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)

The objectives of this study were to determine the effects of 10 consecutive days of moderate-intensity training on 1) the muscular metabolic response to exercise at 100% of the pre-training maximum rate of oxygen consumption (VO2max); and 2) mitochondrial enzyme markers (citrate synthase, CS; succinate dehydrogenase, SDH; 3-hydroxy-acyl-CoA dehydrogenase, HAD) of oxidative capacity in middle gluteal muscle. Six mature, unfit Thoroughbred horses completed both incremental (for determination of VO2max) and high-intensity exercise protocols before (HI1) and after (HI2) training. Training consisted of 10 consecutive days of running at 55% VO2max for 60 min per day (13-14 km/day). For the HI, horses completed a 10 min warm-up, followed by exercise at 100% of pre-training VO2max (mean speed 9.8 m/s) until fatigue. Training resulted in an 8.9% increases in VO2max (Pre: 142 +/- 4 ml/kg bwt/min; Post: 155 +/- 4 ml/kg bwt/min) and a 24% increase in run time to fatigue during HI. Whereas VO2 during HI was not altered by training, peak values for VCO2 and R were significantly lower following training. Compared to HI1, there was a 45% reduction in the net rate of muscle glycogenolysis during HI2. Peak (end exercise) values for plasma and muscle lactate concentrations decreased by 22 and 23%, respectively, after training. Training also attenuated the exercise-associated increase in plasma norepinephrine, but there was no effect on plasma epinephrine concentrations. Maximal activities of CS, SDH, and HAD were unaltered by training. We conclude that 10 days of moderate-intensity exercise results in decreases in muscle glycogenolysis and anaerobic metabolism during high-intensity exercise at the same absolute workload. Furthermore, development of measurable increases in mitochondrial oxidative potential may not be required for expression of these metabolic adaptations in early training.
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PMID:Muscular and metabolic responses to moderate-intensity short-term training. 1065 74

The purpose of this study was to examine the effect of acute (24 h) and chronic (5 wk) hypobaric hypoxic exposure equivalent to a simulated altitude of 4,300 m (446 mmHg) on the enzymes of fat metabolism. Heart, liver, and skeletal muscle were taken from 32 male Sprague-Dawley rats. Altitude exposure did not affect the activity of citrate synthase in any of the tissues, suggesting that mitochondrial content was unchanged. Carnitine palmitoyltransferase-I (CPT-I) activity was significantly reduced in the heart by both acute and chronic high altitude exposure compared with controls. A similar reduction was found for CPT-I activity in extensor digitorum longus after acute and chronic exposure compared with control animals. CPT-I activity was not affected by altitude exposure in the soleus muscle or the liver. 3-Hydroxyacyl-CoA dehydrogenase (beta-HAD) activity was significantly depressed in the hearts of chronically exposed animals compared with controls. No difference between acute and control animals was found in the heart for beta-HAD activity. Liver beta-HAD activity was also significantly decreased in the acclimatized as well as in the acute animals compared with the control group. Quadriceps beta-HAD activity was reduced for the chronic animals only compared with controls. These data suggest that acclimatization to high altitude selectively decreases key enzymes in fat utilization and oxidation in the heart, liver, and select skeletal muscles.
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PMID:Alterations in enzymes involved in fat metabolism after acute and chronic altitude exposure. 1113 88

The activity of muscle metabolic enzymes depends on the amount and type of physical training. We examined muscle enzyme adaptation to prolonged training followed by a period of lowered activity in spinal-cord-injured individuals (SCI). Ten SCI [mean age 35 (SEM 2) years, mean body mass 78 (SEM 4) kg, mean time post-injury 12 (SEM 2) years and range of lesion C5-T4] were given 12 months of functional electrical stimulation of an upright cycling motion for 30 min a day, three times a week, followed by 6 months of training once a week. Activities of glycolytic (hexokinase HK, lactate dehydrogenase LDH) and oxidative (citrate synthase CS, 3-hydroxyacyl-CoA dehydrogenase HAD) enzymes were determined in biopsies of the vastus lateralis muscle taken at 0, 3, 6, 12, and 18 months of training. The degree of sympathoadrenergic activity was evaluated from arterial concentrations of catecholamines in response to acute exercise. Training three times a week induced increases (P < 0.05) in HK (150%), LDH (40%), CS (100%), and HAD (70%) activities that reached a plateau after 3 months. Peak oxygen uptake and power output during exercise by electrical stimulation rose continuously over the first 12 months. After reducing the amount of training by two-thirds, HK, LDH and CS activities remained elevated above basal levels (P < 0.05), whereas HAD, power output and maximal oxygen uptake returned to pretraining levels (P > 0.05). It is concluded that most improvements in glycolytic and mitochondrial oxidative enzyme activities induced by long-term training can be maintained in spinal-cord-injured individuals despite a marked reduction in training frequency unrelated to performance or to the degree of sympathoadrenergic impairment.
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PMID:Muscle enzyme adaptation to training and tapering-off in spinal-cord-injured humans. 1141 39

