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

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

A 15-year-old girl with a four-month history of cardiac failure from undetermined cause was admitted to the hospital with weakness, fatigue, and weight loss. During her hospitalization she was found to have abused diet aids, laxatives, and cathartics. Although an electrocardiogram revealed nonspecific T-wave abnormalities and laboratory studies showed supranormal enzyme test results for creatine kinase and lactate dehydrogenase, no definite explanation of the cardiomyopathy was forthcoming. Ipecac abuse leading to cardiomyopathy was suspected early in the hospitalization. HPLC analysis of a urine sample showed emetine, a principle component of ipecac, the presence of which was later confirmed by more-specific HPLC analysis with photodiode array detection.
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PMID:Emetine identified in urine by HPLC, with fluorescence and ultraviolet/diode array detection, in a patient with cardiomyopathy. 292 Apr 26

Lactic acid is formed and accumulated in the muscle under conditions of high energy demand, rapid fluctuations of the energy requirement and insufficient supply of O2. During intense exercise sustained to fatigue muscle pH decreases to about 6.4-6.6. Force generation does not appear to be limited by the high H+ ion concentration per se but is more related to the PCr level. Phosphofructokinase may be inhibited by high H+ concentration but the inhibition is adequately overcome by increases in the activators AMP and ADP. A high concentration of H+ will decrease PCr by a direct effect on the creatine kinase equilibrium and indirectly by an increase in ADP. The effect of acidosis on glycolysis and on the PCr level will result in a decreased rate of ADP rephosphorylation, and it is suggested that ADP increases transiently above the steady-state level in the contracting muscle fibre. It is further suggested that the function of Na-K-ATPase is impaired by the increase of ADP resulting in an altered ionic balance over the muscle cell membrane. Muscle fatigue is thus considered to be due to an insufficient rate of ADP rephosphorylation resulting in a block in the activation process or in the excitation/contraction coupling.
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PMID:Muscle fatigue and lactic acid accumulation. 347 Oct 61

Muscle fatigue and pain are together common symptoms which can be analysed physiologically. For many patients attending a medical clinic the problem for the doctor is to decide whether the problem is "in the mind" or "in the muscle". A history of the symptoms occurring at rest without any exercise is a hint of psychological origin. Exercise fatigue or pain should ideally be reproduced by an appropriate provoking exercise test. Needle biopsy with histochemistry is cost-effective as a means of reaching a diagnosis while blood determinations of erythrocyte sedimentation rate and plasma creatine kinase and lactate are more specific but less sensitive indicators of a muscle cause. Fatigue is analysed by force and action potential measurements with electrically stimulated contractions. Pain worse after exercise can be related to muscle damage. A programme of therapeutic exercise may be tried as a further means of assessment of these symptoms.
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PMID:Muscle fatigue and pain. 353 9

During muscular fatigue two metabolites, hydrogen ions (H+) and inorganic phosphate (Pi), increase in concentration. The effect of increase in [H+] has been modeled mathematically for a system containing creatine kinase (EC 2.7.3.2), adenylate kinase (EC 2.7.4.3), and the appropriate concentrations of their substrates. Assuming that no other equilibrium reactions are involved, the result of acidification should be a useful increase in the ratio [ATP]/[ADP]. It is also shown by a reanalysis of earlier 31P NMR studies that the observed combination of increased [H+] and increased [Pi] leads to an increase in the monobasic phosphate concentration [Pi-] that is inversely proportional to the force of contraction. This suggests that Pi- may be a direct inhibitor of the actomyosin ATPase system.
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PMID:Muscular fatigue: effects of hydrogen ions and inorganic phosphate. 353 90

Five women and three men (aged 24-43 yr) performed maximal eccentric contractions of the elbow flexors (for 20 min) on three occasions, spaced 2 wk apart. Muscle pain, strength and contractile properties, and plasma creatine kinase (CK) were studied before and after each exercise bout. Muscle tenderness was greatest after the first bout and thereafter progressively decreased. Very high plasma CK levels (1,500-11,000 IU/l) occurred after the first bout, but the second and third bouts did not significantly affect the plasma CK. After each bout the strength was reduced by approximately 50% and after 2 wk had only recovered to 80% of preexercise values. Each exercise bout produced a marked shift of the force-frequency curve to the right which took approximately 2 wk to recover. The recovery rate of both strength and force-frequency characteristics was faster after the second and third bouts. Since the adaptation occurred after the performance of maximal contractions it cannot have been a result of changes in motor unit recruitment. The observed training effect of repeated exercise was not a consequence of the muscle becoming either stronger or more resistant to fatigue.
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PMID:Repeated high-force eccentric exercise: effects on muscle pain and damage. 369 72

