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

We studied the physiologic adaptation of patients with mitochondrial myopathies to aerobic training. Ten patients underwent individually supervised, moderate-intensity aerobic training on a treadmill for 8 weeks. Biochemical and functional measures improved with training. Estimated aerobic capacity increased by 30%. Blood lactate concentrations at rest and after exercise decreased by 30%. Muscle phosphorus magnetic resonance spectroscopy measurements of adenosine diphosphate recovery after exercise improved by more than 60%. Fatigue and tolerance to daily activities also improved. Although the improvement in exercise tolerance may be due in part to reversal of the effects of secondary deconditioning, this uncontrolled clinical trial suggests that aerobic training can benefit patients with mitochondrial myopathies.
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PMID:Effects of aerobic training in patients with mitochondrial myopathies. 956 94

A decline of isometric force production is one characteristic of skeletal muscle fatigue. In fatigue produced by repeated short tetani, this force decline can be divided into two components: a reduction of the cross-bridges' ability to generate force, which comes early; and a reduction of the sarcoplasmic reticulum Ca2+ release, which develops late in fatigue. Acidification due to lactic acid accumulation has been considered as an important cause of the reduced cross-bridge force production. However, in mammalian muscle it has been shown that acidification has little effect on isometric force production at physiological temperatures. By exclusion, in mammalian muscle fatigue, the reduction of force due to impaired cross-bridge function would be caused by accumulation of inorganic phosphate ions, which results from phosphocreatine breakdown. The reduction of sarcoplasmic reticulum Ca2+ release in late fatigue correlates with a decline of ATP and we speculate that the reduced Ca2+ release is caused by a local increase of the ADP/ATP ratio in the triads.
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PMID:Mechanisms underlying the reduction of isometric force in skeletal muscle fatigue. 957 70

Limitations in energy supply is a classical hypothesis of muscle fatigue. The present paper reviews the evidence available from human studies that energy deficiency is an important factor in fatigue. The maximal rate of energy expenditure determined in skinned fibres is close to the rate of adenosine triphosphate (ATP) utilisation observed in vivo and data suggest that performance during short bursts of exercise (<5 s duration) primarily is limited by other factors than energy supply (e.g. Vmax of myosine adenosine triphosphatase (ATPase), motor unit recruitment, engaged muscle mass). Within 10 s of exercise maximal power output decreases considerably and coincides with depletion of phosphocreatine. During recovery, maximal force and power output is restored with a similar time course as the resynthesis of phosphocreatine. Increases in muscle store of phosphocreatine through dietary supplementation with creatine increases performance during high-intensity exercise. These findings support the hypothesis that energy supply limits performance during high-intensity exercise. It is well documented that pre-exercise muscle glycogen content is related to performance during moderate intensity exercise. Recent data indicates that the interfibre variation in phosphocreatine is large after prolonged exercise to fatigue and that some fibres are depleted to the same extent as after high-intensity exercise. Despite relatively small decreases in ATP, the products of ATP hydrolysis (Pi and free ADP) may increase considerably. Free ADP calculated from the creatine kinase reaction increases 10-fold both after high-intensity exercise and after prolonged exercise to fatigue. It is suggested that local increases in ADP may reach inhibitory levels for the contraction process.
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PMID:Energy supply and muscle fatigue in humans. 957 71

1. The mechanism behind the reduction in shortening velocity in skeletal muscle fatigue is unclear. In the present study we have measured the maximum shortening velocity (V0) with slack tests during fatigue produced by repeated, 350 ms tetani in intact, single muscle fibres from the mouse. We have focused on two possible mechanisms behind the reduction in V0: reduced tetanic Ca2+ and accumulation of ADP. 2. During fatigue V0 initially declined slowly, reaching 90 % of the control after about forty tetani. The rate of decline then increased and V0 fell to 70 % of the control in an additional twenty tetani. The reduction in isometric force followed a similar pattern. 3. Exposing unfatigued fibres to 10 microM dantrolene, which reduces tetanic Ca2+, lowered force by about 35 % but had no effect on V0. 4. In order to see if ADP might increase rapidly during ongoing contractions, we used a protocol with a tetanus of longer duration bracketed by standard-duration tetani. V0 in these three tetani were not significantly different in control, whereas V0 was markedly lower in the longer tetanus during fatigue and in unfatigued fibres where the creatine kinase reaction was inhibited by 10 microM dinitrofluorobenzene. 5. We conclude that the reduction in V0 during fatigue is mainly due to a transient accumulation of ADP, which develops during contractions in fibres with impaired phosphocreatine energy buffering.
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PMID:Mechanisms underlying reduced maximum shortening velocity during fatigue of intact, single fibres of mouse muscle. 962 83

