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)

Nineteen bulimic women and 22 age-matched controls were randomly assigned to receive 25 g of glucose or a placebo injection under double-blind conditions. Blood samples of glucose, insulin, and glucagon, and psychometric assessments of mood and food cravings were obtained 10 min before, and 0, 5, 10, 20, 30, 45, and 60 min after injection. Blood levels of the large neutral amino acids (LNAAs) tryptophan, tyrosine, leucine, valine, phenylalanine, and leucine were determined at 10 min before and 60 min after the injection. Bulimic subjects were found to report more symptoms of distressed mood throughout the entire monitoring period than controls. Five minutes following glucose ingestion the self-reports of depression, fatigue, anxiety, and bewilderment rose to a level among the bulimic subjects that was above that at baseline, and was higher than that of bulimia nervosa (BN) subjects receiving placebo. No comparable change in mood was observed among controls. Blood glucose levels were correlated with mood in the bulimic group, but not in controls. In addition, the glucose injection induced a heightened urge to binge in the bulimic group (compared to placebo at 10 and 60 min), whereas reducing food cravings (for sweets) in the controls (at 5 min). When collapsed across time and injection condition, the blood glucose level of bulimics was lower than that of controls. There were no differences in insulin response between the groups. The bulimic group was found to have lower baseline levels of blood tryptophan, whereas no differences in the tryptophan/LNAA ratio were observed either at baseline or following glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A double-blind placebo-controlled glucose challenge in bulimia nervosa: psychological effects. 844 64

Six subjects performed isometric contraction (66% maximal force) to fatigue with the knee extensor muscles. Biopsies were taken from the quadriceps femoris muscle at rest, at fatigue and 1 min after termination of contraction. In three of the subjects recovery from contraction occurred in the presence of an intact circulation (non-occluded, NON) to the thigh, whereas in the other three the circulation during recovery was occluded (OCC). Glycogen synthase fractional activity (GSF) decreased in all subjects from (mean +/- SE) 0.53 +/- 0.06 at rest to 0.37 +/- 0.04 at fatigue (P < 0.001). In the OCC group GSF returned to the pre-exercise value within 1 min after termination of contraction (0.59 +/- 0.07 at rest vs. 0.57 +/- 0.04 at 1 min post-exercise), whereas in the NON group GSF increased to a higher extent (0.48 +/- 0.09 at rest vs. 0.70 +/- 0.06 at 1 min post-exercise). The increase in GSF during the 1-min recovery was almost three-fold higher in the NON group (0.15 +/- 0.02 vs. 0.38 +/- 0.03). Cyclic AMP-dependent protein kinase (cAMP-PK) (assayed at 0/100 microM and 0.2/100 microM cAMP) did not change at fatigue or during recovery in either group. Glycogen synthase phosphatase (GSP) increased at fatigue by approximately 30% (P < 0.05 vs. rest). It is concluded that isometric contraction mediated inactivation of GS (i.e. phosphorylation of GS) is due to activation of a protein kinase(s) but not cAMP-PK. The rapid activation of GS in the NON group demonstrates that a humoral factor(s), possibly insulin and/or oxygen, is responsible for this phenomenon.
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PMID:Regulation of glycogen synthase in human muscle during isometric contraction and recovery. 845 44

The chronic fatigue syndrome is poorly understood. We believe the underlying causes in many atopics and women are a persistent infection and hypersensitivity to the immune-suppressive effects of histamine and certain pathogens. We believe much to the symptomatology can be explained by all four types of hypersensitivity (Gell and Coombs classification) in reaction to a pathogen, electrolyte disturbances which include sometimes permanent changes in cell membranes' ability to pass electrolytes, sometimes permanent biochemical changes in mitochondrial function, and disturbances of insulin and T3-thyroid hormone functions. We also explain in detail what 'fatigue' means for these patients. We present evidence from the medical literature for the plausibility of our hypotheses.
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PMID:Chronic fatigue syndrome: influence of histamine, hormones and electrolytes. 845 68

The effect of carbohydrate (CHO) feedings on exercise-mediated changes in glycogen synthase fractional (GSF) activity has been investigated. Subjects cycled at approximately 70% of maximal oxygen uptake on two occasions: the first to fatigue (135 +/- 17 min; mean +/- SE) (control, CON), and the second at the same workload and duration as the first, but with the addition of frequent ingestion of CHO during exercise (0.27 g kg-1 body weight every 15 min). Biopsies were taken from the quadriceps femoris muscle before and immediately after exercise. Plasma glucose and insulin decreased during CON exercise, but remained elevated throughout CHO exercise (end of exercise: glucose = 4.4 +/- 0.2 mM CON vs. 5.8 +/- 0.2 CHO, P < 0.01; insulin = 9 +/- 1 uU ml-1 CON vs. 19 +/- 3 CHO, P < 0.05). Glycogen decreased to approximately 10% of the basal value during CON and to approximately 20% during CHO, and there was no significant difference in net glycogenolysis between treatments. GSF activity averaged 0.25 +/- 0.03 and 0.22 +/- 0.05 at rest, and increased to 0.51 +/- 0.08 and 0.48 +/- 0.09 after exercise in CON and CHO, respectively (P > 0.05 between treatments). It is concluded that under the present conditions CHO feedings do not alter the exercise-mediated changes in GSF activity. The increase in GSF during exercise is attributed at least in part to the decrease in muscle glycogen (which increases the suitability of GS as substrate for GS phosphatase).
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PMID:No effect of carbohydrate feeding on glycogen synthase in human muscle during exercise. 851 62

