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

Force-velocity, power-velocity and unloaded shortening data were obtained from in situ medial gastrocnemius muscle-tendon complexes (stimulated at 60 Hz) with intact circulation of mature male rats (approximately 125 days old). Measurements were carried out at the end of a long (15 s) contraction (fatigued muscles) or with a short (1 s) contraction either in the fresh state (fresh muscles) or in muscles which had recovered for 15 min after a long contraction. Compared to the fresh state fatigue reduced isometric force by 57%, maximal shortening velocity by approximately 40% and maximal power output by 81%. These reductions were similar to data previously obtained with younger rats (40 days old). However, the velocity data of the muscles which had recovered for 15 min after a long contraction showed a greater reduction in the mature rats. This difference between the two age groups together with a difference in the changes in the initial parts of the isometric force time curves suggest an age-dependent response of the fast-fatigable fibre population of these mixed muscles. In a separate series of experiments the underlying mechanism of the recovery from fatigue was studied in a group of young rats. Fatigue was induced with five long (15 s) contractions (each at 5 min intervals). The recovery of isometric force and power output was monitored with short contractions which indicated a plateau of recovery but the absolute values were still reduced after 60 min (85 and 71% of prefatigue values, respectively). Phosphocreatine concentration recovered rapidly, whereas the ATP concentration was still markedly reduced after 1 h of recovery. The time courses of recovery of inosine-5'-monophosphate (IMP) and lactate concentrations resembled those of force and power output. Thus it is possible that age-dependent differences in IMP and/or lactate production may play a role in fatigue and recovery from fatigue.
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PMID:Age-related effects of fatigue and recovery from fatigue in rat medial gastrocnemius muscle. 259 30

By the use of invasive techniques, skeletal muscle has been shown to contribute to thermogenesis induced by glucose in humans. In an attempt to study this phenomenon by a non-invasive method, this study investigated intracellular high-energy phosphorous compounds in calf muscle by 31P MR spectroscopy during an oral glucose load in healthy lean subjects. The inorganic phosphate concentration increased gradually (P less than 0.05) after glucose intake. The phosphocreatine/inorganic phosphate rate decreased (P less than 0.05) and the estimated ADP concentration increased. ATP and intracellular pH remained unchanged after the glucose administration. No changes were seen in the control experiments. The processes responsible for the decreased energy state of the skeletal muscle cell may be an obligatory conversion of glucose to glycogen. Also, facultative processes, such as sodium/potassium pumping and substrate cycles stimulated by the sympatho-adrenal system, may be partly responsible.
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PMID:Changes of high-energy phosphorous compounds in skeletal muscle during glucose-induced thermogenesis in man. A 31P MR spectroscopy study. 259 28

1. Maximal calcium-activated force (Fmax) and calcium sensitivity were markedly decreased in detergent-skinned fibres from skeletal and cardiac muscle by solutions that mimicked the total milieu changes associated with fatigue and hypoxia. Further experiments determined the relative contribution of each of the individual changes in milieu. 2. Both Ca2+ sensitivity and Fmax of skeletal and cardiac fibres were decreased with increased [H+] or inorganic phosphate (Pi). These effects were greater in cardiac muscle. 3. Decreasing MgATP over the range observed with fatigue and hypoxia (6.8-4.7 mM) had no effect on Fmax or Ca2+ sensitivity of either muscle type. 4. Decreasing phosphocreatine (PCr: 15-1 mM) increased Fmax but had little effect on Ca2+ sensitivity in both muscle types. In cardiac fibres, the effect on Fmax could be mimicked by inhibition of endogenous creatine kinase. 5. ADP (0.7 mM) increased Fmax and Ca2+ sensitivity, while AMP (0.06 mM) slightly increased Fmax but had no effect on Ca2+ sensitivity of either skeletal or cardiac fibres. 6. Creatine (25 mM) had no significant effect on either Ca2+ sensitivity or Fmax of skeletal and cardiac muscle fibres. At higher levels (50 mM), however, creatine depressed Fmax and slightly altered Ca2+ sensitivity. 7. Thiophosphorylation of myosin P light chains (phosphorylatable light chains of myosin) in rabbit psoas fibres had no effect on Ca2+ sensitivity, yet slightly but significantly increased Fmax under fatigue conditions. 8. Reducing the affinity for ATP hydrolysis (by adding ADP, AMP and creatine) over the range calculated for fatigue/hypoxia (60-45 kJ/mol) produced the enhancement in Fmax expected from added ADP and AMP in cardiac but not skeletal muscle, indicating that changes in affinity influence Fmax of skeletal muscle. Reducing affinity produced little change in Ca2+ sensitivity of skeletal muscle. In contrast, the change produced in cardiac muscle was greater than that expected from addition of ADP and AMP; i.e. decreasing affinity increases calcium sensitivity of the heart. 9. Simple summation of all significant changes expected from each constituent altered by fatigue/hypoxia adequately predicted the observed changes in Fmax and Ca2+ sensitivity in both cardiac and skeletal muscle fibres with but one exception (the change in Ca2+ sensitivity of skeletal muscle at pH 7 was slightly overestimated).
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PMID:Changes of intracellular milieu with fatigue or hypoxia depress contraction of skinned rabbit skeletal and cardiac muscle. 260 Aug 30

