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)

In order to find out how short-time denutrition changes the concentration of some substances in the rumen fluid and the blood, tests with full-grown sheep were carried out. Fodder was withheld from sheep with inserted Jarrett fistulae for 48 hours after normal feeding. After 48 hours the animals were given concentrated fodder, after 52 hours exclusively hay. From the 72nd hour onwards the animals were provided with fodder as usual. Samples of the rumen fluid and blood samples were taken at the beginning of the test, after the last normal feeding and then in the 24th, 32nd, 48th, 52nd, 56th, 72nd and 96th hour. We could find out that, during the 48-hour denutrition, the pH-value of the rumen fluid turned alkaline and the concentrations of ammonia, volatile fatty acids and lactic acid decreased. The protein metabolism underwent a rapid change in the organism. The protein content of the blood plasma decreased, above all the albumin content, as well as the concentration of glycoproteins and volatile amino acids. Among the various amino acids, the concentration of glycine increased highly, that of alanine and valine just slightly. The concentration of most amino acids decreased or--of some of them remained the same. Among the paramters that are characteristic of lipid and carbohydrate metabolism, the total content of lipids and cholesterin decreased, and so did the concentration of blood sugar, lactic acid and pyruvic acid in the blood plasma. The results indicate that short-time denutrition has a considerable influence on the rumen fermentation and the intermediary metabolism of ruminants. The quickly arising lack of energy of ruminants slows down the protein synthesis and increases the glyconeogenesis from amino acids. The tissue is supplied with energy by the mobilisation of lipids.
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PMID:[Effect of food deprivation on various parameters of rumen juice and blood of sheep]. 3 36

Nineteen patients, each hospitalized with a major depressive episode, were deprived of sleep for one night. Ten patients responded with clear improvement in depressive symptoms; the substantial clinical change was transient, usually lasting one day. Those who responded had significantly higher initial depression ratings (P less than .01) and tended to be older than nonresponders who experienced mild increases in irritability, fatigue, and discomfort following sleep deprivation. Amine metabolites, 5-hydroxyindoleacetic acid (5HIAA), and homovanillic acid (HVA) were not substantially affected by sleep deprivation, although there was a significant interaction of clinical response and direction of 3-methoxy-4-hydroxyphenylglycol (MHPG) change. Sleep deprivation thus produces acute, but only transient improvement in a selected group of severely depressed patients; it appears to be an important tool in the study of the affective disorders.
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PMID:Effects of sleep deprivation on mood and central amine metabolism in depressed patients. 126 78

Adenine nucleotide (AN) degradation has been shown to occur during intense exercise in the horse and in man, at or close to the point of fatigue. The aim of the study was to compare the concentrations of muscle inosine 5'-monophosphate (IMP) and plasma ammonia (NH3) during intense exercise with the concentrations of muscle and blood lactate. Seven trained thoroughbred horses were used in the study. Each exercised on a treadmill for periods of between 30 s and 150 s, at 11 and/or 12 m.s-1. Blood and muscle samples were taken and analysed for lactate and NH3 and adenosine 5'-triphosphate (ATP), phosphorylcreatine (PCr), IMP, creatine, lactate and glycerol-3-phosphate respectively. Horses showed varying degrees of AN degradation as indicated by plasma [NH3] and muscle [ATP] and [IMP]. Comparisons of [IMP] with muscle [lactate], and plasma [NH3] with that of blood [lactate] indicated a threshold to the start of AN degradation. This threshold corresponded to a lactate content of around 80 mmol.kg-1 dry muscle and 15 mmol.l-1 in blood. We discuss the mechanisms which have been proposed to account for AN degradation and suggest that IMP formation occurs as a result of a sudden rise in the concentration of adenosine 5'-diphosphate (ADP) and consequently the concentration of adenosine 5'-monophosphate. The data suggest a critical pH below which there may be a substantial reduction in the kinetics of ADP rephosphorylation provided by PCr resulting in an increase in [ADP], which is the stimulus to AN degradation during intense exercise.
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PMID:Adenine nucleotide degradation in the thoroughbred horse with increasing exercise duration. 139 58