The aim of the present study was to relate changes in muscle oxidative capacity and free fatty acid flux in response to oil supplementation to fuel utilisation during subsequent exercise of varying intensities. Following 10 weeks of oil supplementation there was an increased capacity for fat utilisation during low and moderate intensity exercise as indicated by a lower respiratory exchange ratio (RER) (P<0.05). We suggest that this was contributed to by a parallel increase in the oxidative capacity of muscle as indicated by a significant increase in the activity of muscle citrate synthase (CS) (P<0.05) and trend towards an increase in beta-Hydroxy acyl CoA dehydrogenase (beta-HAD), (P>0.05). In addition, low and moderate intensity exercise was associated with an exercise-induced increase in plasma free fatty acids (FFA) and there was an increased facility for uptake of FFA by working muscle from circulating triglycerides, as suggested by an increase in TL activity (P<0.01). The response to oil supplementation varied between individual horses and the magnitude of response, during the low intensity exercise test, in terms of difference in RER was correlated to the increase in CS activity (r2 = 0.95, P<0.05) following oil supplementation. There was no similar significant correlation with respect to FFA, TL or beta-HAD activity (P>0.05). The hypothesis in this study was that the metabolic adaptation to oil supplementation, in terms of exercise response, was related to individual increases in the activities of CS, beta-HAD or TL. However, the relationship between these parameters was unequivocal and requires further investigation, ideally with a larger group of horses.
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PMID:Effect of dietary lipid on response to exercise: relationship to metabolic adaptation. 1240 63

The purpose of this study was to determine if there were differences in the capacity of skeletal muscle from morbidly obese Black and White American women to oxidize fatty acids. The oxidation rates of (14)C-palmitate, (14)C-palmitoyl-CoA, and (14)C-palmitoyl-carnitine were measured in whole homogenates of rectus abdominus from Black and White women who were similar in age and body mass index (BMI). The activities of muscle citrate synthase (CS), beta-hydroxy acyl-CoA dehydrogenase (beta-HAD), and mitochondrial and microsomal acyl-CoA synthetase (ACS) were measured in the 2 groups. The results showed that the rate of (14)C-palmitate oxidation by muscle of Black women was 25% that of Whites (8.7 +/- 1.5 v 34.4 +/- 6.8 nmol (14)CO(2) produced/gram tissue wet weight/ hour; P <.05), but the rates of (14)C-palmitoyl-CoA and (14)C-palmitoyl-carnitine oxidation were not different in the 2 groups. No differences were found in the activities of CS or beta-HAD. However, the activities of both mitochondrial and microsomal ACS were lower in the Black women than the Whites (mitochondrial ACS 25.1 +/- 3.9 v 36.4 +/- 5.0 nmol/mg protein/min; P <.05; microsomal ACS 6.2 +/- 0.5 v 8.5 +/- 0.5; nmol/mg protein/min; P <.005). The lower rate of palmitate oxidation, and the lack of differences in the rates of palmitoyl-CoA and palmitoyl-carnitine oxidation indicate that there is a defect in the activation of the fatty acid in the muscle of the Black women. This was confirmed by the decrease in mitochondrial ACS activity in the Black women. The decreased fatty acid oxidation by skeletal muscle of obese Black women could result in shunting these fuels from muscle to adipose tissue for storage, which may contribute to the maintenance of obesity in the Black women.
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PMID:Fatty acid oxidation by skeletal muscle homogenates from morbidly obese black and white American women. 1280 Jan

