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 purpose of the present study was to relate the training-induced alterations in lactate kinetics parameters to the concomitant changes in time to exhaustion (T(lim)) at a work rate corresponding to maximal oxygen uptake (Pa(peak)). Eight subjects performed before and after training i) an incremental exercise up to exhaustion to determine Pa(peak), ii) a 5-min 90 % Pa(peak) exercise followed by a 90-min passive recovery to determine an individual blood lactate recovery curve fitted to the bi-exponential time function: La(t) = La(0) + A1(1 - e -gamma1 x t) + A2(1 - e -gamma2 x t), and iii) a time to exhaustion at Pa peak to determine T lim. A biopsy of the vastus lateralis muscle was made before and after training. The training programme consisted in pedalling on a cycle ergometer 2 h a day, 6 days a week, for 4 weeks. Training-induced increases (p < 0.05) in Pa(peak), muscle capillary density, citrate synthase activity, gamma2 that denotes the lactate removal ability (from 0.0547 +/- 0.0038 to 0.0822 +/- 0.0071 min (-1)) and T(lim) (from 299 +/- 23 to 486 +/- 63 s), decreases (p < 0.05) in activities of lactate dehydrogenase (LDH) and muscle type of LDH, the phosphofructokinase/citrate synthase activities ratio and the estimated net amount of lactate released (NALR) during exercise recovery (from 66.5 +/- 8.6 to 47.2 +/- 11.1 mmol) were also observed. The improvement of T (lim) with training was related to the increase in gamma2 (r = 0.74, p = 0.0367) and to the decrease in NALR (r = 0.77, p = 0.0250). These results suggest that the post-training greater ability to remove lactate from the organism and reduced muscle lactate accumulation during exercise account for the concomitant improvement of the time to exhaustion during high-intensity exercise performed at the same relative work rate.
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PMID:Effects of training on lactate kinetics parameters and their influence on short high-intensity exercise performance. 1638 44

We hypothesized that specific muscular transcript level adaptations participate in the improvement of endurance performances following intermittent hypoxia training in endurance-trained subjects. Fifteen male high-level, long-distance runners integrated a modified living low-training high program comprising two weekly controlled training sessions performed at the second ventilatory threshold for 6 wk into their normal training schedule. The athletes were randomly assigned to either a normoxic (Nor) (inspired O2 fraction = 20.9%, n = 6) or a hypoxic group exercising under normobaric hypoxia (Hyp) (inspired O2 fraction = 14.5%, n = 9). Oxygen uptake and speed at second ventilatory threshold, maximal oxygen uptake (VO2 max), and time to exhaustion (Tlim) at constant load at VO2 max velocity in normoxia and muscular levels of selected mRNAs in biopsies were determined before and after training. VO2 max (+5%) and Tlim (+35%) increased specifically in the Hyp group. At the molecular level, mRNA concentrations of the hypoxia-inducible factor 1alpha (+104%), glucose transporter-4 (+32%), phosphofructokinase (+32%), peroxisome proliferator-activated receptor gamma coactivator 1alpha (+60%), citrate synthase (+28%), cytochrome oxidase 1 (+74%) and 4 (+36%), carbonic anhydrase-3 (+74%), and manganese superoxide dismutase (+44%) were significantly augmented in muscle after exercise training in Hyp only. Significant correlations were noted between muscular mRNA levels of monocarboxylate transporter-1, carbonic anhydrase-3, glucose transporter-4, and Tlim only in the group of athletes who trained in hypoxia (P < 0.05). Accordingly, the addition of short hypoxic stress to the regular endurance training protocol induces transcriptional adaptations in skeletal muscle of athletic subjects. Expressional adaptations involving redox regulation and glucose uptake are being recognized as a potential molecular pathway, resulting in improved endurance performance in hypoxia-trained subjects.
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PMID:Exercise training in normobaric hypoxia in endurance runners. III. Muscular adjustments of selected gene transcripts. 1654 Jul 10