Recent investigations from our and other laboratories indicate that glycogen is a carbon-chain precursor in muscle for the synthesis of TCA cycle intermediates and glutamine. During intense exercise and in conditions of a relative lack of energy (hypoxia, trauma, sepsis) the metabolism of branched-chain amino acids (BCAA) is accelerated in muscle. In the primary BCAA aminotransferase reaction 2-oxoglutarate is used as amino-group acceptor (putting a carbon-drain on the TCA cycle) under formation of glutamate. Glutamate will subsequently react with ammonia, generated in the AMP deaminase reaction or by deamination of amino acids, under formation of glutamine in a reaction catalysed by glutamine synthetase (glutamate + ammonia + ATP--> glutamine + ADP). Muscle glycogen stores may be smaller or less available at high altitude. It is hypothesized that this will lead to premature fatigue (due to both a lack of fuel and of TCA cycle carbon-precursor) and to a reduction in the synthesis rate of glutamine. A chronic reduction in the synthesis rate of glutamine during a long term stay at high altitude on its turn may lead to gut atrophy, bacterial translocation, endotoxemia, muscle protein catabolism and a weakened immune status.
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PMID:Amino acid metabolism, muscular fatigue and muscle wasting. Speculations on adaptations at high altitude. 148 45

We studied plasma ammonia and exercise tolerance in six patients with McArdle's disease (myophosphorylase deficiency, type V glycogenosis) during incremental cycle ergometry. Tests were performed either in the postabsorptive state or after supplementation with branched-chain amino and 2-oxoacids and glucose. Glucose and branched-chain 2-oxoacid combined increased total work performed from control 49 +/- 22 to 80 +/- 36 kJ (P less than 0.05). Glucose alone also improved total work performed from 49 +/- 22 to 64 +/- 33 kJ (P less than 0.05). Branched-chain 2-oxoacids alone had a variable effect, and branched-chain amino acids were of no benefit. Correlations between plasma ammonia and heart rate for individual patients were r = 0.99, P less than 0.01; r = 0.95, P less than 0.01; r = 0.84, P less than 0.01; r = 0.76, P less than 0.01; r = 0.73, P less than 0.01; and r = 0.63, P less than 0.05 and between ammonia and perceived exertion for all patients combined was r = 0.70, P less than 0.0001. In two patients, correlation of ammonia with heart rate at a power output of 60 W was r = 0.91, P less than 0.001 and at 40 W was r = 0.77, P less than 0.001. We conclude that ammonia is either a mediator or a marker of the metabolic events leading to fatigue.
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PMID:Relationship between ammonia, heart rate, and exertion in McArdle's disease. 153 42

The relationship between elevated plasma ammonia (NH3) levels, fatigue development and muscle metabolism were examined in horses during a submaximal fatigue test. Eight Quarter Horse mares were intravenously infused prior to exercise with either sodium acetate (control) or ammonium acetate (AMINF), and exercised to fatigue on an 11% grade treadmill, carrying 27 kg of lead. Time to fatigue was not different (P greater than 0.05) between groups. Intramuscular NH3 and lactate increased (P less than 0.001) during exercise; however, the treatment did not (P greater than 0.05) affect either. A treatment by exercise interaction (P less than 0.01) occurred for plasma NH3. The reciprocal relationship between changes in plasma and intramuscular alanine (ala) and glutamate (glu) indicated activation of the glucose-alanine cycle. Plasma glutamine (gln) increased (P less than 0.001) during exercise; however intramuscular gln was not (P greater than 0.05) altered. The excretion of urea-N was depressed as a result of exercise while the orotic acid/creatinine ratio did not (P greater than 0.05) change. The amino acids and urinary metabolites were not (P greater than 0.05) affected by treatment. These results did not show any metabolic evidence for a role of increased plasma NH3 levels in fatigue development. However this study did provide insight into other aspects of nitrogen metabolism during exercise in the horse.
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PMID:Metabolic responses to ammonium acetate infusion in exercising horses. 168 73

Six thoroughbred horses exercised on a motorised treadmill on two separate occasions at a speed of 11 or 12 m.s-1 for up to 2 min. 4 h prior to exercise each horse was given a 21 test solution of sodium bicarbonate (NaHCO3; 0.6 g.kg-1 body mass) or a control solution of water by nasogastric intubation, the order of administration of the two solutions was randomised. Blood samples (n = 15) were obtained before and during the 4 h after intubation, during exercise and for 30 min after exercise. NaHCO3 ingestion resulted in changes in pre-exercise acid-base status. The changes in blood lactate and base excess with exercise were greater after NaHCO3 administration; after 1 min of exercise in the case of lactate (P less than 0.05) and immediately after exercise in the case of base excess (P less than 0.05). Plasma ammonia levels were lower during (P less than 0.05) and immediately after (P less than 0.05) exercise following NaHCO3 ingestion. The peak change in plasma ammonia with exercise was also lower after NaHCO3 ingestion (P less than 0.05). Following exercise after NaHCO3 ingestion, five horses demonstrated lower muscle adenosine 5-triphosphate loss (P less than 0.05) and inosine 5-monophosphate formation (P = 0.05) and higher glycerol 3-phosphate formation (P less than 0.05). There is evidence to suggest that metabolic alkalosis may delay the onset of fatigue by decreasing the extent of adenine nucleotide loss during high-intensity exercise.
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PMID:The influence of metabolic alkalosis upon exercise metabolism in the thoroughbred horse. 174 3