Earlier work on Notothenioids led to the hypothesis that a reduced glycolytic capacity is a general adaptation to low temperatures in Antarctic fish. In our study this hypothesis was reinvestigated by comparing changes in the metabolic status of the white musculature in two related zoarcid species, the stenothermal Antarctic eelpout Pachycara brachycephalum and the eurythermal Zoarces viviparus during exercise and subsequent recovery at 0 degreesC. In both species, strenuous exercise caused a similar increase in white muscle lactate, a drop in intracellular pH (pHi) by about 0.5 pH units, and a 90% depletion of phosphocreatine. This is the first study on Antarctic fish that shows an increase in white muscle lactate concentrations. Thus the hypothesis that a reduced importance of the glycolytic pathway is characteristic for cold-adapted polar fish cannot hold. The recovery process, especially the clearance of white muscle lactate, is significantly faster in the Antarctic than in temperate eelpout. Based on metabolite data, we calculated that during the first hour of recovery aerobic metabolism is increased 6.6-fold compared with resting rates in P. brachycephalum vs. an only 2.9-fold increase in Z. viviparus. This strong stimulation of aerobic metabolism despite low temperatures may be caused by a pronounced increase of free ADP levels, in the context of higher levels of pHi and ATP, which is observed in the Antarctic species. Although basal metabolic rates are identical in both species, the comparison of metabolic rates during situations of high-energy turnover reveals that the stenothermal P. brachycephalum shows a higher degree of metabolic cold compensation than the eurythermal Z. viviparus. Muscular fatigue after escape swimming may be caused by a drop of the free energy change of ATP hydrolysis, which is shown to fall below critical levels for cellular ATPases in exhausted animals of both species.
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PMID:High-energy turnover at low temperatures: recovery from exhaustive exercise in Antarctic and temperate eelpouts. 984 52

The purpose of this study was to develop a standardised maximal treadmill exercise test performed until fatigue in order to find reproducible markers for anaerobic metabolism, specifically adenine nucleotide degradation. Six Standardbred trotters performed an incremental maximal treadmill exercise test in 1 min steps (starting with 7 m/s) until they could no longer keep pace with the treadmill. The test was performed twice with at least one week between the tests. Heart rate was recorded and venous blood samples were obtained during the test and in the recovery period for determination of plasma lactate, hypoxanthine, xanthine and uric acid. Muscle biopsy samples (m. gluteus) were collected at rest, immediately post exercise, and after 15 min recovery and analysed for their concentrations of glycogen, creatine phosphate (CP), adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), inosine monophosphate (IMP) and muscle lactate (MLa). Significant decreases in glycogen, CP and ATP and significant increases in IMP and MLa were seen immediately post exercise. None of these metabolites had returned to resting levels after 15 min of recovery. A marked increase in plasma lactate (PLa) occurred during exercise and the peak concentration (mean value = 27.2 mmol/l) was reached within 5 min of recovery. Plasma uric acid concentration did not increase during exercise but rose markedly immediately post exercise, reaching the highest level (mean value = 121.5 micromol/l) at 20-30 min recovery. The duration of the maximal test was related to peak PLa and the uric acid concentration at 30 min of recovery. A correlation was also found between the ATP and IMP concentrations immediately post exercise and the plasma uric acid concentration at 30 min of recovery. The results show that this treadmill test triggered anaerobic metabolism and also that uric acid concentration post exercise seems to be a marker for the adenine nucleotide degradation that occurs during intense exercise. No significant differences were seen in metabolic response between the 2 test occasions.
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PMID:Muscle anaerobic response to a maximal treadmill exercise test in Standardbred trotters. 984 69

To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate.
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PMID:Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise. 1006 3