isometric tension and maximum velocity of shortening of frog sartorious and biceps muscles were measured at varying pH and compared with the values obtained for muscles treated with DNFB. Both To and Vmax exhibited increase with increase in pH above neutral pH upto pH 9, and decreased as the pH was decreased up to 5. Muscle treated with DNFB at pH 7 showed about 30% decrement but these too improved at pH 9 to almost 105% and 130% respectively compared to untreated muscle at pH 7. Using the number of short duration tetanic contractions, which reduce To and Vmax by half, as an index for the onset of fatigue, high pH was found to have a positive effect in both normal and DNFB-treated muscle. Thus, the crucial factor for onset of fatigue is not a fall in ATP level but acidification and treatment with high pH Ringer's solution partially annuls the effect of acidosis, arising either naturally or from DNFB treatment. One additional role of creatine kinase activity to that of ATP regeneration is suggested to be the maintenance of neutral pH in the sarcoplasm.
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PMID:Effect of extracellular pH and DNFB treatment on the mechanical performance of frog skeletal muscle. 262 70

Muscular fatigue is of critical importance to performance and as such has been the subject of numerous investigations. However, a clear cause remains elusive. Although many factors have been identified, this review deals only with those which occur distal to the neuromuscular junction. Factors discussed include: energy supply (ATP/creatine phosphate, glycogen, oxygen, and free fatty acids); the accumulation of metabolites (lactate/hydrogen ions, calcium, ammonium, electrolyte and water shifts); and, the special case of eccentric work. The results of many studies using various methodologies are examined. Peripheral fatigue appears to be a complex series of interactions with variable influence on the development of fatigue depending upon the nature of the work performed.
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PMID:Biochemical aspects of peripheral muscle fatigue. A review. 264 71

The study of skeletal muscle disorders is providing potentially important insights into regulatory mechanisms in human exercise and fatigue and information useful for diagnostic and treatment purposes. This review primarily concerned the general metabolic and physiological factors which set upper limits to performance of various types of exercise in patients with a variety of muscle disorders. From the standpoint of exercise performance, skeletal muscle diseases can be classified into three major groups. One group consists of primary disorders of muscle energy metabolism, including defects in muscle carbohydrate and lipid metabolism, disorders of mitochondrial electron transport, and abnormalities of purine nucleotide metabolism. Exercise performance largely reflects the capacity for ATP resynthesis. Oxidative phosphorylation is the dominant quantitative source of energy for ATP resynthesis under most exercise conditions. Consequently, patients with disordered oxidative metabolism (i.e., patients with defects in the availability or utilization of oxidizable substrate, such as those with phosphorylase or PFK deficiency or those with defects in mitochondrial electron transport) typically demonstrate severely impaired exercise performance. Intolerance to sustained exercise and premature fatigability are salient features of muscle oxidative disorders. Maximal oxygen uptake and maximal a-v O2 difference are markedly subnormal related to an attenuated muscle oxygen extraction. Muscle weakness and atrophy are less common. Anaerobic muscle performance is dramatically limited in patients with virtually complete defects of glycogenolysis/glycolysis but appears relatively normal in those with electron transport defects. A second major group of disorders includes patients with decreased muscle mass due to muscle necrosis, atrophy, and replacement of muscle by fat and connective tissue. These disorders are exemplified by the various muscular dystrophies (Duchenne's dystrophy, Becker's dystrophy, LG dystrophy, FSH dystrophy, and myotonic dystrophy) in which exercise performance is severely impaired due to muscle wasting and weakness in spite of largely normal pathways for muscle ATP resynthesis. In muscular dystrophy patients, the degree to which maximal oxygen uptake and anaerobic muscle performance are impaired appears to be a function of the severity of muscle weakness and atrophy. A third group of disorders includes patients with impaired activation of muscle contraction or relaxation. These disorders may be considered in two subcategories. In the first, impaired activation or relaxation of contractile activity is due to intrinsic muscle dysfunction (e.g., diseases associated with myotonia or periodic paralysis). In the second subcategory, there is impaired muscle activation due to a primary abnormality in the central nervous system, motor nerves, or neuromuscular junction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Skeletal muscle disorders and associated factors that limit exercise performance. 267 57

A review of metabolic pathways is presented, which are involved in muscular energy production during hypoxia according to recent experimental findings. By means of own exercise examinations the course of reactions providing ATP anaerobically in the muscles of limbs with poor circulation is analysed. Therefore, the arteriovenous differences in the concentrations of lactate, pyruvate, ammonia, hypoxanthine and alanine in the femoral blood of patients with stage II AOD were determined. In addition, the intracellular phosphorus compounds ATP, PCr and Pi as well as the tissue pH were measured noninvasively in the calf muscles using 31P magnetic resonance spectroscopy. The results give evidence for marked activation of the creatine kinase reaction, of glycolysis, of the myokinase reaction and of the purine nucleotide cycle in the ischaemic musculature at loads of short duration, which are in total sufficient to maintain the concentration of ATP even during claudication pain. In spite of salvage pathways like alanine formation, the end products of these "emergency reactions", Pi, H+ and NH4+, accumulate and exert deleterious cytotoxic effects, which are thought to be responsible for rapid muscle fatigue and claudication pain in PAOD.
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PMID:[Regulation of ischemic muscle metabolism in peripheral arterial occlusive disease]. 267 1

