Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.1.99.3 (PRE)
1,923 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phosphate has been proposed as an ergogenic aid since it may enhance O2 delivery and cardiac work efficiency by increasing plasma phosphate (P Pi), red blood cell phosphate (RBC Pi), 2,3-diphosphoglycerate (DPG), RBC adenosine triphosphate (ATP), and P50. In 10 normal, fasting males we measured cardiac output (Q) by CO2 rebreathing, heart rate (HR), O2 deficit (O2DEF), and O2 consumption (VO2) during cycle ergometer exercise (60% of peak VO2). Stroke volume (SV) and arteriovenous O2 difference (A-VO2) were calculated. Following a baseline blood sample (BASE) for P Pi, RBC Pi, DPG, RBC ATP, and P50 (3 h before exercise), a single oral dose of dicalcium phosphate (129 mmol) and glucose (500 ml/10% sol, PHOS), or placebo (PLA), was administered in a random, crossover, double-blind fashion. Blood sampling was repeated immediately before and after exercise (PRE-EX and POST-EX). PHOS induced increases in P Pi (3.87 to 4.35 mg.dl-1, P less than 0.05), RBC Pi (3.86 to 4.63 mg.dl-1, P = 0.08), DPG (11.8 to 13.1 mumol.g-1 Hb, P less than 0.05), RBC ATP (4.2 to 4.4 mumol.g-1 Hb, P less than 0.05), and P50 (26.8 to 27.9 mm Hg, P less than 0.05) from BASE to PRE-EX. All variables remained elevated through the exercise period, as evidenced by higher levels than BASE at POST-EX (P less than 0.05). However, P50 was not different across conditions at PRE-EX (PHOS P50 = 27.9, PLA P50 = 28.3 mm Hg) or POST-EX (PHOS P50 = 28.0, PLA P50 = 28.1 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen delivery and cardiac output during exercise following oral phosphate-glucose. 238 2

The effects of simple-carbohydrate (CHO)- and complex-CHO-rich diets on skeletal muscle glycogen content were compared. Twenty male marathon runners were divided into four equal groups with reference to dietary consumption: depletion/simple, depletion/complex, nondepletion/simple, and nondepletion/complex. Subjects consumed either a low-CHO (15% energy [E] intake), or a mixed diet (50% CHO) for 3 days, immediately followed by a high-CHO diet (70% E intake) predominant in either simple-CHO or in complex-CHO (85% of total CHO intake) for another 3 days. Skeletal muscle biopsies and venous blood samples were obtained one day prior to the start of the low-CHO diet or mixed diet (PRE), and then again one day after the completion of the high-CHO diet (POST). The samples were analysed for skeletal muscle glycogen, serum free fatty acids (FFA), insulin, and lactate and blood glucose. Skeletal muscle glycogen content increased significantly (p less than 0.05) only in the nondepletion/simple group. When groups were combined, according to the type of CHO ingested and/or utilization of a depletion diet, significant increases were observed in glycogen content. Serum FFA decreased significantly (p less than 0.05) for the nondepletion/complex group only, while serum insulin, blood glucose, and serum lactate were not altered. It is concluded that significant increases in skeletal muscle glycogen content can be achieved with a diet high in simple-CHO or complex-CHO, with or without initial consumption of a low-CHO diet.
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PMID:Simple and complex carbohydrate-rich diets and muscle glycogen content of marathon runners. 334 97

We have purified large quantities of Escherichia coli photoreactivating enzyme (EC 4.1.99.3) to apparent homogeneity and have studied its physical and chemical properties. The enzyme has a molecular weight of 36 800 and a S020,W of 3.72 S. Amino acid analysis revealed an apparent absence of tryptophan, a low content of aromatic residues, and the presence of no unusual amino acids. The N terminus is arginine. The purified enzyme contained up to 13% carbohydrate by weight. The carbohydrate was composed of mannose, galactose, glucose, and N-acetylglucosamine. The enzyme is also associated with RNA (approximately 10 nucleotides/enzyme molecule) containing uracil, adenine, guanine, and cytosine with no unusual bases detected.
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PMID:Escherichia coli photoreactivating enzyme: purification and properties. 677 46

Exercise metabolism was examined in 13 endurance athletes who exercised on three occasions for 40 min at 70% of maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (RTT) or 40 degrees C and 20% relative humidity before (PRE ACC) or after (POST ACC) 7 days of acclimation. Exercise in the heat resulted in a lower (P < 0.05) mean O2 uptake (0.13 l/min) and higher (P < 0.01) heart rate and respiratory exchange ratio. Acclimation resulted in a lower (P < 0.01) mean heart rate and respiratory exchange ratio. Postexercise rectal temperature, muscle temperature, muscle and blood lactate, and blood glucose were higher (P < 0.01) in the PRE ACC than in the RTT trial, but all were reduced (P < 0.01) in the POST ACC compared with the PRE ACC trial. Muscle glycogenolysis and percentage of type I muscle fibers showing glycogen depletion were greater (P < 0.05) in the PRE ACC than in the RTT trial. Muscle glycogenolysis was unaffected by acclimation during exercise in the heat, although the percentage of depleted type I fibers was higher (P < 0.05) in the unacclimated state. Plasma epinephrine was higher (P < 0.01) during exercise in the heat in the unacclimated individual relative to RTT but was lower (P < 0.01) in the POST ACC than in the PRE ACC trial. The greater reliance on carbohydrate as a fuel source during exercise in the heat appears to be partially reduced after acclimation. These alterations are consistent with the observed changes in plasma epinephrine concentrations.
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PMID:Muscle metabolism during exercise and heat stress in trained men: effect of acclimation. 817 68

