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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The basic scientific achievements of the Department of Biochemistry of Muscles organized at the Academy of Sciences of Ukrainian SSR in 1944 are presented in this short historical overview. The basic guidelines for activities in the scientific field are as follows: study of biochemical processes in the working muscles as well as during misfunctions and disabilities, processes of adenine nucleotides exchange and ammonia creation, biochemical characterization of Ca2+ and H+ transport through the plasma and sarcoplasmic reticulum membranes. It is shown that creatine and creatine phosphate as well as adenine nucleotide content and metabolism affect the muscle functioning, glycogen metabolism proceeds simultaneously with the lowering of content of inorganic phosphate. The facts of glucose phosphorylation and its conversion via glycolytic pathways and the backward reaction of glycolysis (the aerobic synthesis of phosphopyruvate, glycogen synthesis from glucose in the presence of phosphorylase) were determined. After the muscle work up to tiredness adenine nucleotide depletion is not limited by its dephosphorylation, but goes up to formation of inosine acid and ammonia. Deamidation is shown to be in myofibrillar fraction and in sarcoplasmic reticulum of the skeletal muscle. Deamidation activity is not registered in myocardium myofibrillar fraction but it is registered in sarcoplasmic reticulum. AMP-phosphohydrolase and adenosine desaminase were found in membranes of the sarcoplasmic reticulum. The decrease in activity of all enzymes mentioned above is registered during myocardium hypertrophy, because of aorta narrowing. These data permit creating the methods for obtaining substance "adenosine phosphate" for treatment of cardiac pathologies. Glutaminase was found to be active in the muscles. This activity depended on the organism functioning. The ammonia usage by the muscle cells goes with glutamine synthesis and consumption of energy of ATP, e.g. protein amidation. The later is of all-biological significance and is used in the fields of medicine actualls concerned with the following fact: the velocity of hydrolysis of amidated protein is different for such pathology as epilepsia, tuberculosis, poisoning with manganese oxides. The methods for diagnostics of the above pathological states were developed on this basis. It is proved that glutamine nitrogen can be also used in the reaction of transamination, particularly during synthesis of purines, inosine acid and it is stored in a form of glutaminic acid. Changes in carbohydrate and phosphorus metabolism, in nitrogen and energetic exchanges and mitochondria overfilling with calcium were determined under E-avitaminosis dystrophy.(ABSTRACT TRUNCATED)
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PMID:[Department of the Biochemistry of Muscles]. 757 Oct 74

We investigated the mechanisms of muscle fatigue in ALS. In the muscles of ALS patients and healthy control subjects, we examined (1) fatigue using measurements of muscle force, (2) energy metabolism using phosphorus-31 magnetic resonance spectroscopy, and (3) activation using neurophysiologic measures and MRI. During 25 minutes of intermittent isometric exercise of the tibialis anterior muscle, both maximum voluntary and tetanic force declined more in patients than in controls, indicating greater fatigability in ALS. There was a similar decline of voluntary and tetanic force, suggesting that much of the fatigue was not central. Evoked compound muscle action potential amplitudes were preserved during exercise in both groups, indicating no failure of neuromuscular transmission; this result suggests that the source of fatigue was not at the neuromuscular junction or within the muscle membrane. In spite of greater fatigability, changes during exercise in energy metabolites and proton signal intensity tended to be less in ALS patients compared with controls, suggesting impaired muscular activation. We conclude that the greater muscle fatigue in ALS patients results from activation impairment, due in part to alterations distal to the muscle membrane.
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PMID:Physiology of fatigue in amyotrophic lateral sclerosis. 772 63

31P-nuclear magnetic resonance spectroscopy and evoked electromyography were applied to rat skeletal muscle to examine the mechanism of muscle fatigue and the recovery of muscle phosphorus metabolites and pH during fatigue. When the sciatic nerve was electrically stimulated at 1 Hz, the contraction force of the gastrocnemius muscle decreased gradually to 46% of the maximal force, accompanied by a decrease in phosphocreatine (PCr) and a corresponding increase in inorganic phosphate (P(i)) and diprotonated inorganic phosphate (H2PO4-). Neither the amplitudes of compound muscle action potentials (CMAP) nor muscle pH changed significantly. At 10-Hz stimulation, contraction force rapidly decreased to 26% of maximal force, accompanied by a decrease in PCr and increases in P(i) and H2PO4-. Muscle pH decreased for a few minutes, then gradually recovered during continued stimulation. The amplitude of the CMAP also decreased for a few minutes and then reached steady values. At 100-Hz stimulation, the contraction force decreased to 6% of the maximal force and there was a decrease in the amplitude of the CMAP. However, the changes in the phosphorus metabolites and pH were transient and recovered to the control value during the stimulation. These results indicated that fatigue at 1 and 100-Hz stimulation was mainly caused by the change in phosphorus metabolite concentrations and electrical failure, respectively, and that fatigue at 10-Hz stimulation might have been due to both of these factors. These results also indicated that electrical failure might have been the cause of the recovery of the phosphorus metabolites and pH during 100-Hz stimulation and of pH during 10-Hz stimulation.
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PMID:Fatigue and recovery of phosphorus metabolites and pH during stimulation of rat skeletal muscle: an evoked electromyography and in vivo 31P-nuclear magnetic resonance spectroscopy study. 780 63