The aim of the present study was to examine the differences in fat oxidation between endurance trained (ET) and untrained (UT) women. Eight ET and nine UT women performed a progressive cycle ergometer test until exhaustion. The rate of fat oxidation was similar at low work rates (<or=90 W) but was 80-200% higher in ET subjects at 120-180 W. When related to relative exercise intensity, the fat oxidation was similar in the low-intensity domain (<or=40% VO2max), but higher in the ET subjects both at moderate intensities (45-60% VO2max; +22% vs. UT) and at high intensities (65-80% VO2max; +35% vs. UT). There was no difference in the maximal fat oxidation rates between the trained and untrained women. The relative exercise intensity that elicited the highest rate of fat oxidation (Fatmax) was 56+/-3% and 53+/-2% VO2max in ET and UT women, respectively (NS). In biopsies from m. vastus lateralis, the activity of the enzymes citrate synthase, beta-hydroxy acyl CoA dehydrogenase (HAD), and hormone sensitive lipase was higher in the ET subjects. The HAD activity correlated significantly with fat oxidation at moderate and high intensities. We conclude that the ET women had a higher fat oxidation at moderate- and high-exercise intensities both at same relative and at absolute intensity compared with the UT women. The HAD activity and fat oxidation rates were highly correlated indicating that training-induced adaptation in muscle fat oxidative capacity is an important factor for enhanced fat oxidation. Interestingly, maximal fat oxidation occurred at the same exercise intensity.
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PMID:Maximal fat oxidation rates in endurance trained and untrained women. 1700 14

Inspiring a hyperoxic (H) gas permits subjects to exercise at higher power outputs while training, but there is controversy as to whether this improves skeletal muscle oxidative capacity, maximal O(2) consumption (Vo(2 max)), and endurance performance to a greater extent than training in normoxia (N). To determine whether the higher power output during H training leads to a greater increase in these parameters, nine recreationally active subjects were randomly assigned in a single-blind fashion to train in H (60% O(2)) or N for 6 wk (3 sessions/wk of 10 x 4 min at 90% Vo(2 max)). Training heart rate (HR) was maintained during the study by increasing power output. After at least 6 wk of detraining, a second 6-wk training protocol was completed with the other breathing condition. Vo(2 max) and cycle time to exhaustion at 90% of pretraining Vo(2 max) were tested in room air pre- and posttraining. Muscle biopsies were sampled pre- and posttraining for citrate synthase (CS), beta-hydroxyacyl-coenzyme A dehydrogenase (beta-HAD), and mitochondrial aspartate aminotransferase (m-AsAT) activity measurements. Training power outputs were 8% higher (17 W) in H vs. N. However, both conditions produced similar improvements in Vo(2 max) (11-12%); time to exhaustion (approximately 100%); and CS (H, 30%; N, 32%), beta-HAD (H, 23%; N, 21%), and m-AsAT (H, 21%; N, 26%) activities. We conclude that the additional training stimulus provided by training in H was not sufficient to produce greater increases in the aerobic capacity of skeletal muscle and whole body Vo(2 max) and exercise performance compared with training in N.
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PMID:The effects of training in hyperoxia vs. normoxia on skeletal muscle enzyme activities and exercise performance. 1717 Feb 2

Well-trained endurance athletes undergo periods of high-intensity interval training (HIT) or high-volume training (HVT) to improve exercise performance, but little is known about the mechanistic changes that occur during this time. The purpose of this study was to examine the influence of HIT and HVT on the activities of citrate synthase (CS) and phosphofructokinase (PFK), and on intramuscular buffering capacity (betam) in already well-trained rats. At 4 weeks of age, Wistar rats were divided into sedentary (SED; n=18) and exercise training groups (n=38). Following a 10 week preliminary training program, trained rats were divided randomly into 3 further groups that completed 4 additional weeks of continued endurance (CON, n=14), high-intensity training (HIT, n=12), or high-volume training (HVT, n=12). Soleus (SOL), red and white gastrocnemius (RG and WG), and red and white vastus (RV and WV) muscles were removed 24-48 h after a final run-to-fatigue performance test (30 m.min(-1) 25% grade) to determine the activities of CS, PFK, and betam. No differences in run time to exhaustion were found between the groups. However the HIT group possessed CS and PFK activities and betam in WV muscle that were 60%, 24%, and 10% higher, respectively (all p<0.05), compared with the HVT group; differences were not found between the HIT and CON groups. Although no differences in run performance were found, HIT compared with HVT in already well-trained rats resulted in significantly higher oxidative and glycolytic capacities of fast-contracting fibres. No differences were shown in fast-contracting muscle between HIT and CON.
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PMID:Manipulating training intensity and volume in already well-trained rats: effect on skeletal muscle oxidative and glycolytic enzymes and buffering capacity. 1751 Jun 78

