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

Work conditions in the synthetic detergents production according to the new technology created by Sumitomo (Japan) were evaluated from hygienic point of view. The main unfavourable factor is the contamination of air by initial products (aerosols of sodium tripoli phosphate, carboxy methylcellulose, optic bleacher, enzymes et al.) and dust of the final product. Sulphur oxides appear in the air of the sulphating unit. Levels of noise and vibration are surpassed. At the same time the studied technology is more profitable than the current ones. Parameters of the cardiovascular, central nervous and neuromuscular systems do not indicate the physical and neuropsychic fatigue.
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PMID:[Industrial hygiene in the modern manufacture of synthetic detergents]. 142 39

1. The role of the myoplasmic free Mg2+ concentration ([Mg2+]i) in fatigue was studied in intact single fibres isolated from mouse skeletal muscle. Fatigue was produced by repeated tetanic stimulation. The fluorescent Mg2+ indicator furaptra was pressure injected into fibres. In vivo calibrations were performed to convert fluorescence signals into [Mg2+]i. 2. [Mg2+]i at rest was 0.78 +/- 0.05 mM (mean +/- S.E.M., n = 14). An increase of the extracellular [Mg2+] from 0.5 to 20 mM resulted in a small elevation of [Mg2+]i (86 microM in 5 min). Removal of extracellular Na+ did not affect [Mg2+]i. An intracellular alkanization of about 0.6 pH units gave a [Mg2+]i reduction of 65 microM. 3. During fatiguing stimulation [Mg2+]i initially remained almost constant and it then suddenly started to rise towards the end of the stimulation period. The onset of the [Mg2+]i rise was always followed by a rapid tension decline. In fatigue [Mg2+]i was approximately twice as high as at rest. 4. Fibres were injected with MgCl2 to study if the rise in [Mg2+]i could explain the tension decline in fatigue. An elevation of [Mg2+]i was accompanied by a tension reduction but the [Mg2+]i for a given tension was generally much higher in rested fibres injected with MgCl2 than in fatigued fibres. Thus the rise in [Mg2+]i as such cannot explain the tension reduction in fatigue. 5. Injection of MgCl2 was also used to assess the intracellular Mg2+ buffering. The mean Mg2+ buffer power (i.e. the ratio of the change in [Mg2+]i to the amount of Mg2+ added) was 0.62. 6. ATP is the quantitatively most important binding site for Mg2+ at rest and ATP breakdown is then a likely source of the [Mg2+]i increase in fatigue. The role of ATP breakdown in the increase of [Mg2+]i was studied with metabolic inhibition: fibres were exposed to iodoacetic acid to inhibit glycolysis and cyanide to inhibit oxidative phosphorylation. The pattern during metabolic inhibition was similar to that observed during fatigue. After remaining almost constant during a lengthy period, [Mg2+]i rose rapidly and this rise preceded a period of rapid tension decline. The fibres thereafter went into rigor and [Mg2+]i stabilized at an elevated level; the mean [Mg2+]i increase in rigor was 1.30 mM. 7. We have used modelling to determine the likely change in the intracellular ATP concentration ([ATP]i) for the observed changes in [Mg2+]i.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myoplasmic free Mg2+ concentration during repetitive stimulation of single fibres from mouse skeletal muscle. 146 36

A sixty nine-year-old woman was admitted to the hospital because of further examination of hypercalcemia. On July 1990, she complained of general fatigue and loss of appetite. She was pointed out to have hypercalcemia (15.1mg/dl), urolithiasis, and renal insufficiency. CT films of the chest showed swelling of the mediastinal lymphnodes and CT of the abdomen nephrocalcinosis. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in the mediastinum. Levels of the parathyroid hormone was normal. Levels of the serum calcium (13.7mg/dl), angiotensin converting enzyme (30.4IU/L) and 1.25 (OH)2D (87PG/ml) were elevated. Giant cells were found in the biopsy specimen of the lung. A significant relationship between the serum calcium and creatinine were observed (r = 0.76, p < 0.02). Proximal fractional reabsorption of sodium showed to be suppressed (47.7%), and distal fractional reabsorption of sodium showed to be normal (88.4%). From these findings hypercalcemia and urolithiasis was suggested to result from sarcoidosis. The hypercalcemia and renal insufficiency improved with corticosteroid therapy.
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PMID:[A case of sarcoidosis with hypercalcemia, urolithiasis, nephrocalcinosis and renal insufficiency]. 148 16