The purpose of this study was to test the hypothesis that calcineurin, a calcium-dependent protein phosphatase recently implicated in the signaling of skeletal muscle hypertrophy and fiber type conversion, is required to induce some mitochondrial enzyme adaptations to endurance exercise training in skeletal muscle. Three- to four-week-old male Sprague-Dawley rats with an initial body weight ranging from 45 to 55 g were used in this study. The rats were randomly assigned to groups injected with either a specific calcineurin inhibitor, cyclosporin A (CsA), (group CI) or vehicle (group VI). CsA was subcutaneously injected into the rats at a rate of 50 mg.kg(-1) body weight per day for 10 days. The CI and VI groups were further assigned to sedentary (SED) or exercise training (EX) groups. In the EX group, the rats were trained for 10 days (90 min.day(-1), approximately 14-20 m.min(-1), 10% grade). The citrate synthase (CS) activities in the soleus and plantaris muscles of the EX group rats were significantly higher than those of the SED group rats ( p<0.001). Furthermore, 3-beta-hydroxyacyl-CoA dehydrogenase (3-HAD) activities in the soleus and plantaris muscles were significantly higher in the EX group rats than in the SED group rats ( p<0.001). However, there were no significant differences in CS and 3-HAD activities between the VI and CI groups. The interactions between CsA injection and exercise training were not statistically significant in any of the parameters. These results may suggest that calcineurin is not involved in some mitochondrial enzyme adaptations to endurance exercise training.
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PMID:Calcineurin is not involved in some mitochondrial enzyme adaptations to endurance exercise training in rat skeletal muscle. 1285 86

To examine whether genes associated with cellular defense against oxidative stress are associated with insulin sensitivity, patients with type 2 diabetes (n = 7) and age-matched (n = 5) and young (n = 9) control subjects underwent a euglycemic-hyperinsulinemic clamp for 120 min. Muscle samples were obtained before and after the clamp and analyzed for heat shock protein (HSP)72 and heme oxygenase (HO)-1 mRNA, intramuscular triglyceride content, and the maximal activities of beta-hydroxyacyl-CoA dehydrogenase (beta-HAD) and citrate synthase (CS). Basal expression of both HSP72 and HO-1 mRNA were lower (P < 0.05) by 33 and 55%, respectively, when comparing diabetic patients with age-matched and young control subjects, with no differences between the latter groups. Both basal HSP72 (r = 0.75, P < 0.001) and HO-1 (r = 0.50, P < 0.05) mRNA expression correlated with the glucose infusion rate during the clamp. Significant correlations were also observed between HSP72 mRNA and both beta-HAD (r = 0.61, P < 0.01) and CS (r = 0.65, P < 0.01). HSP72 mRNA was induced (P < 0.05) by the clamp in all groups. Although HO-1 mRNA was unaffected by the clamp in both the young and age-matched control subjects, it was increased (P < 0.05) approximately 70-fold in the diabetic patients after the clamp. These data demonstrate that genes involved in providing cellular protection against oxidative stress are defective in patients with type 2 diabetes and correlate with insulin-stimulated glucose disposal and markers of muscle oxidative capacity. The data provide new evidence that the pathogenesis of type 2 diabetes involves perturbations to the antioxidant defense mechanism within skeletal muscle.
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PMID:Intramuscular heat shock protein 72 and heme oxygenase-1 mRNA are reduced in patients with type 2 diabetes: evidence that insulin resistance is associated with a disturbed antioxidant defense mechanism. 1294 74

The purpose of the present study was to investigate the relationship among intra-abdominal adipose storage, adaptation in the serum leptin concentration and skeletal muscle enzyme activity after a 4-week energy restriction (ER). Thirty-one male Wistar rats were divided into 40% energy restricted (n=24) or ad libitum-fed control (CL) rats (n=7). The energy-restricted rats were grouped into the most fat (MF, n=7), medium (n 10) and the least fat (LF, n=7) by their intra-abdominal fat pads mass (epididymal, mesenteric, and perirenal) after ER. A superficial portion of M. gastrocnemius tissue obtained before and after the diet period were analyzed to determine the activities of hexokinase (HK), beta-hydroxyacyl CoA dehydrogenase (beta-HAD) and citrate synthase (CS). Blood samples were also collected for a serum leptin assay. At the baseline, no difference was found in either the leptin concentration or the enzyme activities among LF, MF and CL. The serum leptin concentration was positively correlated with the muscle activities of beta-HAD and CS, while it negatively correlated with HK/beta-HAD. After ER, the activities of HK, beta-HAD and CS were all significantly lower in LF than in CL. Among the energy-restricted rats, the intra-abdominal fat pad weight, leptin concentration and the activities of beta-HAD, CS, beta-HAD/CS all significantly correlated with one another. The changes in leptin and the activity of beta-HAD were also positively correlated. These findings indicate that parallel decreases in the serum leptin and skeletal muscle enzyme activities with the energy restriction-induced intra-abdominal adipose reduction, thus may suggest the leptin to have a regulative effect on the muscle enzyme activity during ER.
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PMID:Decreased serum leptin and muscle oxidative enzyme activity with a dietary loss of intra-abdominal fat in rats. 1471 57