High-intensity aerobic interval training (HIIT) is a compromise between time-consuming moderate-intensity training and sprint-interval training requiring all-out efforts. However, there are few data regarding the ability of HIIT to increase the capacities of fat and carbohydrate oxidation in skeletal muscle. Using untrained recreationally active individuals, we investigated skeletal muscle and whole-body metabolic adaptations that occurred following 6 weeks of HIIT (~1 h of 10 x 4 min intervals at ~90% of peak oxygen consumption (VO2 peak), separated by 2 min rest, 3 d.week-1). A VO2 peak test, a test to exhaustion (TE) at 90% of pre-training VO2 peak, and a 1 h cycle at 60% of pre-training VO2 peak were performed pre- and post-HIIT. Muscle biopsies were sampled during the TE at rest, after 5 min, and at exhaustion. Training power output increased by 21%, and VO2 peak increased by 9% following HIIT. Muscle adaptations at rest included the following: (i) increased cytochrome c oxidase IV content (18%) and maximal activities of the mitochondrial enzymes citrate synthase (26%), beta-hydroxyacyl-CoA dehydrogenase (29%), aspartate-amino transferase (26%), and pyruvate dehydrogenase (PDH; 21%); (ii) increased FAT/CD36, FABPpm, GLUT 4, and MCT 1 and 4 transport proteins (14%-30%); and (iii) increased glycogen content (59%). Major adaptations during exercise included the following: (i) reduced glycogenolysis, lactate accumulation, and substrate phosphorylation (0-5 min of TE); (ii) unchanged PDH activation (carbohydrate oxidation; 0-5 min of TE); (iii) ~2-fold greater time during the TE; and (iv) increased fat oxidation at 60% of pre-training VO2 peak. This study demonstrated that 18 h of repeated high-intensity exercise sessions over 6 weeks (3 d.week-1) is a powerful method to increase whole-body and skeletal muscle capacities to oxidize fat and carbohydrate in previously untrained individuals.
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PMID:High-intensity aerobic interval training increases fat and carbohydrate metabolic capacities in human skeletal muscle. 1908 69

The purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and endurance performance in trained cyclists. Ten well-trained cyclists (mean +/- SD; age 24.4 +/- 2.8 years, body mass 73.2 +/- 8.3 kg, VO(2max) 58 +/- 7 ml kg(-1) min(-1)) completed three endurance performance tasks [incremental exercise test to exhaustion, 2 and 10 min time trial (TT)]. In addition, a muscle biopsy sample from the vastus lateralis muscle was analysed for MCT1 and MCT4 expression levels together with the activity of citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD). There was a tendency for VO(2max) and peak power output obtained in the incremental exercise test to be correlated with MCT1 (r = -0.71 to -0.74; P < 0.06), but not MCT4. The average power output (P (average)) in the 2 min TT was significantly correlated with MCT4 (r = -0.74; P < 0.05) and HAD (r = -0.92; P < 0.01). The P (average) in the 10 min TT was only correlated with CS activity (r = 0.68; P < 0.05). These results indicate the relationship between MCT1 and MCT4 as well as cycle TT performance may be influenced by the length and intensity of the task.
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PMID:The relationship between monocarboxylate transporters 1 and 4 expression in skeletal muscle and endurance performance in athletes. 1931 62

In the present study, we tested the hypothesis that chronic ANG I-converting enzyme (ACE) inhibition could improve the training-induced improvement in endurance exercise performance and that this could be related to enhanced skeletal muscle metabolic efficiency. Female Wistar rats were assigned to four groups comprising animals either maintained sedentary or endurance trained (Sed and Tr, respectively), and treated or not for 10 wk with an ACE inhibitor, perindopril (2 mg.kg(-1).day(-1)) (Per and Ct, respectively) (n = 8 each). Trained rats underwent an 8-wk treadmill training protocol that consisted of 2 h/day running at 30 m/min on a 8% decline. Before the start of and 1 wk before the end of experimental conditioning, the running time to exhaustion of rats was measured on a treadmill. The training program led to an increase in endurance time, higher in Tr-Per than in Tr-Ct group (125% in Tr-Ct vs. 183% in Tr-Per groups, P < 0.05). Oxidative capacity, measured in saponin-permeabilized fibers of slow soleus and fast plantaris muscles, increased with training, but less in Tr-Per than in Tr-Ct rats. The training-induced increase in citrate synthase activity also was less in soleus from Tr-Per than Tr-Ct rats. The training-induced increase in the percentage of the type IIa isoform of myosin heavy chain (MHC) (45%, P < 0.05) and type IIx MHC (25%, P < 0.05) associated with decreased type IIb MHC (34%, P < 0.05) was minimized by perindopril administration. These findings demonstrate that the enhancement in physical performance observed in perindopril-treated animals cannot be explained by changes in mitochondrial respiration and/or MHC distribution within muscles involved in running exercise.
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PMID:Decreased muscle ACE activity enhances functional response to endurance training in rats, without change in muscle oxidative capacity or contractile phenotype. 1940 47

