SP. Trained rats ran 1 h/d at 26.8 m/min, 15% grade, 5 d/wk, 10 wk. Both beta-antagonists were given at doses that decreased exercise heart rates by 25%. Training increased skeletal muscle citrate synthase, cytochrome c oxidase (Cyt-Ox), carnitine palmitoyltransferase (CPT), beta-hydroxyacyl coenzyme A dehydrogenase, mitochondrial malate dehydrogenase (MDH), and alanine aminotransferase (ALT) activities significantly in the TC group, but not in TP. These enzyme activities, except Cyt-Ox and CPT, were also significantly increased in TA. Hepatic phosphoenolpyruvate carboxykinase activity did not alter with training or beta-blockade. Fructose 1,6-bisphosphatase activity was lower in TC than in SC, but unchanged in TP or TA. Hepatic mitochondrial MDH and ALT activities increased with training only in TC. It is concluded that beta 2-adrenergic mechanisms play an essential role in the training-induced enzymatic adaptation in skeletal muscle.
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PMID:Enzymatic adaptation to physical training under beta-blockade in the rat. Evidence of a beta 2-adrenergic mechanism in skeletal muscle. 287 82

This study was designed to test the hypothesis that rats trained with marked reductions in exercise heart rate respond with adaptations indicative of increased intrinsic myocardial performance. Therefore, we measured changes in maximum work capacity (VO2max), biochemical-functional indexes of cardiac contractile capacity, and skeletal muscle oxidative capacity in normal-trained (NT) rats and in rats trained while receiving the selective cardiac beta 1-blocking drug atenolol (AT). Training consisted of treadmill running at approximately 80% VO2max (untrained) for 1-h duration, 6 days/wk, for a total of 8 wk. Exercise heart rate of the AT group was markedly reduced and averaged 140 beats/min below the NT group for any given session. Compared with sedentary controls, VO2max was increased by 11%, and red vastus lateralis muscle citrate synthase activity was increased by 28% in both AT and NT groups (P less than 0.05). There were no differences between trained and nontrained groups with regard to Ca2+-regulated myofibril adenosinetriphosphatase. In situ derived left ventricular pressure and the maximum rate of left ventricular pressure development were not augmented relative to sedentary control values when the trained hearts were either stimulated inotropically or maximally afterloaded . These findings suggest that maximum exercise capacity can be enhanced in rodents conditioned with and without limited elevation in exercise heart rate; however, this reduction of exercise heart rate acceleration does not provide a stimulus to enhance the intrinsic functional capacity of the rodent heart.
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PMID:Adaptive responses of rats trained with reductions in exercise heart rate. 623 46