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 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle glycogen and glucose have been suggested to be carbon-chain precursors for glutamine synthesis in skeletal muscle. Therefore, the aim of the present study is to investigate whether carbohydrate supplementation affects plasma glutamine and other amino acids during exercise and 7 h of recovery. Eight well-trained subjects cycled at an alternating workload of 50 and 80% Wmax until exhaustion (59 to 140 min). During the exercise bout the subjects received either water (control) or a carbohydrate (CHO) drink (83 g CHO x l(-1), 2 ml x kg(-1) per kg body weight every 15 min). Plasma glutamine concentration appeared not to be affected by exercise, as a significant increase was only observed at some points in time during the control test. During recovery, however, plasma glutamine concentration decreased from 682+/-24 and 685+/-19 micromol x l(-1) at exhaustion to 552+/-19 and 534+/-12 micromol x l(-1) after 2 h of recovery for the control and CHO test, respectively. Plasma glutamine concentration returned to pre-exercise values after 7 h of recovery. Alanine concentration increased during exercise in both tests. During the recovery period the concentration of alanine (48%), and total amino acids (23%) decreased below the pre-exercise level. The plasma alanine and the total amino acid concentration was still suppressed after 7 h of recovery. In conclusion, carbohydrate supplementation had neither an effect during exercise nor during recovery on the concentration of plasma glutamine or other amino acids. Exercise, however, causes a substantial decrease in the plasma amino acid concentration during recovery.
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PMID:Effect of carbohydrate supplementation on plasma glutamine during prolonged exercise and recovery. 956 14

The participation of hepatic glycogenolysis and gluconeogenesis to the glycemic changes promoted by exercise was investigated. For this purpose, we employed swimming rats (2.5% body weight extra load attached to the tail, at 24 degrees C) using a favorable condition to measure hepatic glycogenolysis (fed rats) and a favorable condition to measure hepatic gluconeogenesis (fasted rats). This experimental approach permits us to compare the contribution of hepatic glycogenolysis and gluconeogenesis to glucose changes for a specific schedule of exercise. The animals were investigated at rest, after 5 minutes of swimming and after swimming to exhaustion. Our results show that hepatic glycogen has a crucial role to determine hyperglycemia during exercise. In contrast, hypoglycemia developed during exercise when glycogen was depleted. However, the ability of the liver to produce glucose from L-lactate, glycerol and L-glutamine was increased during exercise. Taken together, these findings suggest that the hepatic capacity to produce glucose from gluconeogenic substrates (except for L-alanine) was increased when hepatic glycogen stores were depleted. Thus, the increased capacity to produce glucose shown by livers from exercising rats must to be an important metabolic adaptation to protect against severe hypoglycemia.
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PMID:Changes in glycemia induced by exercise in rats: contribution of hepatic glycogenolysis and gluconeogenesis. 1010 May 3

The effects of menstrual cycle phase and carbohydrate (CHO) supplementation were investigated during prolonged exercise. Nine healthy, moderately trained women cycled at 70% peak O(2) consumption until exhaustion. Two trials were completed during the follicular (Fol) and luteal (Lut) phases of the menstrual cycle. Subjects consumed 0.6 g CHO. kg body wt(-1). h(-1) (5 ml/kg of a 6% CHO solution every 30 min beginning at min 30 of exercise) or a placebo drink (Pl) during exercise. Time to exhaustion during CHO increased from Pl values (P < 0.05) by 14.4 +/- 8.5 (Fol) and 11.4 +/- 7.1% (Lut); no differences were observed between menstrual cycle phases. CHO attenuated (P < 0.05) the decrease in plasma glucose and insulin and the increase in plasma free fatty acids, tryptophan, epinephrine, and cortisol observed during Pl for both phases. Plasma alanine, glutamine, proline, and isoleucine were lower (P < 0.05) in Lut than in Fol phase. CHO resulted in lower (P < 0.05) plasma tyrosine, valine, leucine, isoleucine, and phenylalanine. These results indicate that the menstrual cycle phase does not alter the effects of CHO supplementation on performance and plasma levels of related substrates during prolonged exercise.
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PMID:Effect of menstrual cycle phase on carbohydrate supplementation during prolonged exercise to fatigue. 1065 39

