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

Within the last 10 years the indications for a therapeutic regimen with beta-blocking-agents have been differentiated: coronary heart disease with angina pectoris (interval regimen), essential hypertension, especially in younger persons; hyperkinetic heart syndrome; thyreotoxikosis, symptomatic therapy; heart rhythm disorders, extrasystolic or tachysystolic; neurologic-psychiatric diseases. The development of the newer beta-blocking-agents has effected different kinetic data (f.i. long acting effects of Tenormin) and a increased cardioselectivity. The recommendations for the therapeutic regimen have to be outlined to the underlying diseases. The sensitivity against the drugs depends on remarkable individual differences, with the consequence of a careful and low dosage in the beginning in each case. The side-effects of beta-blocking-agents are presumably: bradycardia, bronchospasm, fatigue, adynamia, myocardial insufficiency, gastrointestinal symptoms, hypoglycemia, hypotension.
...
PMID:[Therapy with beta-blocking-agents (author's transl)]. 3 43

The EEG was recorded in 27 subjects during hangover. Male healthy volunteers drank 1.75 g/kg body weight of ethanol in 3 h and the EEG was recorded 14-16 h later when the degree of hangover was highest. For control purposes a second EEG was recorded after a similar session when subjects drank water instead of ethanol. A third record was taken in normal laboratory conditions. T5-A1 and O1-A1 derivations were subjected to computer analysis from which spectral and frequency parameters were calculated. Visual analysis of the EEG during hangover showed a decrease and slowing of alpha activity and an increase in theta activity. Spectral analysis of the EEG gave a statistically significant increase in 7-8 c/sec activity during hangover. The EEG change could not be explained in terms of blood alcohol level, hypoglycaemia or acidosis. Also fatigue could be excluded as a cause of EEG change by means of "water controls". The conclusion is that the slowing of the EEG during hangover is caused by the depressant action of ethanol, or its metabolites, on cortical function.
...
PMID:Electroencephalographic changes during experimental hangover. 5 42

A 3-yr-old boy was investigated for numerous episodes of fatigue, irritability, pallor, and sweating, which began at 11 mo of age, when he had an episode of symptomatic hypoglycemia with ketonuria. He had euphoria, mental confusion, drowsiness, nausea, and vomiting 1-5 hr after oral administration of glycerol in doses of 0.5-1.0gm/kg. Orally administered MCT (1 gm/kg) had similar effects. On one occasion, oral glycerol also provoked hypoglycemia, as had a 16 1/2 hr fast. Intravenously administered glycerol (0.09 gm/kg) induced an immediate loss of consciousness from which he recovered spontaneously after 30 min; there were no changes in blood glucose values. Intravenously administered fructose (0.25 gm/kg) was tolerated normally. Leukocytes showed normal activities for FDPase, glycerol kinase, and glycerol phosphate dehydrogenase. The restriction of dietary intake of fat has been associated with a marked improvement in physical and mental activities. These observations suggest a unique, yet undifined intolerance to glycerol, which suggest caution in the diagnostic use of glycerol in the investigation of hypoglycemia as well as in the therapy of increased intracranial or intraocular pressure.
...
PMID:Glycerol intolerance in a child with intermittent hypoglycemia. 16 54

A new method for the psychological and physical selection of aircrew is described. Data from the literature are cited in support of the proposition that, in muscular work tests, the response of the body to fatigue cannot only be measured by means of the usual spirometric and ECG methods, but also via the plasma cortisol, ACTH and STH response. It is shown that changes in the concentration of these hormones are mainly attributable to fatigue and its accompanying hypoglycaemia. Hitherto overlooked due to the lack of standardisation of its methods, endocrinological examination could, it is suggested, be of considerable assistance in the selection of aircrew, in the interests of greater safety in the air.
...
PMID:[Behavior of plasma cortisol, ACTH and STH in subjects performing controlled work on the bicycle ergometer]. 21 42

The purpose of this study was to determine the influence of diurnal variations of muscle and liver glycogen stores on exercise endurance in male albino rats. Animals were swum to exhaustion at either 0700 or 1900 h, after which samples of soleus, white vastus lateralis, and red vastus lateralis muscles as well as liver were excised and subsequently analyzed for glycogen content. Glycogen content of all tissues from nonexercising control animals was higher in the morning than in the evening. Consequently, animals at 0700 h swam 60% longer than those at 1900 h (209 +/- 20 min vs. 130 +/- 23 min, respectively). However, because the skeletal tissues of the exhausted animals were not totally depleted of glycogen, it was concluded that fatigue under the swim protocol was the result of hypoglycemia secondary to hepatic glycogen depletion. The results of this study demonstrate the physiological consequences of diurnal glycogen fluctuation and establish experimental support for the importance of controlling this variable in rodent exercise investigations.
...
PMID:Muscle and liver glycogen content: diurnal variation and endurance. 57 22

