Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol or without drugs. After propranolol administration the increases during exercise in plasma glucagon and epinephrine concentrations as well as the decrease in plasma glucose concentrations were faster than in control experiments. When euglycemia was maintained by glucose infusion during beta-adrenergic blockade, glucagon and epinephrine responses to exercise, although not abolished, were markedly reduced. The diminution of the exercise-induced decline in glucose concentrations correlated significantly with the diminution of the glucagon as well as the epinephrine responses. Thus decreased glucose concentrations may significantly enhance the secretion of glucagon and epinephrine during prolonged exercise in man. Since the diminution of the glucagon response produced by glucose infusion was not accompanied by significant alterations in the levels of nonesterified fatty acid (NEFA) and glycerol, increased glucagon secretion does not seem to be a major determinant of lipolysis during exercise in man. During glucose infusion, glycogen utilization rates in muscle (n = 4) tended to decrease, whereas carbohydrate combustion rate and concentrations of norepinephrine, insulin, alanine, and lactate were unchanged.
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PMID:Glucose-induced decrease in glucagon and pinephrine responses to exercise in man. 86 12

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol (P), during lipolytic blockade with nicotinic acid (N), or without drugs (C). The total work times (83 +/- 9 (P), 122 +/- 8 (N), 166 +/- 10 (C) min, mean and SE) differed significantly. Epinephrine rose progressively above preexercise levels (0.06 +/- 0.01 ng/ml); at exhaustion concentrations in P experiments (2.15 +/- 0.41) were larger than in N (1.08 +/- 0.31) and C (0.72 +/- 0.28) experiments. Norepinephrine increased consistently while insulin decreased. After an initial decrease glucagon concentrations increased progressively in parallel with declining plasma glucose and were at exhaustion always three times preexercise values. Thus beta-adrenergic blockade did not diminish the glucagon response. Nor was this response increased when alpha-receptor stimulation in P experiments was intensified. Carbohydrate combustion was smaller and NEFA and glycerol concentrations in serum larger during C experiments. Alanine concentrations were never raised at exhaustion. Accordingly, neither stimulation of adrenergic receptors nor NEFA and alanine concentrations are major determinants for the exercise-induced glucagon secretion in man. It is suggested that decreased glucose availability enhances the secretion of glucagon and epinephrine during prolonged exercise.
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PMID:Glucagon and plasma catecholamines during beta-receptor blockade in exercising man. 93 21

It has been demonstrated in several diving vertebrates that succinate, a component of the Krebs cycle, accumulates in blood during breath-hold dives. The production of succinate is thought to result from amino acid catabolism. Our purpose was to determine whether succinate accumulation occurs in man during muscular activity requiring anaerobic energy contribution. Experiments using an endurance athlete included apneic work on an underwater ergometer and treadmill running to exhaustion. During 1 min breath-hold "dives" in cold water while exercising at a work rate equivalent to 62% of VO2max, venous succinate increased from 42 mumoles/l (M X 10(-6)) at rest to 125 M X 10(-6). The treadmill run elicited VO2max and increased succinate from a similar resting value to 93 M X 10(-6). Increases in alanine, lactate, and pyruvate were observed for both types of exercise. The findings confirm that succinate accumulation also occurs in man. It was suggested that amino acid catabolism may provide a source of anaerobic energy production in addition to glycolysis. However, the importance of the proposed energy pathway remains to be quantified.
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PMID:Succinate accumulation in man during exercise. 97 51

The purpose of this research was to measure changes in selected plasma amino acids (AA) during two successive exercise trials to exhaustion. Eleven trained male athletes completed these trials at weeks 4, 6, 8 and 12. Blood samples for each test were collected after a 12-hour fast at times (in minutes) 0 (Resting), 45, 90, 135, 180, at exhaustion (EI), after a 20-minute recovery period, and at the second exhaustion (EII). At the end of EI, subjects consumed an artificially sweetened water replacement (placebo) treatment or a carbohydrate (CHO) replacement (1.1 g CHO/kg BW) in order to determine any effect of CHO replacement on changes in energy substrates or AA, adjusted for plasma volume changes. From baseline to EI, alpha-aminobutyric acid, alanine, glycine, isoleucine, serine, valine threonine, and tyrosine decreased significantly (p less than or equal to 0.05), while taurine increased significantly. During the recovery period following EI, isoleucine, leucine, ornithine, phenylalanine, tyrosine, urea and valine increased significantly. From the end of recovery until EII, alanine, aspartic acid, glycine, isoleucine, leucine, ornithine, phenylalanine, serine, threonine, tyrosine and valine decreased significantly. CHO replacement had no effect on the mean change scores for any AA from EI to the end of the recovery period and affected only serine, citrulline, glycine and threonine from the end of the recovery period to EII.
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PMID:Plasma amino acid responses of trained athletes to two successive exhaustion trials with and without interim carbohydrate feeding. 145 48

