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

The influence of delta sleep-inducing peptide (DSIP) on sleep was studied in 16 chronic insomniac patients according to a double-blind matched-pairs parallel-groups design. Subjects slept for 5 consecutive nights in the laboratory. Night 1 was used for adaptation, night 2 for baseline measurements. In the afternoon before the 3rd, 4th and 5th night, half of the patients received intravenously 25 nmol/kg body weight DSIP, and half of the patients a glucose solution (placebo). Measures for sleep structure, objective (polysomnography) and subjective sleep quality and for subjective tiredness were assessed. The results for objective sleep quality indicated higher sleep efficiency and shorter sleep latency with DSIP as compared to placebo. One measure of subjectively estimated tiredness decreased within the DSIP group. Data analysis suggested, however, that the statistically significant effects were weak and in part could be due to an incidental change in the placebo group. As none of the other measures, including subjective sleep quality, showed any change, it was concluded that short-term treatment of chronic insomnia with DSIP is not likely to be of major therapeutic benefit.
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PMID:Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients. A double-blind study. 129 94

The clinical and biochemical manifestations of secondary adrenocortical insufficiency are not well defined in the medical literature. This study was designed to determine the clinical and laboratory features suggesting the diagnosis of adrenal insufficiency in 15 chronic ACTH deficiency patients during low and normal cortisol states. Except for fatigue and weakness, the characteristic clinical manifestations of primary adrenal insufficiency occurred rarely. ACTH deficiency did not significantly modify blood glucose, serum calcium, sodium, potassium and differential white blood cell count. However, serum T4 was lower (65 +/- 19 vs 95 +/- 21 nmol/l, p less than 0.001) during cortisol deficiency, while T3 was higher (2.4 +/- 0.67 vs 2.0 +/- 0.60 nmol/l, p less than 0.001). Furthermore, rT3 decreased significantly during hypocorticism (0.27 +/- 0.07 vs 0.18 +/- 0.07 nmol/l, p less than 0.001). The T4/T3 ratio was significantly lower than the normal in 15 out of the 17 episodes of ACTH deficiency (29 +/- 12.5 vs 57 +/- 9.4, p less than 0.0001). We conclude that the increase in T3 and decrease in T4 levels are associated with chronic secondary adrenocortical insufficiency. This laboratory feature could be due, at least in part, to the increased peripheral conversion of T4 to T3 during cortisol deficiency.
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PMID:Increase in T3 levels during hypocorticism in patients with chronic secondary adrenocortical insufficiency. 131 31

The burnout syndrome denotes a constellation of physical fatigue, emotional exhaustion, and cognitive weariness resulting from chronic stress. Although it overlaps considerably with chronic fatigue as defined in internal medicine, its links with physical illness have not been systematically investigated. This exploratory study, conducted among 104 male workers free from cardiovascular disease (CVD), tested the association between burnout and two of its common concomitants--tension and listlessness--and cardiovascular risk factors. After ruling out five possible confounders (age, relative weight, smoking, alcohol use, and sports activity), the authors found that scores on burnout plus tension (tense-burnout) were associated with somatic complaints, cholesterol, glucose, triglycerides, uric acid, and, marginally, with ECG abnormalities. Workers scoring high on tense-burnout also had a significantly higher low density lipoprotein (LDL) level. Conversely, scores on burnout plus listlessness were significantly associated with glucose and negatively with diastolic blood pressure. The findings warrant further study of burnout as a predictor of cardiovascular morbidity and mortality.
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PMID:Burnout and risk factors for cardiovascular diseases. 139 14

Ingestion of approximately 30-60 g of carbohydrate during each hour of exercise will generally be sufficient to maintain blood glucose oxidation late in exercise and delay fatigue. Since the average rates of gastric emptying and intestinal absorption exceed 1,250 ml.h-1 for water and solutions containing up to 8% carbohydrate, exercising people can be supplemented with both carbohydrate and fluids at relatively high rates. When cyclists exercise at competitive intensities for 2 h in the heat with a sweat rate of 1,400 ml.h-1, it is clear that the closer that fluid consumption matches sweating rate (at least up to 80% of sweating rate), the better. Increasing dehydration, due to inadequate fluid consumption, directly impairs stroke volume, cardiac output, and skin blood flow, which results in larger increases in body core temperature, heart rate, and ratings of the difficulty of exercise. This same phenomenon probably also applies to running, which argues against the notion that a certain amount of dehydration (i.e., up to 3%) is permissible and without major cardiovascular consequences. However, runners generally drink only 500 ml.h-1 of fluid and thus allow themselves to dehydrate at rates of 500-1,000 ml.h-1. The performance question boils down to "Will the time lost as a result of drinking larger volumes be compensated by the physiological benefits drinking produces and the faster running pace that might be achieved during the last half of the race?" However, if the goal is safety, which means minimizing hyperthermia, there is no question that the closer that the rate of drinking can match the rate of dehydration, the better.
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PMID:Benefits of fluid replacement with carbohydrate during exercise. 140 5