The relative contribution of genetic and environmental influences to individual exercise capacity is difficult to determine. Accordingly, animal models in which these influences are carefully controlled are highly useful to understand the determinants of intrinsic exercise capacity. Studies of systemic O(2) transport during maximal treadmill exercise in two diverging lines of rats artificially selected for endurance capacity showed that, at generation 7, whole body maximal O(2) uptake ((.)V(O(2)(max)) was 12% higher in high capacity (HCR) than in low capacity runners (LCR) during normoxic exercise. The difference in (.)V(O(2)(max) between HCR and LCR was larger during hypoxic exercise. Analysis of the linked O(2) conductances of the O(2) transport system showed that the higher (.)V(O(2)(max) was not due to a higher ventilatory response, a more effective pulmonary gas exchange, or an increased rate of O(2) delivery to the tissue by blood. The main reason for the higher (.)V(O(2)(max) of HCR was an increased tissue O(2) extraction, due largely to a higher tissue diffusive O(2) conductance. The enhanced tissue O(2) diffusing capacity was paralleled by an increased capillary density of a representative locomotory skeletal muscle, the gastrocnemius, in HCR. Activities of skeletal muscle oxidative enzymes citrate synthase and beta-HAD were also higher in HCR than LCR. Thus, the functional characteristics observed during exercise are consistent with the structural and biochemical changes observed in skeletal muscle that imply an enhanced capacity for muscle O(2) uptake and utilization in HCR. The results indicate that the improved (.)V(O(2)(max) is solely due to enhanced muscle O(2) extraction and utilization. However, the question arises as to whether it is possible to maintain a continually expanding capacity for O(2) extraction at the tissue level with successive generations, without a parallel improvement in the capacity to deliver O(2) to the exercising muscles.
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PMID:Systemic oxygen transport in rats artificially selected for running endurance. 1634 8

Some evidence suggests that resistance training may lower relative muscle mitochondrial content via "dilution" of the organelle in a larger muscle fibre. Such an adaptation would reduce fatigue resistance, as well as compromise oxidative ATP synthesis and the capacity for fatty-acid oxidation. We investigated the effect of resistance training on mitochondrial enzymes of the citric acid cycle (citrate synthase; CS) and beta-oxidation (beta-hydroxyacyl CoA dehydrogenase; beta-HAD), as well as markers of the potential for glucose phosphorylation (hexokinase; HK) and glycolysis (phosphofructokinase; PFK). Twelve untrained men (21.9 +/- 0.5 y; 1.79 +/- 0.03 m; 83.2 +/- 3.2 kg) participated in a 12 week progressive resistance-training program. Muscle biopsies were taken from the vastus lateralis before (PRE) and after (POST) training. Training increased mean muscle fibre cross-sectional area (p < 0.05) and the activities of CS (PRE = 4.53 +/- 0.44 mol.kg protein(-1).h(-1); POST = 5.63 +/- 0.40 mol.kg protein(-1).h(-1); p < 0.001) and beta-HAD (PRE = 2.55 +/- 0.28 mol.kg protein(-1).h(-1); POST = 3.11 +/- 0.21 mol.kg protein(-1).h(-1); p < 0.05). The activity of HK increased 42% (p < 0.05), whereas the activity of PFK remained unchanged. We conclude that resistance training provides a stimulus for improving muscle oxidative potential, as reflected by the increased activities of CS and beta-HAD following resistance training induced hypertrophy.
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PMID:Increased muscle oxidative potential following resistance training induced fibre hypertrophy in young men. 1711 Oct 3


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