To determine the effects of neutralizing exercise systemic acidosis via the intravenous route upon endurance and metabolic responses, eight lean, normal, postabsorptive men exercised to exhaustion at about 80% of their VO2 max (69 +/- 3%, mean +/- SEM, of maximum power output) on a cycle ergometer. Exercise studies were performed either with no infusion (control) or with a total infusion volume of about 1.5 L, mainly as 1.3% sodium bicarbonate or as 0.9% sodium chloride (NaCl), infused (double-blind) throughout exercise. The sodium bicarbonate was to prevent acid-base change, the sodium chloride was as a control for the volume infused. Arterialized venous blood and breath-by-breath analysis of expired gases were obtained. [H+] (nmol.L-1) and [HCO3-] (mmol.L-1) at exhaustion were similar in control and NaCl (46.5 +/- 1.8, 19.9 +/- 0.9), but remained unchanged from rest values with bicarbonate (38.4 +/- 0.9, 24.8 +/- 1.5, p less than 0.005 vs control and NaCl). At exhaustion, VO2, VCO2, RER, heart rate, and systolic BP as well as FFA, glycerol, alanine, insulin, norepinephrine, and epinephrine did not differ among protocols. Endurance was markedly prolonged (p less than 0.01) with bicarbonate (31.9 +/- 5.8 min) and NaCl (31.8 +/- 4.1 min) compared with the control (19.0 +/- 2.9 min) condition. Plasma glucose at exhaustion was higher (p less than 0.025) in the control compared to bicarbonate and NaCl experiments, while lactate was higher (p less than 0.025) in the bicarbonate than in the control and NaCl experiments. Thus, the prolonged endurance with sodium bicarbonate infusion could not be explained either by its effect of maintaining blood acid-base equilibrium or concomitant metabolic changes.
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PMID:Intravenous bicarbonate and sodium chloride both prolong endurance during intense cycle ergometer exercise. 240 23

Intermittent claudication is associated with adaptation in muscle metabolism. This study has evaluated the metabolism of amino acids at rest and during non-steady state exercise in patients with arterial insufficiency of at least six months duration in comparison with matched control individuals. The exchange of amino acids were measured during two periods of acute exercise; one initial exercise period with a standardized work load and exercise time and a second exercise period which continued until further exercise was impossible due to pain in the patients and exhaustion in the controls. The maximum blood flow was reduced by 40% in the patients but the maximum oxygen uptake per unit power developed was almost the same in patients and controls. The patients had significantly lower concentrations of glutamine, lysine and taurine at rest compared with the controls. The exchange of amino acids across the resting leg did not differ between the two groups. Exercise increased the efflux of amino acids in both patients and controls. The efflux of glutamine (896 +/- 205 vs. 48 +/- 359 nmol/100 ml/min/watt) was higher in the patients compared to the controls at the first exercise period with inverse changes in the opposite direction of asparagine (149 +/- 105 vs. 799 +/- 121 and 27 +/- 70 vs. 633 +/- 334 nmol/100 ml/min/watt at the first and second exercise, respectively. Alanine release did not differ between the groups. The complementary patterns of glutamine and asparagine during hypoxic exercise in the patients may reflect the fact that these amino acids share a common carrier system. The similarity in the efflux of non-metabolized amino acids, such as methionine, phenylalanine, tyrosine and 3-methylhistidine, indicated that muscle hypoxia in claudication patients did not promote net degradation of either globular or myofibrillar proteins, although exercise increased the efflux of 3-methylhistidine three- to fourfold in both patients and control individuals (from 1 +/- 0.4 to 4 +/- 1.8 and from 0 +/- 0.7 to 6 +/- 2.5 nmol/100 ml/min/watt, respectively). The exercise-induced alterations in leg exchange of amino acids were restored within 10-20 min following exercise regardless of hypoxia. The results demonstrate that patients with arterial insufficiency have altered intermediary metabolism of amino acids during exercise. However, muscle hypoxia in such patients does not seem to promote a negative protein balance or induce serious alterations in cell membrane integrity.
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PMID:Leg exchange of amino acids during exercise in patients with arterial insufficiency. 340 84

Six men were studied during exercise to exhaustion on a cycle ergometer at 73% of VO2max following ingestion of glycerol, glucose or placebo. Five of the subjects exercised for longer on the glucose trial compared to the placebo trial (p less than 0.1; 108.8 vs 95.9 min). Exercise time to exhaustion on the glucose trial was longer (p less than 0.01) than on the glycerol trial (86.0 min). No difference in performance was found between the glycerol and placebo trials. The ingestion of glucose (lg X kg-1 body weight) 45 min before exercise produced a 50% rise in blood glucose and a 3-fold rise in plasma insulin at zero min of exercise. Total carbohydrate oxidation was increased by 26% compared to placebo and none of the subjects exhibited a fall in blood glucose below 4 mmol X 1-1 during the exercise. The ingestion of glycerol (lg X kg-1 body weight) 45 min before exercise produced a 340-fold increase in blood glycerol concentration at zero min of exercise, but did not affect resting blood glucose or plasma insulin levels; blood glucose levels were up to 14% higher (p less than 0.05) in the later stages of exercise and at exhaustion compared to the placebo or glucose trials. Both glycerol and glucose feedings lowered the magnitude of the rise in plasma FFA during exercise compared to placebo. Levels of blood lactate and alanine during exercise were not different on the 3 dietary treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the effects of pre-exercise feeding of glucose, glycerol and placebo on endurance and fuel homeostasis in man. 353 95

