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

A 19-year-old patient presented with exercise-related myalgia, fatigue and elevated creatine kinase levels. Histology of a muscle biopsy was characterized by the presence of very large amounts of tubular aggregates. Both his father and paternal grandfather had elevated creatine kinase and large amounts of tubular aggregates in their muscle biopsies. The aggregates consisted of closely packed vesicles and tubules filled with electron-dense material or with one to several smaller tubules. Disorders with tubular aggregates in the muscle fibres such as hyperornithinaemia with gyrate atrophy of the retina, hypokalaemic periodic paralysis, hyperkalaemic periodic paralysis, myotonia congenita, alcoholism, osteomalacic myopathy etc. have been excluded. Tubular aggregates can be found in muscle disorders characterized by exercise-induced cramps, pain and stiffness. They also represent the predominant histological feature of some familial myopathies due to a yet unidentified genetic defect. In our family, there was male-to-male transmission, confirming dominant inheritance.
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PMID:On a dominantly inherited myopathy with tubular aggregates. 944 9

To examine some possible sites of fatigue during short-lasting maximally intensive stretch-shortening cycle exercise, drop jumps on an inclined sledge apparatus were analyzed. Twelve healthy volunteers performed jumps until they were unable to maintain jumping height > 90% of their maximum. After the workout, the increases in the blood lactate concentration and serum creatine kinase activation were statistically significant (P < 0.001 and P < 0.05, respectively) but rather small in physiological terms. The major changes after the workout were as follows: the single twitch was characterized by smaller peak torque (P < 0.05) and shorter time to peak (P < 0.05) and half-relaxation time (P < 0.01). The double-twitch torque remained at the same level (P > 0.05), but with a steeper maximal slope of torque rise (P < 0.05); during 20- and 100-Hz stimulation the torque declined (both P < 0.01) and the maximal voluntary torque changed nonsignificantly but with a smaller maximal slope of torque rise (P < 0.01) and a higher activation level (P < 0.05), accompanied by an increased electromyogram amplitude. These findings indicate that the muscle response after the short-lasting consecutive maximum jumps on the sledge apparatus may involve two distinct mechanisms acting in opposite directions: 1) The contractile mechanism seems to be potentiated through a shorter Ca2+ transient and faster cross-bridge cycling, as implied by twitch changes. 2) High-frequency action potential propagation shows an impairment, which is suggested as the possible dominant reason for fatigue in exercise of this type.
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PMID:Neuromuscular fatigue after maximal stretch-shortening cycle exercise. 945 55

The purpose of this experiment was to test the hypothesis that chronic (89 days) administration of recombinant equine somatotropin (eST) would increase aerobic capacity and improve exercise performance in old mares. Fifteen, healthy, unfit, aged (20-26 year old) mares were randomly assigned to a treatment (eST, 12.5 mg day-1 in 3 ml glycine/manitol buffer, s.c., n = 7) or control (vehicle, 3 ml day-1, s.c., n = 8) group. Aerobic capacity and exercise performance were measured using a standardized exercise test (SET) performed on a high speed treadmill. Tests were conducted before (-21 days), during (+43 days and +89 days) and after (+127 days) treatment. During the SET, resting data were collected and the horses then ran up a fixed 6% grade, starting at 4 m s-1, with a 1 m s-1 increase every 60 s (omitting 5 m s-1) until fatigue. Oxygen uptake (VO2) was measured using an open flow calorimeter and blood lactate concentration (LA) via a lactate analyser. Venous blood samples (10 ml) were collected at rest, during the last 10 s of each step of the SET, and after exercise and used to measure LA, plasma protein concentration (PP), hematocrit (HCT), and the plasma concentrations of creatine kinase (CK) and aspartamine transferase (AST). There were no differences (P > 0.05) in resting VO2, LA, TPP, or HCT due to treatment or test time. Furthermore, there were no differences (P > 0.05) in maximal oxygen uptake (VO2max), top run velocity, run time, watts at VO2max, velocity to produce a lactate of 4 mmoll-1 (VLA4), watts at VLA4, peak HCT or peak LA. Finally, there were no differences (P > 0.05) in resting or post-exercise CK or AST. These data indicate that chronic eST administration does not affect aerobic capacity or indices of exercise performance in unfit aged mares.
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PMID:Chronic recombinant equine somatotropin (eST) administration does not affect aerobic capacity or exercise performance in geriatric mares. 945 54

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40 min of bench stepping (knee high step; 15 steps x min[-1]). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150 W, with increments of 50 W every 2 min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P < 0.05). Endurance time and peak VO2 during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P < 0.05) during cycling after eccentric exercise compared with the control condition. Peak blood lactate concentration, observed at 2 min post-exercise was also higher [12.6 (SD 1.4) vs 10.9 SD (1.3) mM; P < 0.01]. The higher blood lactate concentration during cycling exercise after prior eccentric exercise may be attributable to an increased rate of glycogenolysis possibly arising from an increased recruitment of Type II muscle fibres. It follows that determination of lactate thresholds for the purpose of fitness assessment in subjects experiencing DOMS is not appropriate.
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PMID:Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans. 953 93

