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

Tension and metabolite concentrations were measured in single frog muscle fibers at 15 degrees C in vitro, in response to electrical stimulation or to immersion in caffeine- or potassium chloride-Ringer. Sarcomere length equaled 2.3 micrometers. Interrupted stimulation for 150 s at 20 Hz or stimulation for 7.5 min at 1 Hz was followed by at least 20 min of fatigue, evidenced by a reduced 200-ms test contraction. Fatigued fibers contracted maximally in potassium chloride- or caffeine-Ringer. They had high lactate and glucose 6-phosphate concentrations and a reduced phosphocreatine (PCr) concentration. Adenosine 5'-triphosphate (ATP) concentration was approximately normal but was markedly reduced by a caffeine contracture. A plot of PCr consumption against the tension-time integral at different stimulation frequencies (25, 35, or 50 Hz) and durations had an intercept of 25.5 nmol PCr/mg protein at time zero and a corrected slope of 0.65 nmol approximately P/mg protein per kg . s . cm-2. Prolonged fatigue is not due to energy exhaustion or to the inability of muscle fibers to consume residual ATP but probably arises from long-lasting interference in excitation-contraction coupling, which can be reversed by KCl- or caffeine-induced release of Ca2+ from intracellular stores.
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PMID:Fatigue and metabolism of frog muscle fibers during stimulation and in response to caffeine. 697 5

Phosphocreatine has been shown having significant effects on striated skeletal musculature. In fact, it was shown, by experimental researches, that phosphocreatine interfered with the state of fatigue induced in the Mus musculus and in rats, by the swimming test.
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PMID:[Phosphocreatine and skeletal musculature: in vivo research]. 707 47

The present study was designed to investigate the effects of different types of physical fatigue-past demand for exertion-on the performance of a visual detection task performed with and without masking. 31 male subjects were first administered a VO2 max test and familiarized with the detection task. They were divided into two groups to control potential effects of masking. They were subjected to three experimental treatment involving the utilization of different sources of energy: (a) a short anaerobic alactic acid effort recruiting phosphocreatine, (b) a supramaximal effort (anaerobic lactic acid) recruiting glycogen without oxygen, and (c) a progressive (partially anaerobic) effort recruiting glycogen and oxygen. All three were performed on a treadmill. Blood samples were collected for the anaerobic lactacid and the partially anaerobic exercises. Once fatigued, all subjects undertook the detection task. A 2 X 3 X 2 X 8 analysis of variance, with repeated measures on the last three factors, was applied to the data (mask/no mask X type of exercise X pre-post performance measures X location of the letter to be detected). No significant difference was found for either the main effects or interactions, except for the location of the letter and the mask/no mask condition. It appears therefore that a physically fit population (mean VO2 max = 62.39 ml X kg(-1) X min(-1)) shows no detectable decrement in a perceptual task performed after fatiguing exercises recruiting various types of energy sources.
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PMID:Influence of different types of physical fatigue on a visual detection task. 732 75

The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation-contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation-contraction coupling) components.
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PMID:Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis. 747 63

Metabolic status and intracellular pH were investigated using 31-P nuclear magnetic resonance spectroscopy during mechanical fatigue induced in rat gastrocnemius muscle in vivo by continuous stimulation either at low or high frequency. During high frequency stimulations, force decreased to low level (10% of initial in 3-6 min) while phosphocreatine declined abruptly to 28-30% of its initial level and pH fell to 6.36 in 45 seconds. Force then continued to fall but PCr and pH rose again to reach 80-85% of the initial phosphocreatine value and 6.96 (pH) at the end of the stimulation period. The major feature of these results at high frequency was that the muscle could not generate force despite high energy stores and normal pH. During low frequency stimulation, force decreased in 9 min, to 10% of initial level. Phosphocreatine decreased abruptly to become undetectable while pH declined to 6.08 in 90 seconds. But later, phosphocreatine rose again to 35% and pH recovered to 6.84 while force continued to fall. Our results showed that intracellular pH and energy stores are not involved in the development and maintenance of mechanical fatigue.
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PMID:Rat gastrocnemius high and low frequency fatigue without metabolic impairment by 31P NMR. 751 31

