Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle biopsies taken from the musculus quadriceps femoris of man were analysed for pH, ATP, ADP, AMP, creatine phosphate, creatine, lactate and pyruvate. Biopsies were taken at rest, after circulatory occlusion and after isometric contraction. Muscle pH decreased from 7.09 at rest to 6.56 after isometric exercise to fatigue. Decrease in muscle pH was linearly related to accumulation of lactate plus pyruvate. An increase of 22mumol of lactate plus pyruvate per g of muscle resulted in a fall of 0.5pH unit. The apparent equilibrium constant of the creatine kinase reaction (apparent K(CK)) increased after isometric contraction and a linear relationship between log(apparent K(CK)) and muscle pH was obtained. The low content of creatine phosphate in muscle after contraction as analysed from needle-biopsy samples is believed to be a consequence of an altered equilibrium state of the creatine kinase reaction. This in turn is attributed mainly to a change in intracellular pH.
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PMID:Creatine kinase equilibrium and lactate content compared with muscle pH in tissue samples obtained after isometric exercise. 0 60

This study was designed to investigate electromyographic (EMG), muscle glycogen and blood lactate changes in quadriceps muscle group during repeated 40 maximal eccentric and concentric contractions, and to follow the recovery in EMG, muscle glycogen and serum creatine kinase values during a 4 day period following the work test. The subjects were normal males and test order (eccentric or concentric) was randomly selected. The results indicated first, that the EMG parameters (IEMG, AMUP), muscle glycogen and blood lactate changed in a similar manner during the both fatigue loads. Despite the high tension work no selective depletion of glycogen could be observed in the slow or fast twitch muscle fibres in either type of work. The restoring of muscle glycogen occurred in a similar manner after the both fatigue loads, and no significant differences were present between eccentric and concentric works in the serum creatine kinase levels for a 2 days period. The eccentric work was associated with muscle soreness, which was strongest during the second day after the termination of the work test. The recovery of the EMG parameters were also delayed in eccentric fatigue. After concentric fatigue EMG-activity returned to normal values within 2 days.
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PMID:Changes in motor unit activity and metabolism in human skeletal muscle during and after repeated eccentric and concentric contractions. 88 14

Symptoms of depression in the majority of patients immediately following acute myocardial infarctions (AMI) resolve rapidly; they are an adjustment reaction. However, in a group of 552 male patients there were 80 (14.5%) patients with persistent major depressive symptoms during a finite period after AMI. Infarction size was assessed by maximum creatine kinase levels, the QRS-complex and the occurrence of late potentials. These measures did not correlate with the degree of depressed moods in these groups. An arrhythmic event in the early hospitalization phase, a recurrent infarction, dyspnoea, and persistent angina pectoris before the AMI were significantly related to more profound degrees of depression. Patients who reported serious life-events in the last 2 yr before AMI, or who suffered from exhaustion and fatigue in the prehospital phase were subject to significantly higher levels of depression. A prodromal phase prior to hospitalization free of bodily symptoms and the use of denial were related to low levels of depression. The logistic regression model incorporating all univariate significant variables revealed that symptoms of exhaustion and fatigue prior to AMI had the strongest independent correlation with post AMI depression.
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PMID:Factors which provoke post-infarction depression: results from the post-infarction late potential study (PILP). 143 62

This study has measured the pattern of elevated serum enzyme activity (ESEA) during extended daily training in a dose-response manner and compared ESEA to the pattern of accumulated fitness and fatigue predicted from a mathematical model previously described. Blood samples were taken regularly during the study from each subject and the activity of lactate dehydrogenase (LDH), creatine kinase (CK), and aspartate aminotransferase (AST) in the serum was measured. Although no single physiological/biochemical correlate of the hypothesized fatigue compartment of performance is firmly identified it is significant that the pattern of variation of model fatigue and ESEA throughout training were similar although slightly out of phase. With continued hard training, model fatigue began to plateau and concomitantly ESEA declined exponentially from its initial high value in early training. During relative rest throughout a tapering period following training both ESEA and fatigue reverted quickly towards baseline and follow the similar but earlier time course in blood of a degradative membrane enzyme phospholipase A2 observed in clinical studies.
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PMID:Dose/response effects of exercise modeled from training: physical and biochemical measures. 164 35

We identified a cohort of 300 individuals who had paralytic polio between 1935 and 1955. All lived in Olmsted County, Minnesota. From the 247 survivors, we selected 50 subjects for detailed historical, functional, psychological, clinical, and electrophysiologic evaluation. Sixty-four percent of these 50 survivors complained of new symptoms of muscle pain, fatigue, and weakness after a period of prolonged stability. This led to changes in lifestyle or activity in only 18%. The likelihood of expressing new complaints was not related to present age or interval since polio, and electrophysiologic testing did not distinguish between those with or without new problems. The development of new difficulties in a limb was most strongly predicted by significant paralysis of that limb at the time of the acute illness. Patients with leg weakness were twice as likely to complain of new problems compared to those with arm weakness. Elevated creatine kinase levels were present only in those with new complaints.
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PMID:Late effects of paralytic poliomyelitis in Olmsted County, Minnesota. 201 Dec 46

