Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight men exercised at 66% of their maximal isometric force to fatigue after prior decrease in the glycogen store in one leg (low-glycogen, LG). The exercise was repeated with the contralateral leg (control) at the same relative intensity and for the same duration. Muscle (quadriceps femoris) glycogen content decreased in the LG leg from 199 +/- 17 (mean +/- S.E.M.) to 163 +/- 16 mmol of glucosyl units/kg dry wt. (P less than 0.05), and in the control leg from 311 +/- 23 to 270 +/- 18 mmol/kg (P less than 0.05). The decrease in glycogen corresponded to a similar accumulation of glycolytic intermediates. Muscle glucose increased in the LG leg during the contraction, from 1.8 +/- 0.1 to 4.3 +/- 0.6 mmol/kg dry wt. (P less than 0.01), whereas no significant increase occurred in the control leg (P greater than 0.05). It is concluded that during exercise glucose is formed from glycogen through the debranching enzyme when muscle glycogen is decreased to values below about 200 mmol/kg dry wt.
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PMID:Glucose formation in human skeletal muscle. Influence of glycogen content. 273 May 75

Changes in glucose 1,6-bisphosphate and regulators of glucose-1,6-bisphosphate synthase and phosphatase during isometric contraction have been determined. Biopsies were obtained from the quadriceps femoris muscle before and after 20 s of contraction and at fatigue. Glucose 1,6-bisphosphate increased by 35% after 20 s of contraction (P less than 0.001) with no further change at fatigue (P greater than 0.05 versus 20 s). Pi, fructose 1,6-bisphosphate and glycerate 3-phosphate, all inhibitors of the synthase, increased significantly during the first 20 s (P less than 0.05-0.001), whereas muscle pH (decrease in which inhibits synthase) decreased continuously. The decrease in the total adenine nucleotide pool, which is stoichiometric with the increase in IMP (an activator of phosphatase), was not significant after 20 s, but was 15% at fatigue (P less than 0.001). The rapid increase in glucose 1,6-bisphosphate, despite increases in the inhibitors of synthase, suggests that the synthase was activated, possibly by the substrate glycerate 1,3-bisphosphate and/or a yet unknown activator(s). The lack of any further change in glucose 1,6-bisphosphate during the latter part of contraction may be due to concomitant activation of the synthase and phosphatase.
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PMID:Transient increase in glucose 1,6-bisphosphate in human skeletal muscle during isometric contraction. 273 May 76

The relationship between changes in muscle metabolites and the contraction capacity was investigated in humans. Subjects (n = 13) contracted (knee extension) at a target force of 66% of the maximal voluntary contraction force (MVC) to fatigue, and the recovery in MVC and endurance (time to fatigue) were measured. Force recovered rapidly [half-time (t 1/2) less than 15 s] and after 2 min of recovery was not significantly different (P greater than 0.05) from the precontraction value. Endurance recovered more slowly (t 1/2 approximately 1.2 min) and was still significantly depressed after 2 and 4 min of recovery (P less than 0.05). In separate experiments (n = 10) muscle biopsy specimens were taken from the quadriceps femoris muscle before and after two successive contractions to fatigue at 66% of MVC with a recovery period of 2 or 4 min in between. The muscle content of high-energy phosphates and lactate was similar at fatigue after both contractions, whereas glucose 6-phosphate was lower after the second contraction (P less than 0.05). During recovery, muscle lactate decreased and was 74 and 43% of the value at fatigue after an elapsed period of 2 and 4 min, respectively. The decline in H+ due to lactate disappearance is balanced, however, by a release of H+ due to resynthesis of phosphocreatine, and after 2 min of recovery calculated muscle pH was found to remain at a low level similar to that at fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of contraction capacity to metabolic changes during recovery from a fatiguing contraction. 279 65

We reported a case of halothane-induced fulminant hepatitis with acute renal failure which developed 6 days after reexposure to halothane. The patient was a 58-year-old female. She had a history of liver dysfunction after exposure to halothane 6 years previously. She had surgical treatment of clubfoot under halothane anesthesia in other hospital. Preoperative physical examination and laboratory data were normal. On the 6th post-operative day she abruptly developed high fever and general fatigue. Next day, she was transferred to our hospital. At admission, fulminant hepatitis complicated with acute renal failure was diagnosed with severe liver and renal damage. She was immediately treated with plasma exchange, glucose-insulin therapy, and hemodialysis. Serum transaminase level returned to normal value within a week. However, despite repeated hemodialysis, renal function did not improve, and she died of P. aeruginosa sepsis on 28th day after the operation. It may be suggested that in this patient hypersensitivity to halothane has persisted during the six years.
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PMID:[A case of fulminant hepatitis after reexposure to halothane six years later]. 281 Jul 19