At presentation the history of an 87-year-old woman included progressive memory loss, repeated transient ischaemic attack, increasing fatigue, dizziness, palpitations and frequent falls. Investigations revealed erythrocytosis, leukocytosis, thrombocytosis, normal arterial oxygen concentration and an increased red cell volume. Polycythaemia vera was diagnosed and was successfully managed by phlebotomy with half a unit twice a week and rechecks of her haematocrit, initially; she reported marked improvement after 2 weeks of treatment. The alternative treatments for polycythaemia vera are discussed; in addition to venesection, conventional treatments include bone-marrow depressive agents such as phosphorus-32 and chemotherapy with agents such as hydroxyurea. More recent developments include isovolumic erythrocytophoresis, alpha-interferon and ticlopidine. All of the treatments are associated with complications, or other disadvantages, thrombotic complications in the case of phlebotomy, malignancies in the case of most myelosuppressive treatments, and problems of compliance in others. The optimal treatment for polycythaemia vera is a judicious combination of the alternatives, depending on the phase of the disease, the age of the patient, and other prognostic factors.
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PMID:Primary polycythaemia vera in the elderly. 802 Jun 39

This article describes the use of combining spectral electromyographic signal techniques with phosphorus magnetic resonance (31P-NMR) spectroscopy for the purpose of studying muscle disorders. The quantification of muscle fatigue by electromyographic spectral variables such as the median frequency is summarized. Its development as a laboratory and clinical tool is presented, with an emphasis toward its potential as an assessment procedure. Similarly, the use of 31P-NMR spectroscopy for noninvasive measurement of phosphate metabolites and intracellular pH during fatigue are described. The limitations of this procedure are presented and compared with surface electromyographic techniques. Suggestions are made for combining these techniques for the purpose of monitoring muscle metabolic and electrophysiologic changes in situ during fatiguing exercises. A recent study in which these techniques were combined to evaluate the underlying mechanisms of fatigue in patients with fibromyalgia is described.
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PMID:Combined use of surface electromyography and 31P-NMR spectroscopy for the study of muscle disorders. 824 97

Phosphorus nuclear magnetic resonance (31P NMR) spectroscopy is a non-destructive analytical laboratory technique that, due to recent technical advances, has become applicable to the study of high-energy phosphate metabolism in both animal and human extremity muscles (in vivo). 31P NMR can assay cellular phosphocreatine, ATP, inorganic phosphate, the phosphorylated glycolytic intermediates, and intra-cellular pH in either resting or exercising muscle, in a non-invasive manner. NMR uses non-perturbing levels of radio-frequency energy as its biophysical probe and can therefore safely study intact muscle in a repeated fashion while exerting no artifactual influence on ongoing metabolic processes. Compared with standard tissue biopsy and biochemical assay techniques, NMR possesses the advantages of being non-invasive, allowing serial in situ studies of the same tissue sample, and providing measurements of only active (unbound) metabolites. NMR studies of exercising muscle have yielded information regarding fatigue mechanisms at the cellular level and are helping resolve long-standing questions regarding the metabolic control of glycolysis, oxidative phosphorylation, and post-exercise phosphocreatine re-synthesis. NMR is also being utilized to measure enzymatic reaction rates in vivo. In the near future, other forms of NMR spectroscopy may also permit the non-invasive measurement of tissue glycogen and lactate content.
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PMID:Phosphorus nuclear magnetic resonance: a non-invasive technique for the study of muscle bioenergetics during exercise. 832 Nov 1

A 57-yr-old man presented with a long history of undiagnosed fatigue but no evidence of bone disease. He was noted to have hypophosphatemia due to an idiopathic phosphaturia. Marked abnormalities of exercising skeletal muscle detected by phosphorus magnetic resonance spectroscopy and by plasma metabolite measurements were consistent with mitochondrial dysfunction. Oral phosphate supplements restored plasma phosphate concentration and muscle biochemistry to normal and produced considerable improvement in symptoms and exercise tolerance, although the phosphate concentration in muscle was only marginally low and increased little by treatment. We conclude that hypophosphatemia should be excluded in unexplained fatigue.
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PMID:Oral phosphate supplements reverse skeletal muscle abnormalities in a case of chronic fatigue with idiopathic renal hypophosphatemia. 801 97