1) Ingesting CHO during prolonged, moderate-intensity (60-85% VO2max) exercise can improve performance by maintaining plasma glucose availability and oxidation during the later stages of exercise. 2) Plasma glucose may be oxidized at rates in excess of 1 g.min-1 late in exercise. Athletes therefore need to ingest sufficient quantities of CHO in order to meet this demand. This can be accomplished by ingesting CHO at 40-75 g.h-1 throughout exercise or by ingesting approximately 200 g of CHO late in exercise. Ingesting CHO after fatigue has already occurred, however, is generally ineffective in restoring and maintaining plasma glucose availability, CHO oxidation, and/or exercise tolerance. 3) No apparent differences exist between glucose, sucrose, or maltodextrins in their ability to improve performance. Ingesting fructose during exercise, however, does not improve performance and may cause gastrointestinal distress. 4) The form of CHO (i.e., solid vs liquid) ingested during exercise is unlikely to be important provided that sufficient water is also consumed when ingesting CHO in solid form. 5) Ingesting 50-200 g of CHO 30-60 min before exercise results in transient hypoglycemia early in exercise, but this does not affect the rate of muscle glycogen utilization or, in most people, cause overt symptoms of neuroglucopenia. Whether performance is impaired, unaffected, or enhanced by such pre-exercise CHO feedings remains equivocal. 6) Ingesting 200-350 g of CHO 3-6 h before exercise appears to improve performance, possibly by maximizing muscle and/or liver glycogen stores or by supplying CHO from the small intestine during exercise itself.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nutritional manipulations before and during endurance exercise: effects on performance. 140 6

A 44-year-old female with 16-year history of rheumatoid arthritis visited Akiru Hospital with complaints of a thirst, a dry mouth and a general fatigue. One week prior to admission, the patient manifested excessive thirsty feeling, a body weight loss and a sleepless by the polyuria. She has been given 5-10 mg of prednisolone and 240 mg of lobenzarit disodium (CCA) in a day for 11 months. A hematologic examination showed no abnormality, and the examination of her serum showed the following values: BUN, 9.3 mg/dl; creatinine, 0.9 mg/dl; sodium, 139 mEq/l; chloride, 102 mEq/l; potassium, 3.9 mEq/l; osmolality, 290 mOsm/l. Plasma antidiuretic hormone (ADH) level increased slightly (6.0 pg/ml). Examination of her urine revealed specific gravity, 1.005; no trace of glucose, protein, blood and ketones; normal sediment; and osmolality, 209 mOsm/l. The patient was given exogenous ADH (10 units of vasopressin tannate in oil, intramuscularly) to obtain a diagnosis, and she was found to be unable to concentrate her urine more than 1.008 in the specific gravity. A water restriction, as a test for diabetes insipidus, also failed to concentrate her urine in the specific gravity and in the osmolality. Together with these findings, the patient was diagnosed to be a diabetes insipidus, and CCA was seemed to account for the disease. This unfavorable effect of CCA appeared to be reversible, since the patient recovered her urinary concentrating ability after the medication of CCA was discontinued.
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PMID:[Lobenzarit disodium (CCA)--induced diabetes insipidus in a patient with rheumatoid arthritis]. 141 95

A 40-year-old white woman presented with hirsutism, amenorrhea, generalized fatigue, diffuse weight gain, acral changes, and coarsened facial features. Physical examination revealed mild diastolic hypertension, acromegalic features, hirsutism, and seborrhea. The growth hormone concentration was elevated and did not suppress after glucose administration. Urinary free cortisol excretion was increased and was not suppressed during a 2 mg low-dose dexamethasone suppression test. Magnetic resonance imaging of the sella demonstrated a 1.3 x 1.2 x 0.8 cm pituitary adenoma. Trans-sphenoidal resection was performed, and portions of the resected tumor were analyzed by routine pathologic methods. Histopathologic and immunohistochemical findings indicated discrete growth hormone- and adrenocorticotropic hormone-producing pituitary adenomas. Coexisting acromegaly and Cushing's syndrome due to pituitary neoplasia was previously reported in two patients. However, to the authors' knowledge, this represents the first description of a patient with acromegaly and Cushing's disease resulting from discrete synchronous adenomas of the pituitary gland as defined by modern histopathologic techniques.
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PMID:Case report: acromegaly and Cushing's disease in a patient with synchronous pituitary adenomas. 144 69