Beta adrenoceptor antagonists are effective in the symptomatic management of angina pectoris. This paper examines critically the possible influence of the ancillary properties of beta 1 selectivity, partial agonism and membrane-stabilizing action on the response in anginal patients. The response is categorized according to experimental, pharmacological and clinical endpoints, placing emphasis on the possible errors which may arise from extrapolation from the former to the latter. It is concluded: That selective beta adrenoceptor antagonism confers limited, but tangible advantages over non-selective antagonists in regard to patients with reversible airways obstruction, and also in the metabolic and haemodynamic response to acute hypoglycaemia. Cardioselectivity does not influence the central haemodynamic response to exercise, but lessens adrenaline-mediated hypertensive responses to smoking and hypoglycaemia. Non-selective partial agonists cause less reduction in resting ventricular function, but their effects on cardiac output during exercise are indistinguishable from full antagonists. Membrane stabilizing properties have a marked influence on the tolerability of these agents in terms of unwanted, nonspecific central nervous system symptoms. Unresolved questions relate to the influence of partial agonism on fatigue, metabolic responses, especially blood lipids and glucose, and the possibility of lesser efficacy in angina compared to full antagonists.
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PMID:The possible role of the ancillary properties of beta adrenoceptor antagonists in the management of angina pectoris. 286 Jul 71

To determine whether a single carbohydrate feeding could rapidly restore and maintain plasma glucose availability late in exercise, six trained cyclists were studied on two occasions during exercise to fatigue at 70 +/- 1% of VO2max. After 135 min of exercise, the men were fed either an artificially sweetened placebo or glucose polymers (3 g.kg-1 in a 50% solution). Prolonged exercise led to a decline in plasma glucose from 4.6 +/- 0.1 mM at rest to 3.9 +/- 0.2 mM after 135 min (P less than 0.05). Plasma glucose decreased further (P less than 0.05) to 3.2 +/- 2.0 mM at fatigue following placebo ingestion but increased (P less than 0.05) and was then maintained at 4.5-4.9 mM following carbohydrate ingestion. Respiratory exchange ratio (R) fell gradually during the placebo trial from 0.88 +/- 0.01 after 10 min of exercise to 0.81 +/- 0.01 at fatigue (P less than 0.01). R also reached a minimum of 0.81-0.82 in each subject after 135-180 min of exercise during the carbohydrate feeding trial but increased again to 0.84-0.86 as plasma glucose rose following the carbohydrate feeding. Exercise time to fatigue was 21% longer (205 +/- 17 vs 169 +/- 12 min; P less than 0.01) during the carbohydrate ingestion trial. Plasma insulin did not increase significantly, whereas plasma free fatty acids and blood glycerol plateaued following carbohydrate ingestion. These data indicate that a single carbohydrate feeding late in exercise can supply sufficient carbohydrate to restore euglycemia and increase carbohydrate oxidation, thereby delaying fatigue.
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PMID:Metabolism and performance following carbohydrate ingestion late in exercise. 292 2

Hepatocytes from rats deprived of food for 48 h synthesized glucose and urea from glutamine at a rate which, at pH 7.3, was markedly stimulated (175-250%) by dibutyryl cAMP, phenylephrine, and norepinephrine, in agreement with previous investigators. These effectors also stimulated respiration, elevating ATP production by the amount required for the increase in glucose and urea synthesis. Both the basal and stimulated rates were strongly pH dependent with maxima in the region of pH 7.2-7.6 (urea synthesis) and 7.2-7.5 (glucose synthesis) and declined rapidly on either side of these pH values. The inhibitions at acid and alkaline pH were neither due to lack of energy nor to limitation in glutamine uptake. The intracellular concentrations of aspartate, glutamate, and glutamine were lower at pH 6.7 than at pH 7.3 and were differently affected by dibutyryl cAMP and phenylephrine at the two pH values investigated. When calcium was omitted from the suspending medium, the basal rates of glucose and urea production were decreased as was stimulation by the effectors, phenylephrine completely, and the others partially. The stimulations by phenylephrine and dibutyryl cAMP were additive under all conditions tested. The pattern of metabolite changes indicates that although both effectors stimulated glutaminase and increased supply of aspartate to the argininosuccinate synthetase, dibutyryl cAMP gave greater activation of glutaminase whereas the adrenergic agonists gave greater stimulation of later steps on the biosynthetic pathways. It may be physiologically important than at acid pH both ureagenesis and gluconeogenesis are severely suppressed and cannot be effectively stimulated by the major hormonal regulators of these pathways.
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PMID:pH dependence of hormonal regulation of gluconeogenesis and urea synthesis from glutamine in suspensions of hepatocytes. 298 Dec 10