A miniature piglet model that replicates clinical hypothermic (14 degrees C nasopharyngeal) circulatory arrest and low-flow (50 ml/kg per minute) bypass was used to study carotid blood flow with electromagnetic flow probe, cerebral blood flow by microsphere injection, cerebral metabolic rate by arteriovenous oxygen and glucose extractions, lactate production by cerebral arteriovenous difference, and cerebral edema. Data from five animals that underwent circulatory arrest and five animals that underwent low-flow bypass (aged 28.8 +/- 0.4 [mean +/- standard error of the mean] days) were analyzed. The duration of circulatory arrest and low-flow bypass was 1 hour. In a parallel study with the same animal model, phosphorus 31 magnetic resonance spectroscopy was used to assess cerebral phosphocreatine, nucleoside triphosphate (adenosine triphosphate), and intracellular pH. Five animals (aged 31.8 +/- 1.1 days) underwent circulatory arrest, and five underwent low-flow bypass. A brief phase of hyperemic carotid blood flow was seen immediately after the onset of reperfusion in the circulatory arrest group but not in the low-flow group. In the circulatory arrest and low-flow bypass groups, cerebral blood flow (percentage of baseline 71.2% +/- 8.3% and 69.1% +/- 5.8%, respectively), cerebral oxygen consumption (45.6% +/- 10.0%, 44.5% +/- 7.6%), and cerebral glucose consumption (31.5% +/- 30.7%, 83.5% +/- 24.2%) remained depressed after 45 minutes of reperfusion and rewarming to normothermia. However, after 3 more hours of pulsatile normothermic reperfusion, cerebral oxygen consumption and cerebral glucose consumption had returned to baseline. Phosphocreatine, adenosine triphosphate, and pH were maintained at or above baseline levels throughout low-flow bypass and throughout 3 hours of normothermic reperfusion. In contrast, both phosphocreatine and adenosine triphosphate became undetectable 32 +/- 3.7 minutes after onset of circulatory arrest. During and early after circulatory arrest, pH decreased to a minimum of 6.506 +/- 0.129 at 40 minutes after reperfusion. After 3 hours of normothermic reperfusion, phosphocreatine and adenosine triphosphate recovered to 98.6% +/- 9.0% and 90.1% +/- 13.5% of baseline, respectively, and pH was 7.087 +/- 0.051, similar to baseline (7.1755 +/- 0.041). In the low-flow bypass group, the disparity between the depressed level of cerebral oxygen consumption and normal high-energy phosphate levels may reflect incomplete cerebral rewarming or decreased energy consumption. In the circulatory arrest group, the parallel recovery of oxygen consumption and high-energy phosphates eventually achieving baseline levels suggests that the degree of hypothermia used provides adequate protection for acute cerebral recovery after 1 hour of circulatory arrest.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Recovery of cerebral blood flow and energy state in piglets after hypothermic circulatory arrest versus recovery after low-flow bypass. 841 62

Skeletal muscle bioenergetics and control of intracellular pH have been investigated in 46 patients with chronic fatigue syndrome by phosphorus magnetic resonance spectroscopy. The results have been compared with those from healthy controls and from a group of patients with mitochondrial cytopathies affecting skeletal muscle. No consistent abnormalities of glycolysis, mitochondrial metabolism or pH regulation were identified in the group when taken as a whole, although in 12 of the 46 patients the relationship between pH and phosphocreatine utilisation during exercise fell outside the normal range. Of these, 6 patients showed increased acidification relative to phosphocreatine depletion while 6 showed reduced acidification. These findings do not support the hypothesis that any specific metabolic abnormality underlies fatigue in this syndrome although abnormalities may be present in a minority of patients.
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PMID:Skeletal muscle bioenergetics in the chronic fatigue syndrome. 850 83

The estuarine dinoflagellate Pfiesteria piscicida gen. et sp. nov. produces exotoxin(s) that can be absorbed from water or fine aerosols. Culture filtrate (0.22 microns porosity filters, > 250 toxic flagellated cells/ml) induces formation of open ulcerative sores, hemorrhaging, and death of finfish and shellfish. Human exposure to aerosols from ichthyotoxic cultures (> or = 2000 cells/ml) has been associated with narcosis, respiratory distress with asthma-like symptoms, severe stomach cramping, nausea, vomiting, and eye irritation with reddening and blurred vision (hours to days); autonomic nervous system dysfunction [localized sweating, erratic heart beat (weeks)]; central nervous system dysfunction [sudden rages and personality change (hours to days), and reversible cognitive impairment and short-term memory loss (weeks)]; and chronic effects including asthma-like symptoms, exercise fatigue, and sensory symptoms (tingling or numbness in lips, hands, and feet; months to years). Elevated hepatic enzyme levels and high phosphorus excretion in one human exposure suggested hepatic and renal dysfunction (weeks); easy infection and low counts of several T-cell types may indicate immune system suppression (months to years). Pfiesteria piscicida is euryhaline and eurythermal, and in bioassays a nontoxic flagellated stage has increased under P enrichment (> or = 100 micrograms SRP/L), suggesting a stimulatory role of nutrients. Pfiesteria-like dinoflagellates have been tracked to fish kill sites in eutrophic estuaries from Delaware Bay through the Gulf Coast. Our data point to a critical need to characterize their chronic effects on human health as well as fish recruitment, disease resistance, and survival.
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PMID:Insidious effects of a toxic estuarine dinoflagellate on fish survival and human health. 852 74


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