The eosinophilia-myalgia syndrome associated with the use of oral preparations of the amino acid L-tryptophan was recognized in late 1989. We describe the clinical and laboratory manifestations, pathological findings and early clinical course of 20 patients with the eosinophilia-myalgia syndrome. Prominent clinical findings included severe myalgias limiting function, fatigue, rashes, edema and weight gain, weight loss, muscle weakness and shortness of breath. Laboratory findings included eosinophilia (often marked), normal erythrocyte sedimentation rate, and elevated aldolase with normal or low creatine kinase values. On biopsy fascial inflammation was always seen consisting of lymphocytes, histiocytes and eosinophils in a perivascular distribution. Invasion of the vascular wall by lymphocytes was seen in 20%. Capillary and arteriolar endothelial cell thickening was found in most cases on electron microscopy and endothelial cell necrosis or mural invasion by lymphocytes was seen in 25% of cases. Two patients improved with no therapy. Ten patients responded to therapy with prednisone alone. Three patients have had progressive disease and one of these died. The relationship of this syndrome to previously described disease entities associated with eosinophilia is discussed.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan use. 227 99

The Cardiac Arrhythmia Pilot Study tested the feasibility of performing a large-scale study to evaluate the effect of therapy of ventricular arrhythmias after acute myocardial infarction (AMI). Ten clinical sites identified patients with greater than or equal to 10 ventricular premature complexes (VPCs)/hour, recorded 6 to 60 days after AMI in patients with an ejection fraction greater than 0.20. Patients were randomized to receive 1 of 5 agents: encainide, flecainide, imipramine, moricizine or placebo. Successful therapy was defined as greater than or equal to 70% suppression of VPCs and greater than 90% suppression of runs of ventricular tachycardia. Randomization to a second agent occurred if a patient did not achieve adequate suppression with the initial agent. Patients initially randomized to placebo continued to receive placebo. Patients were evaluated at 3-month intervals for the next year. Of 30,763 patients screened, 10,734 (35%) were younger than 70 years old and had a qualifying AMI. A Holter recording was obtained in 3,957 patients, of whom 871 (22%) had qualifying arrhythmias and 687 were eligible. Of the 687 eligible patients, 502 (73%) were randomized. Mean age of enrolled patients was 59 years. One-half of patients were randomized within 1 month after AMI. Mean ejection fraction was 0.45, with 175 (35%) patients having an ejection fraction less than 0.40. On baseline drug-free recording, 173 (35%) patients had less than 30 VPCs/hour; 149 (30%) between 30 and 100/hour and 180 (36%) greater than or equal to 100/hour. At least 1 run of ventricular tachycardia was seen in 172 (34%) patients. Drugs taken at baseline were similar in all groups with 116 (23%) patients taking digitalis, 161 (32%) taking diuretics, 203 (41%) taking beta blockers and 200 (40%) taking calcium antagonists. Slightly more patients, 53 (51%), randomized to flecainide were taking calcium antagonists. No significant relation was noted between baseline VPC frequency and ejection fraction, but baseline VPC frequency was correlated with heart rate, arrhythmia noted before AMI and right bundle branch block. As expected, a high ejection fraction correlated with lower peak creatine kinase values, an inferior location of the infarct and fewer signs of congestive heart failure. At baseline, at least 1 adverse symptom was volunteered by 192 (39%) patients. The most common symptoms were unusual tiredness or fatigue, heart beating fast or skipping beats or headache. In this study, over 20 age- and AMI-eligible patients were identified to obtain each randomized patient. The randomization process successfully distributed baseline variables across drug groups.
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PMID:Recruitment and baseline description of patients in the Cardiac Arrhythmia Pilot Study. The Cardiac Arrhythmia Pilot Study (CAPS) investigators. 245 14

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

The skeletal muscle has the capacity to respond adaptively to increased use. This observation could open up the feasibility of constructing pumping chambers to support or even replace cardiac work. We investigated the changes in enzyme activity due to chronic stimulation in an animal skeletal muscle. In 5 adult sheep the psoas muscle of one side was electrically stimulated through the muscle nerves, with an implantable stimulation unit for 5 weeks. The activity of the hexokinase (E.C.2.7.1.1.), lactate dehydrogenase (E.C.1.1.1.27), malate dehydrogenase (E.C.1.1.1.37), creatine kinase (E.C.2.7.3.2.) choline acetyltransferase and the contents of adenosine triphosphate and adenosine diphosphate were determined in bioptic specimen. The use of only 15 Hertz as a stimulation frequency led to a transformation of an originally fast-twitch muscle into a slow-twitch muscle with reduced susceptibility to fatigue. These results indicate a potential role of the skeletal muscle as an ideal myocardial substitute with the ability to perform hemodynamic work.
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PMID:[Biochemical changes in skeletal muscles after chronic indirect stimulation]. 260 58

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


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