To determine the upper limits of steady-state exercise performance and carbohydrate oxidation late in exercise, seven trained men were studied on two occasions during prolonged cycling that alternated every 15 min between approximately 60% and approximately 85% of VO2max. When fed a sweet placebo throughout exercise, plasma glucose and respiratory exchange ratio (R) declined (P less than 0.05) from 5.0 +/- 0.1 mM and 0.91 +/- 0.01 after 30 min (i.e., at 85% VO2max) to 3.7 +/- 0.3 mM and 0.79 +/- 0.01 at fatigue (i.e., when the subjects were unable to continue exercise at 60% VO2max). Carbohydrate feeding throughout exercise (1 g/kg at 10 min, then 0.6 g/kg every 30 min) increased plasma glucose to approximately 6 mM and partially prevented this decline in carbohydrate oxidation, allowing the men to perform 19% more work (2.74 +/- 0.13 vs. 2.29 +/- 0.09 MJ, P less than 0.05) before fatiguing. Even when fed carbohydrate, however, by the 3rd h of exercise, R had fallen from 0.92 to 0.87, accompanied by a reduction in exercise intensity from approximately 85% to approximately 75% VO2max (both P less than 0.05). These data indicate that carbohydrate feedings enable trained cyclists to exercise at up to 75% VO2max and to oxidize carbohydrate at up to 2 g/min during the later stages of prolonged intense exercise.
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PMID:Effect of carbohydrate feedings during high-intensity exercise. 305 87

Denervated (1-10 days) rat epitrochlearis muscles were isolated, and basal and insulin-stimulated protein and glucose metabolism were studied. Although basal rates of glycolysis and glucose transport were increased in 1-10-day-denervated muscles, basal glycogen-synthesis rates were unaltered and glycogen concentrations were decreased. Basal rates of protein degradation and synthesis were increased in 1-10-day-denervated muscles. The increase in degradation was greater than that in synthesis, resulting in muscle atrophy. Increased rates of proteolysis and glycolysis were accompanied by elevated release rates of leucine, alanine, glutamate, pyruvate and lactate from 3-10-day-denervated muscles. ATP and phosphocreatine were decreased in 3-10-day-denervated muscles. Insulin resistance of glycogen synthesis occurred in 1-10-day denervated muscles. Insulin-stimulated glycolysis and glucose transport were inhibited by day 3 of denervation, and recovered by day 10. Inhibition of insulin-stimulated protein synthesis was observed only in 3-day-denervated muscles, whereas regulation by insulin of net proteolysis was unaffected in 1-10-day-denervated muscles. Thus the results demonstrate enhanced glycolysis, proteolysis and protein synthesis, and decreased energy stores, in denervated muscle. They further suggest a defect in insulin's action on protein synthesis in denervated muscles as well as on glucose metabolism. However, the lack of concurrent changes in all insulin-sensitive pathways and the absence of insulin-resistance for proteolysis suggest multiple and specific cellular defects in insulin's action in denervated muscle.
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PMID:Resistance of protein and glucose metabolism to insulin in denervated rat muscle. 319 84

Twelve trained males, in a fed state, were studied to examine the effect of pre-exercise fructose ingestion on endurance capacity during prolonged cycling exercise. Sixty minutes prior to exercise, subjects ingested either 60 or 85 g fructose or a sweet placebo. Mean exercise intensity initially required 62% of the maximal aerobic power and thereafter increased to elicit 72 and 81% of maximal aerobic power at 90 and 120 min of exercise, respectively. Exercise time (mean +/- SE) to exhaustion was significantly increased after fructose ingestion, as compared to placebo ingestion (145 +/- 4 vs 132 +/- 3 min, P less than 0.01). During the exercise, no differences were observed between both trials for oxygen uptake, heart rate, or perceived exertion. Serum glucose and insulin levels between both trials were not significantly different throughout the experiment. There were also no significant differences in serum-free fatty acids and glycerol levels as well as respiratory exchange ratio between fructose and placebo trials during the exercise. The results suggest that fructose ingestion is of benefit before prolonged exercise, because it provides a carbohydrate source to contracting muscles without transient hypoglycemia and a depression of fat utilization, and thereby delays the fatigue.
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PMID:Effect of pre-exercise fructose ingestion on endurance performance in fed men. 328 17


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