Depletion of muscle glycogen is considered a limiting performance factor during prolonged exercise, whereas the role of the intramyocellular lipid (IMCL) pool is not yet fully understood. We examined 1) intramyocellular glycogen and lipid utilization during prolonged exercise, 2) resynthesis of muscle glycogen and lipids during recovery, and 3) changes in glycogen content between nonexercising and exercising muscles during recovery. Subjects ran on a treadmill at submaximal intensity until exhaustion. Glycogen concentrations were assessed in thigh, calf, and nonexercising forearm muscle, and IMCL content was measured in soleus muscle using magnetic resonance spectroscopy techniques. At the time of exhaustion, glycogen depletion was 2-fold greater in calf than in thigh muscles, but a significant amount of glycogen was left in both leg muscles. The glycogen concentration in nonexercising forearm muscle decreased during the initial 5 h of recovery to 73% of the baseline value. Duringthe exercise, the IMCL content decreased to 67% and subsequently during recovery increased to 83% of the baseline value. In summary, we found during prolonged running 1) significantly greater muscle glycogen utilization in the calf muscle group than in the thigh muscle group, 2) significant utilization of IMCL in the soleus muscle, and 3) a decrease in glycogen content in nonexercising muscle and an increase in glycogen content in recovering muscles during the postexercise phase. These latter data are consistent with the hypothesis that there is transfer of glycogen by the glucose-lactate and the glucose-->alanine cycle from the resting muscle (forearm) to recovering muscles (thigh and calf) after running exercise.
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PMID:Intramuscular glycogen and intramyocellular lipid utilization during prolonged exercise and recovery in man: a 13C and 1H nuclear magnetic resonance spectroscopy study. 1069 Aug 86

The effect of several antibiotics, molybdate and hydrogen sulfide was tested on anoxic tolerance of the cockle Cerastoderma edule, as well as utilisation of glycogen. The aim was to evaluate the role of fuel depletion and growth of bacteria as a cause of mortality. The exponential increase of sulfide and ammonium occurred in anoxic natural seawater incubations and to a lesser extend in artificial, sulfate free, seawater. This could be strongly decreased by antibacterial agents, which led to improved survival time by approximately two-fold. Molybdate suppressed sulfide formation also, but did not affect survival time. Exogenous sulfide showed a negative effect on survival time at pH 6.8 and induced stronger accumulation of free glucose, D-lactate and L-alanine. This was not the case at pH 8.2. Fifty percent (LT50) of cockles in anoxic seawater died after 3.5 days still with half the initial glycogen concentration present. However, in the presence of chloramphenicol (LT50 7.9 days), the cockles utilised their endogenous fuel almost completely. In both incubations there was initially a strong increase of D-lactate and L-alanine. The D-lactate levels subsequently decreased again, probably due to bacterial consumption. This study strongly indicates that in anoxic closed systems, infection by pathogenic bacteria is the first cause of death and not exhaustion of endogenous fuel depots.
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PMID:Factors involved in the (near) anoxic survival time of Cerastoderma edule: associated bacteria vs. endogenous fuel. 1125 6

Phosphate-limited synthetic culture media were designed to investigate the growth and the pristinamycin production of 'Streptomyces pristinaespiralis' using different nitrogen sources. During balanced growth, either mineral or organic nitrogen sources were readily utilized. However, glutamate and alanine were used as both nitrogen and carbon source, sparing the utilization of the primary carbon source, glucose. Valine was utilized only for its nitrogen and consequently 2-ketoisovalerate was excreted in the medium. Ammonium prevented the utilization of nitrate. Upon phosphate limitation, glycerol, originating from the breakdown of teichoic acids, was released, allowing the recovery of phosphate from the cell wall and the continuation of growth. Under such conditions, ammonium was excreted following the consumption of glutamate and alanine and was later reassimilated after exhaustion of the primary nitrogen source. The mode of utilization of valine prevented the production of pristinamycins due to excretion of 2-ketoisovalerate, one of their direct precursors. For other nitrogen sources, pristinamycin production was controlled by nitrogen catabolic regulation linked to the residual level of ammonium. In the case of nitrate, the negative regulation was alleviated by the absence of ammonium and production then occurred precociously. In the case of amino acids and ammonium, production was delayed until after exhaustion of amino acids and depletion of ammonium.
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PMID:Nitrogen source governs the patterns of growth and pristinamycin production in 'Streptomyces pristinaespiralis'. 1153 85

We tested the theory that links the capacity to perform prolonged exercise with the size of the muscle tricarboxylic acid (TCA) cycle intermediate (TCAI) pool. We hypothesized that endurance training would attenuate the exercise-induced increase in TCAI concentration ([TCAI]); however, the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22 +/- 1 yr) cycled at approximately 80% of initial peak oxygen uptake before and after 7 wk of training (1 h/day, 5 days/wk). Biopsies (vastus lateralis) were obtained during both trials at rest, after 5 min, and at the point of exhaustion during the pretraining trial (42 +/- 6 min). A biopsy was also obtained at the end of exercise during the posttraining trial (91 +/- 6 min). In addition to improved performance, training increased (P < 0.05) peak oxygen uptake and citrate synthase maximal activity. The sum of four measured TCAI was similar between trials at rest but lower after 5 min of exercise posttraining [2.7 +/- 0.2 vs. 4.3 +/- 0.2 mmol/kg dry wt (P < 0.05)]. There was a clear dissociation between [TCAI] and endurance capacity because the [TCAI] at the point of exhaustion during the pretraining trial was not different between trials (posttraining: 2.9 +/- 0.2 vs. pretraining: 3.5 +/- 0.2 mmol/kg dry wt), and yet cycle endurance time more than doubled in the posttraining trial. Training also attenuated the exercise-induced decrease in glutamate concentration (posttraining: 4.5 +/- 0.7 vs. pretraining: 7.7 +/- 0.6 mmol/kg dry wt) and increase in alanine concentration (posttraining: 3.3 +/- 0.2 vs. pretraining: 5.6 +/- 0.3 mmol/kg dry wt; P < 0.05), which is consistent with reduced carbon flux through alanine aminotransferase. We conclude that, after aerobic training, cycle endurance capacity is not limited by a decrease in muscle [TCAI].
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PMID:Effect of endurance training on muscle TCA cycle metabolism during exercise in humans. 1512 41