Patients on long-term zidovudine (AZT) therapy experience muscle fatigue and weakness attributed to AZT-induced mitochondrial toxicity in skeletal muscle. To determine if the clinico-pathological abnormalities in these patients correspond to abnormal muscle energy metabolism, we used 31P in vivo magnetic resonance spectroscopy to follow phosphorylated metabolites during exercise. We studied 19 normal volunteers, 6 HIV-positive patients never treated with AZT, and 9 HIV-positive patients who had been treated with AZT for a mean period of 33 mo (range 12-48 mo) and had muscle biopsy-proven AZT-myopathy with abnormal mitochondria. Changes in phosphocreatine, ATP, and intracellular pH in the gastrocnemius muscle were followed during a graded steady state exercise protocol, and the recovery of phosphocreatine was followed on cessation of exercise. We found that graded steady state exercise produced a greater depletion of muscle phosphocreatine levels in the AZT-treated patients, compared to either HIV-positive patients who were not treated with AZT or normal controls. No differences in the effects of steady state exercise on muscle phosphocreatine levels were observed between the control group and the HIV-positive patients who had not been treated with AZT. The results suggest that the effect of AZT on muscle energy metabolism is significant, and similar to the effect observed in patients with known mitochondrial myopathies. Using a well-known model for control of mitochondrial metabolism, the observed differences in steady state phosphocreatine levels during exercise suggest that AZT treatment decreases the maximal work output and the maximal rate of muscle ATP synthesis.
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PMID:Metabolic abnormalities in skeletal muscle of patients receiving zidovudine therapy observed by 31P in vivo magnetic resonance spectroscopy. 761 82

1. The importance of the level of tricarboxylic acid cycle intermediates (malate, citrate and fumarate) for energy transduction during exercise has been investigated in six healthy subjects and in two patients with muscle phosphorylase deficiency (McArdle's disease). 2. Healthy subjects cycled for 10 min at low (50 W), moderate [130 +/- 6 W (mean +/- SEM)] and high (226 +/- 12 W) work rates, corresponding to 26, 50 and 80% of their maximal O2 uptake, respectively. Patients with McArdle's disease cycled for 11-13 min at submaximal (40 W) rates, and to fatigue at maximal work rates of 60-90 W. 3. In healthy subjects, phosphocreatine was unchanged during low work rates, but decreased to 79 and 32% of the initial level during moderate and high work rates. In patients with McArdle's disease, phosphocreatine decreased to 82 and 34% of the initial level during submaximal and peak exercise. Muscle lactate increased in healthy subjects during exercise at moderate and high work rates, but remained low in patients with McArdle's disease. 4. In healthy subjects, tricarboxylic acid cycle intermediates were similar at rest and at low work rates (0.48 +/- 0.04 mmol/kg dry weight), but increased to 1.6 +/- 0.2 mmol/kg dry weight and 4.0 +/- 0.3 mmol/kg dry weight at moderate and high work rates. The tricarboxylic acid cycle intermediate level in patients with McArdle's disease was similar to that in healthy subjects at rest, but was markedly reduced during exercise when compared at the same relative intensity. The peak level of tricarboxylic acid cycle intermediates in patients with McArdle's disease was 22% of that in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tricarboxylic acid cycle intermediates during incremental exercise in healthy subjects and in patients with McArdle's disease. 763 53

1. ADP inhibits the maximum shortening velocity (V0) in skeletal muscle. [ADP] may increase considerably during contractions and reduce V0 in the absence of energy buffering by phosphocreatine (PCr). We have tested this hypothesis by comparing V0 in long and short tetani produced in situations where PCr buffering is absent. 2. Single, intact muscle fibres were dissected from toe muscles of Xenopus and stimulated by current pulses at 20 degrees C. The test sequence consisted of a 400 ms tetanus, followed after 3 s by a 1400 ms tetanus and after an additional 4 s by a 400 ms tetanus. V0 was measured with slack tests at 200 and 1200 ms, respectively. 3. The PCr system was inactivated in three ways: (i) fatiguing fibres with repeated short tetani; (ii) inhibition of the creatine kinase (CK) reaction with dinitrofluorobenzene; and (iii) inhibition of energy metabolism with iodoacetic acid and cyanide. 4. Under control conditions V0 was similar in all three test tetani. With inactive PCr buffering V0 was about 30% lower in the long tetanus. This slowing recovered fully in the second short tetanus in fatigue and with CK inhibition. 5. Calculations suggest that [ADP] can reach very high levels (about 3 mM) during prolonged contractions in the absence of PCr buffering.
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PMID:Reduced maximum shortening velocity in the absence of phosphocreatine observed in intact fibres of Xenopus skeletal muscle. 771 29

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

The relationship between changes in work output (fatigue) and metabolite concentrations was measured in rat skeletal muscle during the course of dynamic exercise (10 s). After 4 s, work output decreased rapidly to approximately 30% at 8 s. In contrast to the changes in phosphocreatine and lactate, the change in ATP concentration paralleled the reduction in work output. A strong linear relationship (r = 0.95) was found between the relative decrease in ATP and the extent of fatigue. Possible mechanisms underlying this relationship are discussed.
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PMID:A linear relationship between ATP degradation and fatigue during high-intensity dynamic exercise in rat skeletal muscle. 781 71


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