This study describes the influence of muscle fiber type composition, enzyme activities and capillary supply on muscle strength, local muscle endurance or aerobic power and capacity. Muscle biopsies were obtained from m. vastus lateralis in thirteen physically active men. Histochemical staining procedures were applied to assess the percentage of fast twitch (FT) fibers, muscle fiber area, and capillary density. Also, the activity of citrate synthase (CS), creatine kinase (CK), hexokinase (HK), lactate dehydrogenase (LDH), and phosphofructokinase (PFK) were analysed using fluorometrical assays. Peak torque at 'low' and 'high' angular velocities was measured during leg extension. Similarly, muscle fatigue (e.g. peak torque decline) and recovery from a short-term exercise task were measured during maximal, voluntary consecutive leg extensions. Aerobic power (VO2max) and aerobic capacity (e.g. onset of blood lactate concentration; OBLA), as defined by a blood lactate concentration of 4 mol X 1(-1) were measured during cycling. Peak torque at a high angular velocity was positively correlated with % FT area (p less than 0.001). Fatigue and recovery were correlated with LDH X CS-1 (p less than 0.001). WOBLA was best correlated with PFK and PFK X CS-1 (p less than 0.001). Hence, muscle strength was partly determined by fiber type composition whereas local muscle endurance, recovery and aerobic capacity reflect mainly capillary supply and the activity of key enzymes involved in aerobic and anaerobic metabolism.
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PMID:The influence of muscle metabolic characteristics on physical performance. 406 7

The diagnosis of acute mild myocarditis in vaguely defined. Therefore we studied 185 consecutive young men in military service with electrocardiographic changes arousing a suspicion of myocarditis in connection with an acute infectious disease. It was possible to classify 160 patients into seven electrocardiographic groups; definite or probable myocarditis was observed in 104 patients. The electrocardiographic patterns considered characteristic for acute myocarditis were: ST segment elevations followed by T wave inversions; gradually changing T wave inversions not corrected by beta blockade; and ventricular extrasystoles more than 10 per minute triggered by acute infection. Thirty-nine subjects without myocarditis had "functional" T wave abnormalities completely normalised by beta blockade, or stable T wave inversion. The leading symptoms in acute myocarditis were fatigue and chest pains; loud S3 gallop, paradoxical cardiac pulsation, pericardial friction rub, or enlargement of the heart were noted altogether in 50% of the patients. Echocardiography disclosed segmental wall motion abnormalities related to the T wave inversions. Serum creatine kinase MB fraction increased in 70% of the acute myopericarditis patients during the ST segment elevation stage. In the non-myocarditis groups the clinical and pertinent laboratory findings remained normal. Thus, we noted in clinically mild acute infectious myocarditis clear-cut and early signs of myocardial dysfunction, suggesting that the direct and often local viral invasion of the myocardium is the basic pathogenetic mechanism. The present electrocardiographic classification based on serial tracings and beta blockade proved useful in the evaluation of patients suspected of having mild acute myocarditis.
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PMID:Evaluation of mild acute infectious myocarditis. 612 67

Isolated extensor digitorum longus muscles from rat were exposed to atmospheres of 30% CO2 (high-CO2 muscles) or 6.5% CO2 (control muscles) in O2 for 95 min. Muscle contraction characteristics were studied before and after the incubation. Tetanic tension decreased in high-CO2 muscles to 55% of initial value but remained unchanged in control muscles. Relaxation time was prolonged in high-CO2 muscles but not in control muscles. Intracellular pH was 6.67 +/- 0.04 (SD) in high-CO2 muscles and 7.01 +/- 0.04 in control muscles. CO2-induced acidosis had a marked influence on the intermediary energy metabolism as shown by a fourfold increase of glucose 6-phosphate, a 14% increase of ADP, and a decrease of phosphocreatine to 44% of the control value. Lactate and pyruvate contents were unchanged. The observed metabolic changes can be explained by an effect of H+ on the activity of phosphofructokinase and on the creatine kinase equilibrium. It can be concluded that H+ concentration causes muscular fatigue. It is, however, uncertain whether this is an effect of increased H+ per se or by high-energy phosphate depletion induced by acidosis.
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PMID:Fatigue and phosphocreatine depletion during carbon dioxide-induced acidosis in rat muscle. 640 27

Patients with neuromuscular diseases have low levels of cardiovascular fitness and they fatigue rapidly during daily activities. The purpose of this investigation was to determine whether patients with slowly-progressive or non-progressive neuromuscular diseases could complete a 12-wk training program without untoward responses, and develop cardiovascular training adaptations. All eight patients completed the training program with better than 90% compliance. Resting creatine kinase and myoglobin in the group as a whole showed no change with training, though two patients did have definite elevations after training. Their VO2max increased by 25 +/- 5% with training and their relative increase in VO2max was not different from that of healthy subjects undergoing the same training. Heart rate reductions during submaximal exercise were somewhat delayed or non-existent in the two patients with Charcot-Marie-Tooth disease, a hereditary neuropathy. However, the six patients with myopathies had heart rate adaptations similar to those in healthy subjects. Thus, some patients with slowly-progressive or non-progressive neuromuscular diseases can undergo exercise training and in many cases demonstrate adaptations not different from those in healthy subjects. Patients with different diseases, however, need not respond uniformly, in terms of training adaptations or markers of muscle damage. Therefore, each disease must be considered individually.
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PMID:Effect of training on the exercise responses of neuromuscular disease patients. 651 64


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