The transcriptional program of yeast cells undergoes dramatic changes during the shift from fermentative growth to respiratory growth. A large part of this response is mediated by the stress responsive transcription factor Msn2. During glucose exhaustion, Msn2 is activated and concentrated in the nucleus. Simultaneously, Msn2 protein levels also drop significantly under this condition. Here we show that the decrease in Msn2 concentration is due to its increased degradation. Moreover, Msn2 levels are also reduced under chronic stress or low protein kinase A (PKA) activity, both conditions that cause a predominant nuclear localization of Msn2. Similar effects were found in msn5 mutant cells that block Msn2 nuclear export. To approximate the effect of low PKA activity on Msn2, we generated a mutant form with alanine substitutions in PKA phosphorylation sites. High expression of this Msn2 mutant is detrimental for growth, suggesting that the increased degradation of nuclear Msn2 might be necessary to adapt cells to low PKA conditions after the diauxic shift or to allow growth under chronic stress conditions.
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PMID:Nuclear localization destabilizes the stress-regulated transcription factor Msn2. 1550 60

During lactate fermentation by Propionibacterium freudenreichii subsp. shermanii ATCC 9614, the only amino acid metabolized was aspartate. After lactate exhaustion, alanine was one of the two amino acids to be metabolized. For every 3 mol of alanine metabolized, 2 mol of propionate, 1 mol each of acetate and CO(2), and 3 mol of ammonia were formed. The specific activity of alanine dehydrogenase was 0.08 U/mg of protein during lactate fermentation, and it increased to 0.9 U/mg of protein after lactate exhaustion. Alanine dehydrogenase and aspartase, key enzymes in the metabolism of alanine and aspartate, respectively, were partially purified, and some of their properties were studied. Alanine dehydrogenase had a pH optimum of 9.2 to 9.6 and high K(m) values for both NAD (1 to 4 mM) and alanine (7 to 20 mM). Activity was inhibited by low concentrations of pyruvate and NADH. The pH optimum of aspartase decreased from approximately 7.5 to approximately 6.4 when the MgCl(2) and aspartate concentrations were decreased. Plots of aspartate concentration versus activity showed either hyperbolic or sigmoidal kinetics (interaction coefficient, up to a value of 3.1), depending on pH and MgCl(2) concentration. MgCl(2) was either an activator or an inhibitor, depending on pH and its concentration. Aspartase activity was inhibited by low concentrations of fumarate. The properties of alanine dehydrogenase and aspartase are consistent with the finding that aspartate is metabolized during lactate fermentation, while alanine is only fermented after lactate exhaustion and then at a slow rate.
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PMID:Properties of Alanine Dehydrogenase and Aspartase from Propionibacterium freudenreichii subsp. shermanii. 1634 14

During prolonged exercise, carbohydrate oxidation may result from decreased pyruvate production and increased fatty acid supply and ultimately lead to reduced pyruvate dehydrogenase (PDH) activity. Pyruvate also interacts with the amino acids alanine, glutamine, and glutamate, whereby the decline in pyruvate production could affect tricarboxycylic acid cycle flux as well as gluconeogenesis. To enhance our understanding of these interactions, we studied the time course of changes in substrate utilization in six men who cycled at 44+/-1% peak oxygen consumption (mean+/-SE) until exhaustion (exhaustion at 3 h 23 min+/-11 min). Femoral arterial and venous blood, blood flow measurements, and muscle samples were obtained hourly during exercise and recovery (3 h). Carbohydrate oxidation peaked at 30 min of exercise and subsequently decreased for the remainder of the exercise bout (P<0.05). PDH activity peaked at 2 h of exercise, whereas pyruvate production peaked at 1 h of exercise and was reduced (approximately 30%) thereafter, suggesting that pyruvate availability primarily accounted for reduced carbohydrate oxidation. Increased free fatty acid uptake (P<0.05) was also associated with decreasing PDH activity (P<0.05) and increased PDH kinase 4 mRNA (P<0.05) during exercise and recovery. At 1 h of exercise, pyruvate production was greatest and was closely linked to glutamate, which was the predominant amino acid taken up during exercise and recovery. Alanine and glutamine were also associated with pyruvate metabolism, and they comprised approximately 68% of total amino-acid release during exercise and recovery. Thus reduced pyruvate production was primarily associated with reduced carbohydrate oxidation, whereas the greatest production of pyruvate was related to glutamate, glutamine, and alanine metabolism in early exercise.
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PMID:Carbohydrate metabolism during prolonged exercise and recovery: interactions between pyruvate dehydrogenase, fatty acids, and amino acids. 1642 76


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