Twenty patients undergoing colonic resection were randomized to either conventional postoperative pain treatment with morphine chloride and acetaminophen (group 1, n = 9) or methylprednisolone sodium succinate 90 minutes before surgery plus intraoperative neural blockade, with a postoperative analgesic regimen with combined bupivacaine hydrochloride-morphine and indomethacin sodium for systemic effect (group 2, n = 11). Assessments of pain, pulmonary function, convalescence, and various injury factors were done several times until 8 days after surgery. Postoperative pain and hyperthermic response were eliminated in group 2. Conventional reduction in pulmonary function measures was improved in group 2, and fatigue and mobility were less pronounced. Prostaglandin E2, interleukin 6, and C-reactive protein levels increased in both groups, but significantly less in group 2. These results suggest that a combined neural and humoral blockade may more effectively inhibit the global stress response to elective surgery than previously observed with neural blockade with or without indomethacin.
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PMID:Effect of combined prednisolone, epidural analgesia, and indomethacin on the systemic response after colonic surgery. 843 Nov 27

A long-lasting impairment of muscular force generation follows fatiguing exercise (fatigue of long duration), the physiological basis of which is not well understood. To investigate the role of reduced calcium release in long-lasting fatigue, we examined the effects of dantrolene sodium, which selectively decreases calcium release from the sarcoplasmic reticulum. The drug impaired muscle function in a pattern identical to that of long-lasting fatigue. The results are consistent with either independent effects of dantrolene and exercise at the same site in the excitation-contraction coupling chain, or independent actions at separate serial sites.
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PMID:Dantrolene sodium and fatigue of long duration. 155 88

A 15-year-old girl who drank excessive amounts of water while walking in the desert on a warm day, is reported. Due to complaints of fatigue and headache she was treated with more fluids and had a generalized seizure. On admission her sodium level was 125 meq/l and serum muscle enzymes were increased. Hyponatremia due to exertion and dilution is well established and may be more common than thought. It can present as a generalized seizure and with rhabdomyolysis. This case illustrates the danger of overzealous water replacement, especially without adequate replacement of salts. When water discipline is in force this possibility should be considered in patients presenting after prolonged, strenuous exercise or marching.
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PMID:[Dilutional hyponatremia and convulsions after strenuous exercise]. 159 97

A 49-year-old woman who had noted increasing fatigue and found it difficult to concentrate became confused and uncoordinated with rapid speech. Anxious and suffering from insomnia she had for 6 weeks taken a prescription-free bromide-containing drug mixture (daily 0.09 g potassium bromide and 1.8 g sodium bromide), to a total bromide intake of 60 g. The admission diagnosis of chronic bromism was confirmed by a markedly increased serum bromide concentration (325 mg/l). Once she had stopped taking the drug and had increased her salt intake she became symptom-free within 8 days. The case demonstrates that, while chronic bromism has become rare, it should still be included in the differential diagnosis, even after intake of supposedly harmless medication.
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PMID:[Chronic bromide intoxication caused by bromide-containing combination drugs]. 161 20

The purpose of this investigation was to examine the effect of ammonium chloride (NH4Cl) and sodium bicarbonate (NaHCO3) ingestion on the physical working capacity at the fatigue threshold (PWCFT). Eighteen adult males (mean age, SD = 23, 2 years) volunteered for two experiments (experiment 1, n = 9; experiment 2, n = 9). In both experiments, the subjects orally ingested 0.3 g.kg-1 body weight of NH4Cl and NaHCO3 over a 3-h period in random order on days separated by 72 h or more. In experiment 1, following ingestion of the substance, the subjects performed a discontinuous incremental cycle ergometer test to the onset of PWCFT which was estimated from integrated electromyography voltages at the vastus lateralis muscle. In experiment 2, the subjects performed a continuous PWCFT test. The results of these experiments indicated that NH4Cl and NaHCO3 ingestion had no significant (P greater than 0.05) effect on PWCFT (experiment 1: NH4Cl = 257, SD 26 W; NaHCO3 = 256, SD 22 W; t = 0.06; r = 0.866; experiment 2: NH4Cl = 231, 14 W; NaHCO3 = 216, 16 W; t = 1.78; r = 0.857).
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PMID:The effect of ammonium chloride and sodium bicarbonate ingestion on the physical working capacity at the fatigue threshold. 164 6