Reactive hypoglycemia was documented in ten postgastrectomy patients by a control oral glucose tolerance test (OGTT). Nine patients experienced nausea, flushing, and fatigue during the first hour of the test. Neuroglycopenic or adrenergic symptoms of hypoglycemia occurred in eight patients two to five hours after oral glucose. The oral administration of phenylephrine elixir, 15 mg., thirty minutes before a repeat OGTT, significantly raised thelowest plasma glucose from 37.5 +/- 2.8 mg./dl. to 45.2 +/- 3.8 mg./dl. (p less than 0.05) but did not affect the occurrence of either the early or the late symptoms. In contrast, propranolol, 10 mg., raised the lowest plasma glucose from 37.5 +/- 2.8 mg./dl. to 57 +/- 5.2 mg./dl. (p less than 0.02) and prevented the occurrence of early and late symptoms. Neither peak nor total plasma insulin levels were affected by either drug. The rate of glucose utilization, as determined by intravenous glucose tolerance tests, did not significantly change after the oral administration of either drug. It is concluded that propranolol ameliorated the symptoms and chemical hypoglycemia after oral glucose and merits more detailed study as a long-term therapy for this disorder.
...
PMID:Effect of adrenergic agents on postgastrectomy hypoglycemia. 118 31

There are at least 5 metabolic causes of fatigue, a decrease in the phosphocreatine level in muscle, proton accumulation in muscle, depletion of the glycogen store in muscle, hypoglycaemia and an increase in the plasma concentration ratio of free tryptophan/branched-chain amino acids. Proton accumulation may be a common cause of fatigue in most forms of exercise and may be an important factor in fatigue in those persons who are chronically physically inactive and also in the elderly: thus, the aerobic capacity markedly decreases under these conditions, so that ATP must be synthesized by the much less efficient anaerobic system. A marked increase in the plasma fatty acid level, which may occur when liver glycogen store is depleted and when hypoglycaemia results, or during intermittent exercise when the rate of fatty acid oxidation may not match the mobilisation of fatty acids, could be involved indirectly in fatigue. This is because such an increase in the plasma level of fatty acids raises the free plasma concentration of tryptophan, which can increase the entry of tryptophan into the brain, which will increase the brain level of 5-hydroxytryptamine: there is evidence that the latter may be involved in central fatigue. In this case, provision of branched-chain amino acids in order to maintain the resting plasma concentration ratio of free tryptophan/branched-chain amino acids should delay fatigue--there is prima facie evidence in support of this hypothesis. This hypothesis may have considerable clinical importance.
...
PMID:Physical and mental fatigue: metabolic mechanisms and importance of plasma amino acids. 136 Mar 9

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)
...
PMID:Nutritional manipulations before and during endurance exercise: effects on performance. 140 6

One of the most important nutritional goals amongst athletes is to maintain adequate energy and fluid balance, since these are subject to relatively rapid changes and are directly related to performance and health. This may especially be the case when exercise intensity is high. Furthermore, when due to exercise and environmental stress food and fluid intake become depressed. In such conditions there may be a dramatic increase in the utilization of carbohydrate (CHO), fluid, and in some instances protein. These increased requirements may then not be covered. Insufficient replacement of CHO may lead to hypoglycemia, altered protein metabolism, central fatigue and exhaustion. Large sweat losses may pose a risk to health by inducing severe dehydration, impaired blood circulation and heat transfer, leading to heat exhaustion and collapse. Inadequate CHO and protein intake leads to a negative nitrogen balance, which over the long term will lead to a loss of muscle mass. In the scope of this presentation we will refer to the most important nutritional factors which are known to affect performance over a short term, at sea level and altitude.
...
PMID:Nutritional aspects of health and performance at lowland and altitude. 148 43

Muscle glycogen and plasma glucose are oxidized by skeletal muscle to supply the carbohydrate energy needed to exercise strenuously for several hours (i.e., 70% maximal O2 consumption). With increasing exercise duration there is a progressive shift from muscle glycogen to blood glucose. Blood glucose concentration declines to hypoglycemic levels (i.e., 2.5 mmol/L) in well-trained cyclists after approximately h of exercise and this appears to cause muscle fatigue by reducing the contribution of blood glucose to oxidative metabolism. Carbohydrate feeding throughout exercise delays fatigue by 30-60 min, apparently by maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously. Carbohydrate feedings do not spare muscle glycogen utilization. Very little muscle glycogen is used for energy during the 3-4-h period of prolonged exercise when fed carbohydrate, suggesting that blood glucose is the predominant carbohydrate source. At this time, exogenous glucose disposal exceeds 1 g/min (i.e., 16 mg.kg-1.min-1) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mmol/L. However, at this time these cyclist cannot exercise more intensely than 74% of maximal O2 consumption, suggesting a limit to the rate at which blood glucose can be used for energy. It is important to realize that carbohydrate supplementation during exercise delays fatigue by 30-60 min, but does not prevent fatigue. In conclusion, fatigue during prolonged strenuous exercise is often due to inadequate carbohydrate oxidation. This is partly a result of hypoglycemia, which limits carbohydrate oxidation and causes muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Carbohydrate supplementation during exercise. 154 49


1 2 3 4 5 6 7 8 9 10 Next >>