The aim of this study was to determine cross-bridge number and kinetics in the diaphragm during fatigue and early recovery. Experiments were conducted in isolated mouse diaphragm (n=10). The force of a single cross-bridge (pi), the number of cross-bridges (m x 10(9) x mm2), the time cycle (tc) and the rate constants for cross-bridge attachment (f1) and detachment (g2) were calculated from the equations of A.F. Huxley. Following the fatigue protocol, peak isometric tension (Po) and maximum unloaded shortening velocity fell by 40+/-1% and 17+/-2%, respectively. In fatigued diaphragm, m fell by approximately 40% and returned to baseline after 10 min. When compared to baseline, g2 fell in fatigued diaphragm and remained significantly lower during the 15-min recovery period. In contrast, fatigue did not significantly modify pi, f1, or tc. There was a strong linear relationship between Po and m (p<0.001, r=0.988). No relationship was observed between tc and g2. These results indicate that changes in tension during fatigue and recovery run parallel to changes in the number of active cross-bridges, with no change in the force generated per cross-bridge. It is conceivable that fatigue durably impairs adenosine diphosphate release from the actomyosin complex without modifying the total duration of the cross-bridge cycle.
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PMID:Cross-bridge kinetics in fatigued mouse diaphragm. 1041 4

A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide pool (TAN = ATP + ADP + AMP), and increase in TAN degradation products inosine 5'-monophosphate (IMP) and hypoxanthine are observed at fatigue during prolonged exercise at 70% maximal O(2) uptake in untrained subjects [J. Baldwin, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study aimed to examine whether these metabolic changes are also prevalent when exercise is performed below the blood lactate threshold (LT). Six healthy, untrained humans exercised on a cycle ergometer to voluntary exhaustion at an intensity equivalent to 93 +/- 3% of LT ( approximately 65% peak O(2) uptake). Muscle biopsy samples were obtained at rest, at 10 min of exercise, approximately 40 min before fatigue (F-40 =143 +/- 13 min), and at fatigue (F = 186 +/- 31 min). Glycogen concentration progressively declined (P < 0.01) to very low levels at fatigue (28 +/- 6 mmol glucosyl U/kg dry wt). Despite this, PCr content was not different when F-40 was compared with F and was only reduced by 40% when F was compared with rest (52. 8 +/- 3.7 vs. 87.8 +/- 2.0 mmol/kg dry wt; P < 0.01). In addition, TAN concentration was not reduced, IMP did not increase significantly throughout exercise, and hypoxanthine was not detected in any muscle samples. A significant correlation (r = 0.95; P < 0. 05) was observed between exercise time and glycogen use, indicating that glycogen availability is a limiting factor during prolonged exercise below LT. However, because TAN was not reduced, PCr was not depleted, and no correlation was observed between glycogen content and IMP when glycogen stores were compromised, fatigue may be related to processes other than those involved in muscle high-energy phosphagen metabolism.
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PMID:Skeletal muscle energy metabolism during prolonged, fatiguing exercise. 1060 Nov 87

When blood is collected into sodium citrate in the proportion of 9 parts blood:1 part sodium citrate, the concentration of plasma sodium citrate in the sample will depend on the packed cell volume (PCV) of the blood sample. This difference in plasma sodium citrate concentration secondary to alterations in PCV significantly affects human platelet aggregation responses. Since horses attain a high PCV in response to high-intensity exercise we investigated the effect of differences in sample plasma sodium citrate concentration on equine platelet aggregability. In addition, low molecular weight heparin (LMWH) was evaluated as an alternative anticoagulant for assessment of platelet aggregability during strenuous exercise in horses. Blood samples were collected pre-exercise and at fatigue after supramaximal treadmill exercise into either 3.8% sodium citrate (9 parts blood:1 part sodium citrate) or 20 u LMWH/ml of blood. Platelet aggregation responses to 1.25 mumol/l adenosine diphosphate (ADP) were measured via optical aggregometry. For samples collected into sodium citrate, aggregability was significantly less than pre-exercise values in samples collected at fatigue and in pre-exercise samples in which sodium citrate concentrations were adjusted to equal those in fatigue samples. However, samples collected into LMWH showed significantly increased platelet aggregability in samples collected at fatigue when compared to pre-exercise samples. In conclusion, higher plasma sodium citrate concentration had a marked inhibitory effect on equine platelet aggregation responses. Low molecular weight heparin was a good alternative anticoagulant for assessment of equine platelet function and results indicate that equine platelet aggregability was enhanced in response to supramaximal exercise.
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PMID:The effect of supramaximal exercise on equine platelet function. 1065 48


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