We have studied the structure of myosin heavy chain (MHC) in the pectoralis muscle of genetically dystrophic (Connecticut Strain) and White Leghorn chicks. MHC was alkylated with N-ethylmaleimide, purified by Sepharose-4B chromatography, and cleaved with cyanogen bromide. The MHC CNBr peptides were analyzed by one-dimensional and two-dimensional isoelectric focusing/sodium dodecyl sulfate gradient gels and by amino acid sequencing. Specific changes were detected in the gel patterns which could be correlated with the loss of muscle function as measured by the exhaustion score (the ability of chicks to rise from a reclining position) in three experimental groups (exhaustion scores: less than 3, 10-20, greater than 30). We have also examined the amino acid sequence of a 3-methyl-histidine-containing peptide which originates from the 20-kDa fragment of pectoralis muscle MHC in dystrophic chicks: Val-Leu-Asn-Ala-Ser-Ala-Ile-Pro-Glu-Gly-*Gln-Phe-*Ile-Asp-Ser-Lys-Lys- Ala-Ser-Leu-Gln-Lys-Leu-Gly-Ser-Ile-Asp-Val-(Asp, 3-methylhistidine, Gln). Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile). Thus, both the peptide map and sequence analyses demonstrate that in avian muscular dystrophy an abnormal pectoralis MHC is synthesized. It is not yet clear whether the "dystrophic" MHC is a variant MHC or if it arises from the abnormal expression of an earlier developmental form (embryonic or neonatal) of pectoralis muscle MHC.
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PMID:Structure of myosin heavy chain in avian muscular dystrophy. 399 78

The amino acid consumption by Bordetella pertussis growing in broth containing casein hydrolysate was examined. Serine, proline, alanine, glycine, aspartate, and glutamate were rapidly consumed, in a manner which suggested that they supplied the energy requirements of the organism; exhaustion of the energy source appeared to be the main factor limiting the yield of cells. There was no correlation between the utilization of individual amino acids and the phase of growth; uptake appeared to depend only upon relative concentrations. Consumption of threonine, phenylalanine, histidine, leucine, and methionine was slight; consumption of valine and lysine was variable, and isoleucine was excreted. The addition of monosodium l-glutamate (3 mg/ml) to the broth in shaken flasks increased the cell yield by an average of 43.5%. It had no detectable adverse effect upon the agglutin-producing capacity, agglutinability in antisera versus smooth and rough growth phases, mouse-lethal toxicity, histamine-sensitizing factor potency, or intracerebral protective potency of the culture. Broth supplemented with monosodium l-glutamate has been used over a 2-year period to prepare experimental vaccines by both batch and continuous cultivation methods at controlled pH; the cell yields obtained from the supplemented broth have been up to 52% higher than those from the basal broth. The use of glutamate to replace a proportion of casein hydrolysate in the broth caused a reduction in the cell yield, an alteration in cell morphology, and reduction in the mouse-lethal toxicity, the histamine-sensitizing factor potency, and the intracerebral protective potency of the cells.
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PMID:Use of glutamic acid to supplement fluid medium for cultivation of Bordetella pertussis. 431 42

The effects of a number of organic substrates on the autotrophic metabolism of Hydrogenomonas eutropha were examined. Dual substrate (mixotrophic) cultivation in the presence of hydrogen plus either fructose or alanine allowed autotrophic growth to begin immediately after the exhaustion of the organic substrate. On the other hand, the presence of acetate, pyruvate, or glutamate caused a lengthy lag to occur before autotrophic growth commenced. With acetate or pyruvate this lag (plateau) in the dicyclic growth curve was due to the repression of ribulose diphosphate carboxylase (RDPC) synthesis during mixotrophic growth. During heterotrophic growth with glutamate, RDPC was partially repressed; however, during mixotrophic growth, RDPC activity was high. Thus the delay of autotrophic growth was not due to a repression of RDPC by glutamate. The data suggest that glutamate interferes with autotrophic metabolism by repressing the incorporation of inorganic nitrogen. The repression of these vital autotrophic functions by acetate, pyruvate, and glutamate occurred both in the presence and absence of hydrogen, i.e., during both heterotrophic and mixotrophic cultivation. The derepression of the affected systems during the plateau phase of the dicyclic growth curves was demonstrated. Carbon dioxide assimilation by whole cells agreed well with the RDPC activity of extracts from cells grown under similar conditions.
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PMID:Autotrophic and heterotrophic metabolism of hydrogenomonas: regulation of autotrophic growth by organic substrates. 498 69


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