Adaptations in fat and carbohydrates metabolism after a prolonged endurance training program were examined using stable isotope tracers of glucose ([6,6-2H2]glucose), glycerol ([2H5]glycerol), and palmitate ([2H2]palmitate). Active, but untrained, males exercised on a cycle for 2 h/day [60% pretraining peak O2 consumption (VO2peak) = 44.3 +/- 2.4 ml.kg-1.min-1] for a total of 31 days. Three cycle tests (90 min at 60% pretraining VO2peak) were administered before training (PRE) and after 5 (5D) and 31 (31D) days of training. Exercise increased the rate of glucose production (Ra) and utilization (Rd) as well as the rate of lipolysis (glycerol Ra) and free fatty acid turnover (FFARa/Rd). At 5D, training induced a 10% (P < 0.05) increase in total fat oxidation because of an increase in intramuscular triglyceride oxidation (+63%, P < 0.05) and a decreased glycogen oxidation (-16%, P < 0.05). At 31D, total fat oxidation during exercise increased a further 58% (P < 0.01). The pattern of fat utilization during exercise at 31D showed a reduced reliance on plasma FFA oxidation (FFA Rd) and a greater dependence on oxidation of intramuscular triglyceride, which increased more than twofold (P < 0.001). In addition, glucose Ra and Rd were reduced at all time points during exercise at 31D compared with PRE and 5D. We conclude that long-term training induces a progressive increase in fat utilization mediated by a greater oxidation of fats from intramuscular sources and a reduction in glucose oxidation. Initial changes are present as early as 5D and occur before increases in muscle maximal mitochondrial enzyme activity.
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PMID:Effects of training duration on substrate turnover and oxidation during exercise. 905 94

To determine the effects of insulin on intracellular calcium and platelet aggregatory responses in hypertensive subjects with insulin resistance, we measured insulin sensitivity in terms of glucose disposal rate (GDR) by the hyperinsulinemic euglycemic clamp technique (GC) in 14 non-diabetic untreated hypertensive subjects, and determined basal ([Ca2+]i) and thrombin-stimulated (T-[Ca2+]i) platelet-free calcium concentrations and thrombin-stimulated platelet aggregatory response (AG) before (PRE[Ca2+]i, T-PRE[Ca2+]i, and PRE AG, respectively) and during (POST[Ca2+]i, T-POST[Ca2+]i, and POST AG, respectively) GC. As a control for GC, vehicle (normal saline) was infused on another day. No significant difference was observed between PRE[Ca2+]i and POST[Ca2+]i, T-PRE[Ca2+]i and T-POST[Ca2+]i, or PRE AG and POST AG, GDR inversely correlated with delta[Ca2+]i (POST [Ca2+]i-PRE[Ca2+]i, r = -0.75, p < 0.02), delta T-[Ca2+]i, (T-POST[Ca2+]i-T-PRE[Ca2+]i, r = -0.63, p < 0.02) and delta AG (POST AG-PRE AG, r = -0.67, p < 0.01). No significant changes were observed in these variables during vehicle infusion. [Ca2+]i, T-[Ca2+]i, and AG decreased during GC as compared with baseline in hypertensive subjects with normal insulin sensitivity, but were unchanged in those with insulin resistance, suggesting that the vasodilatory and anti-platelet aggregatory effects of insulin are impaired in patients with insulin-resistant hypertension.
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PMID:Inhibitory effects of insulin on intracellular calcium and aggregatory response of platelets are impaired in hypertensive subjects with insulin resistance. 932 4

Yeast uses nucleotide excision repair (NER) and photolyase (photoreactivation) to repair cyclobutane pyrimidine dimers (CPDs) generated by ultraviolet light. In active genes, NER preferentially repairs the transcribed strand (TS). In contrast, we recently showed that photolyase preferentially repairs the non-transcribed strands (NTS) of the URA3 and HIS3 genes in minichromosomes. To test whether photoreactivation depends on transcription, repair of CPDs was investigated in the transcriptionally regulated GAL10 gene in a yeast strain deficient in NER [AMY3 (rad1Delta)]. In the active gene (cells grown in galactose), photoreactivation was fast in the NTS and slow in the TS demonstrating preferential repair of the NTS. In the inactive gene (cells grown in glucose), both strands were repaired at similar rates. This suggests that RNA polymerases II blocked at CPDs inhibit accessibility of CPDs to photolyase. In a strain in which both pathways are operational [W303-1a (RAD1)], no strand bias was observed either in the active or inactive gene, demonstrating that photoreactivation of the NTS compensates preferential repair of the TS by NER. Moreover, repair of the NTS was more quickly in the active gene than in the repressed gene indicating that transcription dependent disruption of chromatin facilitates repair of an active gene.
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PMID:RNA polymerase II transcription inhibits DNA repair by photolyase in the transcribed strand of active yeast genes. 938 May