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

Oxygen free radicals have been implicated in exercise-induced cell and tissue injury, indicating an oxidative stress. Fatigue accompanied by a number of physiological and metabolic changes is in indication of overtraining. This study aimed to examine the influence of a continuous 24-h intermittent speed driving (1 h driving/1 h stop), on the response of hormones, antioxidative factors, lipid, and enzyme levels. Seven race car drivers of national level were examined before, during, and immediately after the trial of speed driving on a test designed to check endurance to stress. The parameters measured were: testosterone (Tes), cortisol (Cor), IgM, IgA, cholesterol, HDL, billirubin, ceruloplasmin, urea, uric acid, creatine kinase, and transaminases. Stress hormone Cor declined significantly (p < 0.05), while Tes did not change significantly. Fatigue enzyme, aspartate transaminase (GOT) increased significantly (p < 0.05), while alanine transaminase (GPT) did not change and urea declined. Muscle enzyme, creatine kinase (CK) increased to sixfold (p < 0.01). IgA, IgM and lipids did not change. The primary antioxidant ceruloplasmin increased significantly (p < 0.001), while antioxidants uric acid and glucose remained unchanged. Among the factors measured, ceruloplasmin, cortisol, urea, GOT, and CK seem to give a picture of the organism's alertness and defence capabilities in conditions of stress and fatigue.
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PMID:Stress hormonal factors, fatigue, and antioxidant responses to prolonged speed driving. 967 60

The long term impact of pre-hospital thrombolysis in acute myocardial infarction on the subsequent development of heart failure symptoms was investigated in 362 consecutive patients. The pre hospital strategy, used in 61 patients, allowed for very early administration of streptokinase, within 1.2+/-0.6 (mean+/-S.D.) hours from pain onset. In contrast, 294 patients treated in hospital received lytic treatment within 2.0+/-0.9 hours. The pre hospital group showed faster reperfusion, as measured by the time to peak creatine kinase and to ST segment recovery, but only a slightly better ventricular function, as compared to hospital treated patients. Heart failure symptoms were significantly reduced in the pre hospital group during hospitalization and at long term follow up: there were less dyspnea, fatigue, orthopnea, nocturnal dyspnea, nocturia, peripheral edema and episodes of pulmonary edema. Angina was reduced as well. We conclude that the initial benefit of prehospital thrombolysis translates into long term reduction of heart failure symptoms, thus improving quality of life.
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PMID:Prevention of congestive heart failure by early, prehospital thrombolysis in acute myocardial infarction: a long-term follow-up study. 970 26

Zidovudine is known to be responsible for a mitochondrial myopathy with ragged-red fibres and mitochondrial DNA depletion in muscle. Lactic acidosis alone or associated with hepatic abnormalities has also been reported. A single report mentioned the concomitant occurrence of muscular and hepatic disturbances and lactic acidosis in a patient receiving zidovudine, but muscle and liver tissues were not studied. A 57-year-old man with AIDS, who had been treated with zidovudine for 3 years, developed fatigue and weight loss. Serum creatine kinase and hepatic enzyme levels were high. Lactic acidosis was present. Liver biopsy showed diffuse macrovacuolar and microvacuolar steatosis. After withdrawal of zidovudine, creatine kinase, aspartate aminotransferase, and alanine aminotransferase levels normalised within 5 days, and lactacidaemia decreased. Acidosis persisted. The patient became confused and febrile and died 8 days after detection of high blood lactic acid. A muscle sample obtained at autopsy showed mitochondrial abnormalities with ragged-red fibres and lipid droplet accumulation. Southern blot analysis showed depletion of mitochondrial DNA, affecting skeletal muscle and liver tissue. No depletion was found in myocardium and kidney. This case emphasises that zidovudine treatment can induce mitochondrial multisystem disease, as revealed in our case by myopathy, liver steatosis and lactic acidosis.
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PMID:Zidovudine-induced mitochondrial disorder with massive liver steatosis, myopathy, lactic acidosis, and mitochondrial DNA depletion. 1070 83

The purpose of the present study was to investigate the effect of stretch-shortening-cycle-induced muscle damage on the time course of mechanical behaviour in the drop jump. Ten healthy male subjects performed submaximal stretch-shortening cycle (SSC) exercise on a special sledge apparatus. Exhaustion occurred on average within 3 min. A drop jump (DJ) test from a 50-cm height was performed before and immediately after the sledge exercise as well as 2 h, 2 days and 4 days later. The fatigue exercise showed relatively high blood lactate concentration [12.5 (SD 2.6) mmol x l(-1)] and an increase of serum creatine kinase (CK) activity delayed by 2 days [540 (SD 407) U x l(-1)]. The initial decline in the jump performance (before - immediately after) was related negatively to the early recovery in performance (immediately after 2 h) (P < 0.05). The early recovery of the knee joint moment at the end of stretch showed a negative correlation to the delayed decrease in DJ performance (2 h 2 days) (P < 0.01). Thus, the DJ performance showed an initial decline followed by an early recovery and a secondary decline. Both the initial decline and early recovery in the knee joint moment at the end of stretch were related to the corresponding initial (after 2 h) (P < 0.05) and secondary increases (2 h - 2 days) (P < 0.01) in CK. It is suggested that the early recovery as well as the initial decline in the knee joint function could depend on the degree of muscle damage. Delayed decrease in initial stiffness (2 h - 2 days) was negatively related to the corresponding changes in the knee joint angle at touch down in DJ (P < 0.001). These interactions would imply that the decrease in the stiffness regulation and the modulation of the prelanding motor control might be attributable to secondary muscle damage during 2 days after the SSC exercise. Therefore, it may be suggested that the changes in the DJ performance after the exhausting SSC exercise accompany the progress of muscle damage observed by the corresponding increase in serum CK concentration and the corresponding deterioration of stiffness regulation and motor control in DJ.
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PMID:Effect of exhausting stretch-shortening cycle exercise on the time course of mechanical behaviour in the drop jump: possible role of muscle damage. 1002 37


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