Intense and exhaustive exercise (IEE) is associated with oxidative stress in skeletal muscle, and we recently reported that intestine is sensitive to IEE. In the present study, we investigated the possible relationship between the effects of IEE on morphology and oxidative markers in the ileum and isolated mitochondria. C57BL/6 mice were ascribed either to a control group comprising two subgroups, one sedentary and another exercised for 10 days (E10), or to a corresponding supplemented control group again comprising two subgroups, one sedentary and another exercised for 10 days (E10-V). The IEE program consisted of a single daily treadmill running session at 85% of V(max), until animal exhaustion. Vitamins C (10 mg/kg) and E (10 mg/kg) were concurrently intraperitoneally administered 2 h before the exercise sessions. IEE was shown to cause 1) impairment of ileum internal membrane mitochondria verified by ultramicrography analysis; 2) increase in ileum carbonyl content (117%) and reduction in antioxidant capacity (36%); 3) increase in mitochondria carbonyl content (38%), increase in the percentage of ruptured mitochondria (25.3%), increase in superoxide dismutase activity (186%), and reduction in citrate synthase activity (40.4%) compared with control animals. Observations in the vitamin-supplemented exercised animals (E10-V) were 1) healthy appearance of myocyte mitochondria; 2) decrease in ileum carbonyl content (66%) and increase in antioxidant capacity (53%); 3) decrease in mitochondria carbonyl content (43%), decrease in the percentage of ruptured mitochondria (30%), slight increase in superoxide dismutase activity (7%), and significant increase in citrate synthase activity (121%) compared with E10 animals. Therefore, the present results strongly corroborate the hypothesis that IEE leads to marked disturbances in intestinal mitochondria, mainly in redox status, and affects whole intestinal redox status.
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PMID:Vitamin C and E supplementation prevents mitochondrial damage of ileum myocytes caused by intense and exhaustive exercise training. 1969 58

Two common bean (Phaseolus vulgaris L.) genotypes differing in aluminum (Al) resistance, Quimbaya (Al-resistant) and VAX-1 (Al-sensitive) were grown in hydroponics for up to 25 h with or without Al, and several parameters related to the exudation of organic acids anions from the root apex were investigated. Al treatment enhanced the exudation of citrate from the root tips of both genotypes. However, its dynamic offers the most consistent relationship between Al-induced inhibition of root elongation and Al accumulation in and exclusion from the root apices. Initially, in both genotypes the short-term (4 h) Al-injury period was characterized by the absence of citrate efflux independent of the citrate content of the root apices, and reduction of cytosolic turnover of citrate conferred by a reduced Nicotinamide adenine dinucleotide phosphate-isocitrate dehydrogenase (EC 1.1.1.42) activity. Transient recovery from initial Al stress (4-12 h) was found to be dependent mainly on the capacity to utilize internal citrate pools (Al-resistant genotype Quimbaya) or enhanced citrate synthesis [increased activities of NAD-malate dehydrogenase (EC 1.1.1.37) and ATP-phosphofructokinase (EC 2.7.1.11) in Al-sensitive VAX-1]. Sustained recovery from Al stress through citrate exudation in genotype Quimbaya after 24 h Al treatment relied on restoring the internal citrate pool and the constitutive high activity of citrate synthase (CS) (EC 4.1.3.7) fuelled by high phosphoenolpyruvate carboxylase (EC 4.1.1.31) activity. In the Al-sensitive genotype VAX-1 the citrate exudation and thus Al exclusion and root elongation could not be maintained coinciding with an exhaustion of the internal citrate pool and decreased CS activity.
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PMID:Aluminum resistance in common bean (Phaseolus vulgaris) involves induction and maintenance of citrate exudation from root apices. 2005 83


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