We have previously demonstrated that females oxidize more lipid and less protein and carbohydrate during endurance exercise [21]. Several studies in male rats have demonstrated similar metabolic changes after 4 d of 17-beta-estradiol (E2) administration. Our purpose was to study the effects of E2 administration upon substrate metabolism during 90min of cycle ergometry at 60% VO2peak in 11 healthy, young males. E2 was administered in a single-blind, cross-over, randomized fashion for 11 d (100 microg.d(-1) x 3.5d --> 200 microg.d(-1) x 3.5 d --> 300 microg.d(-1) x 4.0 d). Respiratory exchange ratio (RER), VO2, Ve, HR, lactate, and glucose were measured every 30 min during exercise and E2, testosterone TEST, glycerol and triglycerides were measured prior to exercise T = 0 min. Muscle biopsies were taken from the vastus lateralis before and after exercise for glycogen determination. Estradiol treatment resulted in lower plasma TEST (20.8-->7.8 nmol.L(-1), P<0.0001) and higher plasma E2 (168.1 327.3 pmol.L(-1), P < 0.002). Therewere no effects of E2 treatment upon any of the other measured variables including muscle glycogen: (E2 - PRE = 529.3 --> POST = 237.9; PL-PRE = 582.2 --> POST = 262.4 mmol.kg(-1) [dm]). We concluded that short-term E2 treatment increased plasma E2 to female follicular levels in males but had no effect upon lipid or carbohydrate metabolism.
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PMID:Short-term 17-beta-estradiol administration does not affect metabolism in young males. 1135 19

Adiponectin is an adipocytokine that is hypothesized to be involved in the regulation of insulin action. The purpose of the present investigation was to determine whether plasma adiponectin is altered in conjunction with enhanced insulin action with exercise training. An insulin sensitivity index (S(I)) and fasting levels of glucose, insulin, and adiponectin were assessed before and after 6 mo of exercise training (4 days/wk for approximately 45 min at 65-80% peak O(2) consumption) with no loss of body mass (PRE, 91.9 +/- 3.8 kg vs. POST, 91.6 +/- 3.9 kg) or fat mass (PRE, 26.5 +/- 1.8 kg vs. POST, 26.7 +/- 2.2 kg). Insulin action significantly (P < 0.05) improved with exercise training (S(I) +98%); however, plasma adiponectin concentration did not change (PRE, 6.3 +/- 1.5 microg/ml vs. POST, 6.6 +/- 1.8 microg/ml). In contrast, in a separate group of subjects examined before and after weight loss, there was a substantial increase in adiponectin (+281%), which was accompanied by enhanced insulin action (S(I), +432%). These data suggest that adiponectin is not a contributory factor to the exercise-related improvements in insulin sensitivity.
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PMID:Adiponectin is not altered with exercise training despite enhanced insulin action. 1221 5

We investigated the effects of carbohydrate ingestion during recovery from high-intensity exercise on subsequent high-intensity exercise in trained cyclists. Aerobic power was determined, and the competitive cyclists (N = 7) were familiarized with the 100-kJ test protocol (100 KJ-TEST). The subjects performed a first 100 KJ-TEST (RIDE-1), ingested 0.7 g.(kg body mass)(-1) of Gatorlode (CHO) or placebo (PLC), rested for 60 minutes, and then performed a second 100 KJ-TEST (RIDE-2). Blood samples taken before (PRE-1) and after (POST-1) RIDE-1 and before (PRE-2) and after (POST-2) RIDE-2 were analyzed for plasma glucose ([glucose]), lactate, and nonesterified fatty acids ([NEFA]). No significant differences (p > 0.05) were observed between treatments in time to complete RIDE-1 (CHO = 270.3 +/- 29.0 seconds; PLC = 269.9 +/- 33.0 seconds) and RIDE-2 (CHO = 271.7 +/- 26.6 seconds; PLC = 275.3 +/- 30.6 seconds). Plasma [glucose] significantly decreased during the 60-minute recovery for PLC. There was an interaction effect for [NEFA] during recovery, with [NEFA] increasing for PLC and decreasing for CHO. Carbohydrate ingestion after maximal exercise does not appear to influence subsequent short-duration maximal effort exercise in competitive cyclists but does alter plasma [glucose] and [NEFA] relative to a PLC condition.
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PMID:The effect of liquid carbohydrate ingestion on repeated maximal effort exercise in competitive cyclists. 1258 Jun 51


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