The concentrations of extracellular and intracellular potassium (K+) in skeletal muscle influence muscle cell function and are also important determinants of cardiovascular and respiratory function. Several studies over the years have shown that exercise results in a release of K+ ions from contracting muscles which produces a decrease in intracellular K+ concentrations and an increase in plasma K+ concentrations. Following exercise there is a recovery of intracellular K+ concentrations in previously contracting muscle and plasma K+ concentrations rapidly return to resting values. The cardiovascular and respiratory responses to K+ released by contracting muscle produce some changes which aid exercise performance. Increases in the interstitial K+ concentrations of contracting muscles stimulate CIII and CIV afferents to directly stimulate heart rate and the rate of ventilation. Localised K+ release causes a vasodilatation of the vascular bed within contracting muscle. This, together with the increase in cardiac output (through increased heart rate), results in an increase in blood flow to isometrically contracted muscle upon cessation of contraction and to dynamically contracting muscle. This exercise hyperaemia aids in the delivery of metabolic substrates to, and in the removal of metabolic endproducts from, contracting and recovering muscle tissues. In contrast to the beneficial respiratory and cardiovascular effects of elevations in interstitial and plasma K+ concentrations, the responses of contracting muscle to decreases in intracellular K+ concentrations and increases in intracellular Na+ concentrations and extracellular K+ concentrations contribute to a reduction in the strength of muscular contraction. Muscle K+ loss has thus been cited as a major factor associated with or contributing to muscle fatigue. The sarcolemma, because of changes in intracellular and extracellular K+ concentrations and Na+ concentrations on the membrane potential and cell excitability, contributes to a fatigue 'safety mechanism'. The purpose of this safety mechanism would be to prevent the muscle cell from the self-destruction which is evident upon overload (metabolic insufficiency) of the tissues. The net loss of K+ and associated net gain of Na+ by contracting muscles may contribute to the pain and degenerative changes seen with prolonged exercise. During exercise, mechanisms are brought into play which serve to regulate cellular and whole body K+ homeostasis. Increased rates of uptake of K+ by contracting muscles and inactive tissues through activation of the Na(+)-K+ pump serve to restore active muscle intracellular K+ concentrations towards precontraction levels and to prevent plasma K+ concentrations from rising to toxic levels. These effects are at least partially mediated by exercise-induced increases in plasma catecholamines, particularly adrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Potassium regulation during exercise and recovery. 165 9

Slow-twitch, oxidative skeletal muscles in SHR exhibit several physiological defects, including a reduced ability to maintain force during high frequency repetitive stimulation (1). Muscle fatigue may be produced by one of a variety of factors acting at different levels of the neuromuscular system. Several lines of evidence, however, suggest that SHR soleus fatigues more rapidly than WKY soleus because SHR muscles allow more K+ to accumulate in the extracellular space during repetitive muscle activity. An increase in extracellular K+ can lead to a failure in the generation or conduction of muscle action potentials. Comparison of the compound action potentials recorded from SHR and WKY muscles during repetitive stimulation provided evidence for a decrease in excitability of SHR soleus. Since the K+ released from muscle fibers during exercise is returned to the fiber principally via the activity of the Na+, K+ pump, the increase in extracellular K+ in SHR muscle may reflect a decrease in pump capacity. Measurements including intracellular K+ and Na+ content at rest, the level of hyperpolarization produced by the addition of epinephrine and insulin to SHR soleus and the post-exercise recovery of resting membrane potentials all appear to indicate that Na+, K+ pump capacity is reduced in SHR soleus muscles. Nonetheless, ouabain binding studies show a significantly greater number of pump sites in SHR muscles. The data suggest that Na+ pump activity is decreased in SHR soleus muscles without an apparent reduction in either the number of pump sites or in pump binding affinity.
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PMID:Apparent upregulation of Na+,K+ pump sites in SHR skeletal muscle with reduced transport capacity. 166 34


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