Subjective symptoms and exposure to organic compounds were recorded in road repair and construction workers. Abnormal fatigue, reduced appetite, laryngeal/pharyngeal irritation, and eye irritation were recorded more often in such workers handling asphalt than in a corresponding reference group without asphalt exposure. Mean daily exposure to volatile compounds was only occasionally above 1 ppm. Mean exposure to asphalt fume was 0.358 mg/m3. There was no correlation between symptoms and total amount of volatile compounds, but a significant positive correlation was demonstrated between symptoms and some substances. The highest correlation was found for 1, 2, 4 trimethyl benzene. Symptoms increased with increasing asphalt temperature and with increasing concentrations of asphalt fumes. Amine addition did not increase the sum of symptoms, but soft asphalt seems to result in fewer symptoms than the harder types. Symptoms were not related to external factors like weather, traffic density, or specific working operations. As preventive measures, asphalt temperature should be kept below 150 degrees C, fume concentrations below 0.40 mg/m3, and if possible, the use of harder asphalt types which also require high temperatures should be avoided.
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PMID:Acute effects and exposure to organic compounds in road maintenance workers exposed to asphalt. 180 11

An experimental evaluation of citrulline malate (Stimol, CAS 54940-97-5), an anti-fatigue compound, was undertaken in man and in the animal in order to study the pharmacological activity of the substance at hepatic and renal level. In man, the protocol involved a double-blind randomized, placebo-controlled cross-over technique. The study in the animal was blind and placebo-controlled with two randomized parallel groups. Results showed that citrulline malate stimulates hepatic ureogenesis and favorizes the renal reabsorption of bicarbonates. These metabolic actions had a protective effect against acidosis and ammonia poisoning and explain the anti-fatigue properties of citrulline malate in man.
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PMID:Activity of citrulline malate on acid-base balance and blood ammonia and amino acid levels. Study in the animal and in man. 193 Mar 58

Dietary measures have achieved mixed results in the management of liver disorders. Although a high energy diet may shorten the course of viral hepatitis by a relatively small amount, dietary restriction is usually of no benefit in compensated cirrhosis. Restriction of sodium intake to 22 to 60 mol/day leads to resolution of cirrhotic ascites in approximately 20% of patients, and reduces the requirement for diuretics in the remainder. In advanced liver disease, diet plays an important role in the avoidance of portal-systemic encephalopathy (PSE), with the tolerance of most nutrients, most importantly protein, being sharply reduced. Despite the frequent presence of carbohydrate intolerance in liver disease, carbohydrate supplementation may be required to ensure adequate utilisation of the reduced dietary protein intake. Zinc supplementation may also be required in liver cirrhosis to compensate for a deficiency. Bed rest is an important component of the management of acute and chronic liver disorders, together with the avoidance of fatigue. Abstinence from alcohol is required in alcoholic liver disease patients, who should receive parenteral thiamine 100 mg and other vitamin and mineral supplementation as required. Agents acting on the ascending loop of Henle [such as furosemide (frusemide)] or the distal tubule (such as spironolactone) are the diuretics most frequently employed to mobilise ascites in cirrhosis, the latter drug being the more effective in nonazotaemic patients. In the absence of oedema, the diuresis should be restricted to a maximum of 750 ml/day; however, patients with oedema may safely undergo a diuresis of less than or equal to 1.5 L/day. Diuretic therapy is often associated with renal complications, such as azotaemia (usually reversible) and severe hyponatraemia in cirrhotic patients with ascites; spironolactone may produce antiandrogenic adverse effects. Lactulose, used in the treatment of acute and chronic PSE, acts by inhibiting gastrointestinal absorption of ammonia and other toxic nitrogenous substances, and by reducing urea degradation. Other pharmacological treatments, such as branched-chain amino acids and benzodiazepine antagonists have a limited role in the management of PSE. Chronic cholestasis has been treated with cholestyramine and fat-soluble vitamins, whereas ursodeoxycholic acid appears to be a promising agent in the treatment of primary biliary cirrhosis. In chronic hepatitis, the prevention of development of cirrhosis is a primary treatment goal which has been attempted with variable success using antifibrotic drugs such as penicillamine and colchicine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Traditional management of liver disorders. 208 80


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