A 65-yr-old woman presented for evaluation of a pancreatic mass. She had been suffering from severe constitutional symptoms for 18 months; those symptoms included weight loss, increasing fatigue, night sweats, and recurrent fever attacks up to 40 degrees C. Later, bluish subcutaneous nodules developed on her lower limbs. Laboratory tests yielded signs of chronic inflammation and impaired glucose tolerance with elevated serum insulin and glucagon concentrations. Skin biopsy revealed lobular panniculitis. Ultrasonography and a CT scan demonstrated enlargement of the pancreas, and endoscopic retrograde pancreaticography disclosed displacement and stenosis of the main pancreatic duct. The patient was referred for explorative laparotomy, which was highly suggestive of a malignant pancreatic tumor. However, histological examination of the resected pancreatic and peripancreatic mass revealed tuberculous pancreatitis. This form of isolated tuberculous pancreatitis, associated with lobular panniculitis and laboratory features consistent with a tumor of the endocrine pancreas, has not been reported previously. Active tuberculosis should be a leading differential diagnosis in a patient with an enlarged pancreas when the usual diagnostic reasoning does not yield conclusive results.
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PMID:Isolated tuberculosis of the pancreas masquerading as a pancreatic mass. 854 May 23

Obesity is a particularly important challenge to the health status of Native Americans. This challenge is manifest in the increasing rates of non-insulin-dependent diabetes mellitus among Native Americans. Most studies of Native American infants, preschool children, schoolchildren, and adults have confirmed a high prevalence of overweight. Historical studies suggest that for many Native American communities the high rates of obesity are a relatively recent phenomenon. The specific reasons for the increase in obesity among Native Americans have not been determined, although it has been hypothesized that Native Americans have a genetic predisposition to overweight in a "westernized" environment of abundant food and decreased energy expenditure. Few detailed studies of diet or of physical activity levels of contemporary Native Americans have been published. Community-based interventions to modify diet and activity levels to prevent obesity in Native American communities are needed. Preliminary evidence from two formative school-based programs in the Southwest suggest that Native American communities are receptive to school-based interventions, and that such programs may be able to slow the rate of excess weight gain and to improve fitness in school children. Because of the cultural diversity among Native Americans, future studies should focus on collecting community- and region-specific data, and should emphasize the need for obesity prevention through culturally appropriate community- and school-based behavioral interventions.
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PMID:Toward comprehensive obesity prevention programs in Native American communities. 858 89

An increased extracellular K+ concentration ([K+]0) is thought to cause muscle fatigue. We studied the effects of increasing [K+]0 from 4mM to 8-14mM on tetanic contractions in isolated bundles of fibres and whole soleus muscles from the rat. Whereas there was little depression of force at a [K+]0 of 8-9mM, a further small increase in [K+]0 to 11-14mM resulted in a large reduction of force. Tetanus depression at 11mM [K+]0 was increased when using weaker stimulation pulses and decreased with stronger pulses. Whereas the tetanic force/resting membrane potential (EM) relation showed only moderate force depression with depolarization from -74 to -62mV, a large reduction of force occurred when EM fell to-53mV. The implications of these relations to fatigue are discussed. Partial inhibition of the Na+-K+ pump with ouabain (10(-6 )M) caused additional force loss at 11mM [K+]0. Salbutamol, insulin, or calcitonin gene-related peptide all stimulated the Na+-K+ pump in muscles exposed to 11mM [K+]0 and induced an average 26-33% recovery of tetanic force. When using stimulation pulses of 0.1ms, instead of the standard 1.0-ms pulses, force recovery with these agents was 41-44% which was significantly greater (P < 0.025). Only salbutamol caused any recovery of EM (1.3mV). The observations suggest that the increased Na+ concentration difference across the sarcolemma, following Na+-K+ pump stimulation, has an important role in restoring excitability and force.
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PMID:Relation between extracellular [K+], membrane potential and contraction in rat soleus muscle: modulation by the Na+-K+ pump. 859 43