Eight healthy men cycled at a work load corresponding to approximately 70% of maximal O2 uptake (VO2max) to fatigue (exercise I). Exercise to fatigue at the same work load was repeated after 75 min of rest (exercise II). Exercise duration averaged 65 and 21 min for exercise I and II, respectively. Muscle (quadriceps femoris) content of glycogen decreased from 492 +/- 27 to 92 +/- 20 (SE) mmol/kg dry wt and from 148 +/- 17 to 56 +/- 17 (SE) mmol/kg dry wt during exercise I and II, respectively. Muscle and blood lactate were only moderately increased during exercise. The total adenine nucleotide pool (TAN = ATP + ADP + AMP) decreased and inosine 5'-monophosphate (IMP) increased in the working muscle during both exercise I (P less than 0.001) and II (P less than 0.01). Muscle content of ammonia (NH3) increased four- and eight-fold during exercise I and II, respectively. The working legs released NH3, and plasma NH3 increased progressively during exercise. The release of NH3 at the end of exercise II was fivefold higher than that at the same time point in exercise I (P less than 0.001, exercise I vs. II). It is concluded that submaximal exercise to fatigue results in a breakdown of the TAN in the working muscle through deamination of AMP to IMP and NH3. The relatively low lactate levels demonstrate that acidosis is not a necessary prerequisite for activation of AMP deaminase. It is suggested that the higher average rate of AMP deamination during exercise II vs. exercise I is due to a relative impairment of ATP resynthesis caused by the low muscle glycogen level.
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PMID:Adenine nucleotide degradation in human skeletal muscle during prolonged exercise. 275 35

To investigate the hypothesis that the rate of fatigue development is not influenced by the absolute duration of contraction (train duration) and relaxation (off-phase of duty cycle) at constant duty cycle, strips of the diaphragm from 36 male adult rats (mean +/- SD wt 152 +/- 21 g) were stimulated directly for periods of 180, 250, and 320 ms at a constant duty cycle of 50%. The frequency of stimulation was adjusted to produce 40% of maximal tetanic tension at supramaximal voltages. After 30 min of stimulation, analysis of twitch characteristics between control and experimental groups indicated a prolongation of contraction time of 9% (P less than 0.05), an increase in relaxation time of 75% (P less than 0.05), and a decrease in twitch tension by 78% (P less than 0.05). Similarly, reductions (P less than 0.05) in isometric force output at high stimulation frequency (100 Hz) of 58% and at low frequency (20 Hz) of 67% were also noted. These changes were accompanied by an approximately 60% reduction in the maximal velocity of shortening. No difference was observed for any of the mechanical measures between experimental conditions. After 30-min stimulation, decreases of between 43 and 46% were noted for ATP (P less than 0.05) and increases of between three- and fourfold noted for IMP (P less than 0.05). No changes were found for either ADP or AMP. Total adenine nucleotide concentrations declined (P less than 0.05) an average of 24%. As with the mechanical data, no differences were found between the different stimulation conditions. It is concluded that for the conditions studied, fatigue mechanisms become manifest early in the stimulation period and are only minimally altered by the duration of specific contractions provided the relaxation period is of equal duration.
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PMID:Mechanical and metabolic alterations in rat diaphragm during electrical stimulation. 275 44

The influence of exercise intensity on the accumulation of inosine monophosphate (IMP) in human skeletal muscle has been investigated. Ten men cycled at workloads corresponding to 40%, 75% and 100% of their maximal oxygen uptake (VO2 max). Muscle IMP was below the detection limit (less than 0.01 mmol kg-1 dry wt) at rest and after exercise at 40% of VO2 max, but increased to 0.26 +/- 0.06 (mean +/- SEM) and 3.50 +/- 0.51 mmol kg-1 dry wt after exercise at 75% and 100% of VO2 max respectively. Accumulation of IMP corresponded to a similar decrease in the total adenine nucleotide content. The muscle content of IMP was positively related to lactate and negatively related to phosphocreatine (PCr). IMP was formed in both fibre types, but the IMP content at fatigue was about twice as high in type II fibres as in type I fibres. It was concluded that the IMP content of human skeletal muscle is very low at rest and after low-intensity exercise, but increases after moderate and high-intensity exercise. In contrast to rat muscle, where deamination of AMP predominantly occurs in the fast-twitch muscle fibres, IMP is formed during exercise in both fibre types in human muscle. Accumulation of IMP appears to reflect an imbalance between the rate of utilization and the rate of regeneration of ATP.
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PMID:Formation of inosine monophosphate (IMP) in human skeletal muscle during incremental dynamic exercise. 278 92


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