Experimental therapies for McArdle's disease have been directed toward increasing substrate availability to exercising muscle. Such therapies to date have proven largely unsuccessful. These include administration of isoproterenol to increase blood flow, glucagon treatment to elevate serum glucose and increased dietary fat intake. Each of these therapies also results in greater levels of unesterified fatty acids in blood. More recently, a high protein diet is suggested to provide increased amounts of amino acids which would be available as fuel sources. We hypothesize that the absence of myophosphorylase in McArdle's disease creates an imbalance between the enzymes of the redox systems that control the generation, propagation and inactivation of free radicals. This occurs because muscle cells are forced to rely more heavily on fatty acid oxidation. The resulting free radical damage to cellular components disrupts metabolic control and increases the permeability of membranes. Elevated levels of Ca2+ in the sarcoplasm activate proteases, phospholipases and other catabolic enzymes initiating muscle fatigue and cramping. Lipid peroxidation is a consequence of normal muscle activity and may occur unchecked in individuals with McArdle's disease. Continued muscle activity in the absence of a favorable nutritional environment may promote the progression of the disease by increasing susceptibility to oxidative stress.
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PMID:The role of lipid peroxidation in McArdle's disease: applications for treatment of other myopathies. 146 Nov 77

The development of fatigue was investigated by electrical stimulation in 15 domestic pigs (1 yr old, 70-90 kg body weight) and seven adult dogs (3 yr old, 45 kg body weight). After anaesthesia, silver electrodes were implanted in the anterior and posterior parts of the right masseter muscles. The contralateral muscle was used as control. The bite force was measured. Muscle biopsies were obtained from the anterior, central and posterior parts, and were immediately frozen in liquid nitrogen. A fluorometrical analysis by enzymatic methods for glycogen, glucose, creatine phosphate, NAD, NADH, lactate and pyruvate was made. Blood flow was measured by 133Xe wash-out; oxygen consumption was monitored with an oxygen electrode. The porcine masseter was continuously stimulated for 60 min (100 V, 4 Hz and 2 ms). The canine masseter was intermittently stimulated (100 V, 20 Hz and 2 ms). The contraction was repeated four times, with a 10-min rest between. The porcine masseter could sustain longer endurance times than the canine masseter, which was easily fatigued. A marked substrate depletion was evident. The precontractional contents of glycogen, glucose and creatine phosphate were reduced. Lactate accumulation was evident (2-4 times more in the porcine and 4-8 times more in the canine masseter). The NADH concentration increased and the NAD content decreased. Blood-flow impairment (80% reduction in the dog, 60% in the pig) was observed. After the contraction phase, there was a hyperaemia (58% elevation of blood flow in the pig masseter, 45% in the canine). The oxygen tension followed in magnitude and time the blood-flow changes. These circulatory variables returned to normal after recovery. The high degree of substrate depletion, blood-flow impairment and a simultaneous decrease in oxygen transport to the contracted muscle, in combination with a prominent lactate accumulation, may induce a decrease in bite-force production.
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PMID:Bite-force development, metabolic and circulatory response to electrical stimulation in the canine and porcine masseter muscles. 147 60

Brain serotonin (5-hydroxytryptamine, 5-HT) has been suggested to be involved in central fatigue during prolonged exercise. Changes in the ratio of plasma free tryptophan (free Trp) to branched-chain amino acids (BCAA) are associated with altered brain 5-HT synthesis. The purposes of this study were to describe systematically the effects of prolonged exercise on changes in plasma free Trp and BCAA and to examine the effects of carbohydrate (CHO) feedings on these same variables. Eight well-trained men [VO2max = 57.8 (SE 4.1) ml kg-1 min-1] cycled for up to 255 min at a power output corresponding to VO2 at lactate threshold (approximately 68% VO2max) on three occasions separated by at least 1 week. Subjects drank 5 ml kg-1 body wt-1 of either a water placebo, or a liquid beverage containing a moderate (6% CHO) or high (12% CHO) concentration of carbohydrate beginning at min 14 of exercise and every 30 min thereafter. Exercise time to fatigue was shorter in subjects receiving placebo [190 (SE 4) min] as compared to 6% CHO [235 (SE 10) min] and 12% CHO [234 (SE 9) min] (P < 0.05). Glucose and insulin decreased in the placebo group, and free Trp, free-Trp/BCAA, and free fatty acids increased approximately five- to sevenfold (P < 0.05). These changes were attenuated in a dose-related manner by the carbohydrate drinks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of carbohydrate feedings on plasma free tryptophan and branched-chain amino acids during prolonged cycling. 148 39


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