The effect of chronic stress on tissue-type plasminogen activator (TPA) and plasminogen activator inhibitor-1 (PAI-1) antigens was studied in 69 healthy middle-aged men. Chronic stress, defined as feelings of fatigue, lack of energy, increased irritability, and demoralization, was positively associated with plasma concentrations of PAI-1 antigen but was unrelated to TPA. The association remained unaltered after controlling for age, smoking, alcohol consumption, and physical activity but became nonsignificant after further controlling for abdominal obesity, BMI, and serum insulin and triglyceride levels. This attenuated association implies that the relationship between vital exhaustion and PAI-1 may be secondary to the effects of the metabolic variables. Thus, the present study shows that long-term stress affects the fibrinolytic system and suggests that obesity and insulin and triglyceride concentrations, which are closely correlated with the fibrinolytic parameters, may mediate the association. These findings are consistent with the hypothesis that chronic stress causes increased synthesis of PAI-1, thus promoting the risk for atherothrombotic disease by decreasing the likelihood of spontaneous fibrinolysis and increasing the likelihood of fibrin deposition.
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PMID:Association of chronic stress with plasminogen activator inhibitor-1 in healthy middle-aged men. 863 Jun 60

Skeletal muscles in an animal model of genetic hypertension (the spontaneously hypertensive rat. SHR) exhibit significant deficits in contractile performance. These deficits appear to be unrelated to the rise in blood pressure. Slow-twitch soleus muscles show a decrease in specific muscle tension and a reduced resistance to muscle fatigue during prolonged contractile activity. We tested the hypothesis that the reduced fatigue resistance occurs as a consequence of an impaired ability to maintain or restore Na+ and K+ balance across the sarcolemma during repeated contractions. This may result from a genetically based increase in the Na+ permeability of SHR muscles, coupled with a reduction Na+, K+ pump capacity as the animals mature. Soleus muscles in adult SHR exhibit a significant increase in intracellular Na+ content and a significant decrease in intracellular K+ content at rest. B6RB+ uptake in Na(+)-loaded hypertensive muscles is 45% less than predicted from the number of ouabain-binding sites available. Activation of Na+, K+ pumps using adrenaline or insulin produces a significantly smaller hyperpolarization in hypertensive soleus than in control muscles. Control soleus muscles are hyperpolarized for at least 10 min after a 4 min period of high-frequency activity, but hypertensive soleus muscles remain at resting polarity. Nonetheless, the number of ouabain-binding sites in hypertensive muscle is significantly greater than in control soleus, and binding affinities are similar. This apparent deficit in pump capacity might lead to a greater and more prolonged increase in extracellular K+ during repetitive contractions,and an associated decline in tension. Recently, we have been able to prevent the abnormal decrease in hypertensive soleus fatigue resistance by long-term treatment (8 weeks) with the Ca2+ blocker amlodipine. The therapy prevented or reversed the contractile deficits, but did not restore the responsiveness of the Na+, K+ pump to hormonal stimulation. The current data suggest that both a reduction in Na+, K(+)-pump capacity and changes in Ca2+ distribution play a role in the development of contractile deficits in hypertensive muscles.
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PMID:Na+, K(+)-pump activity and skeletal muscle contractile deficits in the spontaneously hypertensive rat. 872 83

To examine the importance of blood-borne vs. neural mechanisms for hormonal responses and substrate mobilization during exercise, six spinal cord-injured tetraplegic (C5-T1) males (mean age: 35 yr, range: 24-55 yr) were recruited to perform involuntary, electrically induced cycling [functional electrical stimulation (FES)] to fatigue for 24.6 +/- 2.3 min (mean and SE), and heart rate rose from 67 +/- 7 (rest) to 107 +/- 5 (exercise) beats/min. Voluntary arm cranking in tetraplegics (ARM) and voluntary leg cycling in six matched, long-term immobilized (2-12 mo) males (Vol) served as control experiments. In FES, peripheral glucose uptake increased [12.4 +/- 1.1 (rest) to 19.5 +/- 4.3 (exercise) mumol.min-1.kg-1; P < 0.05], whereas hepatic glucose production did not change from basal values [12.4 +/- 1.4 (rest) vs. 13.0 +/- 3.4 (exercise) mumol.min-1.kg-1]. Accordingly, plasma glucose decreased [from 5.4 +/- 0.3 (rest) to 4.7 +/- 0.3 (exercise) mmol/l; P < 0.05]. Plasma glucose did not change in response to ARM or Vol. Plasma free fatty acids and beta-hydroxybutyrate decreased only in FES experiments (P < 0.05). During FES, increases in growth hormone (GH) and epinephrine and decreases in insulin concentrations were abolished. Although subnormal throughout the exercise period, norepinephrine concentrations increased during FES, and responses of heart rate, adrenocorticotropic hormone, beta-endorphin, renin, lactate, and potassium were marked. In conclusion, during exercise, activity in motor centers and afferent muscle nerves is important for normal responses of GH, catecholamines, insulin, glucose production, and lipolysis. Humoral feedback and spinal or simple autonomic nervous reflex mechanisms are not sufficient. However, such mechanisms are involved in redundant control of heart rate and neuroendocrine activity in exercise.
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PMID:Regulation of glucose turnover and hormonal responses during electrical cycling in tetraplegic humans. 876 Feb 20


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