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)

Top-level performances in endurance sports require several years of hard training loads. A major objective of this endurance training is to reach the most elevated metabolic adaptations the athlete will be able to support. As a consequence, overtraining is a recurrent problem that highly-trained athletes may experience during their career. Many studies have revealed that overtraining could be highlighted by various biochemical markers but a principal discrepancy in the diagnosis of overtraining stems from the fact that none of these markers may be considered as universal. In endurance sports, the metabolic aspects of training fatigue appear to be the most relevant parameters that may characterise overtraining when recovery is not sufficient, or when dietary habits do not allow an optimal replenishment of substrate stores. From the skeletal muscle functions to the overall energetic substrate availability during exercise, six metabolic schemes have been studied in relation to overtraining, each one related to a central parameter, i.e. carbohydrates, branched-chain amino acids, glutamine, polyunsaturated fatty acids, leptin, and proteins. We summarise the current knowledge on these metabolic hypotheses regarding the occurrence of overtraining in endurance sports.
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PMID:Biochemical aspects of overtraining in endurance sports: a review. 1239 46

During intense exercise there is an augmented production of ammonia and IMP in the exercised muscle that could be related to the establishment of peripheral fatigue. In order to prevent this accumulation, the urea cycle in the liver eliminates ammonia in the form of urea and the skeletal muscle buffers the increase of ammonia via transamination reactions. In the present study we evaluated the effect of arginine, citrulline and ornithine supplementation, intermediates of the urea cycle, on the performance of sedentary and swimming-trained rats submitted to a single bout of exhaustive exercise. We also measured the glycogen content of the soleus and gastrocnemius muscles and of the liver, as well as the plasma concentrations of ammonia, urea, glutamine, glucose and lactate. The results indicate that arginine, citrulline and ornithine supplementation increased the flux of substrate through the reaction catalysed by glutamine synthetase, leading to increased glutamine production after an exhaustive bout of exercise, and of the mechanism involved in ammonia buffering.
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PMID:Effect of arginine, ornithine and citrulline supplementation upon performance and metabolism of trained rats. 1257 27

Hughlings Jackson at the turn of the century defined epilepsy as a disorder originating in a "morbid nutrition" of the neuron. With the advances in modern neurochemistry, it is becoming increasingly clear that a chronic seizure predisposition or a lowering of the brain's discharge threshold can be demarcated by a number of biochemical markers. They include a tendency for an increased release of glutamate with or without GABAergic impairment, (intra)neural tissue alterations in water redistribution/osmolarity or other distortions of the cytoarchitecture, and an elevation of ionic calcium inside the cell. These changes are dominantly shared parameters of the seizure prone brain. Magnetic resonance spectroscopy (MRS) shows that cerebral levels of glutamate + glutamine (Glx) are increased interictally in epileptogenic regions in human partial epilepsy; other findings using this technique suggest damage to (cellular/mitochondrial) membranes, denoted by N-acetyl-aspartic acid (NAA) changes and a decreased energy capability. The merging of previous in vitro and ex vivo findings in neurophysiology and neurochemistry with magnetic resonance spectroscopy technology provides a powerful new methodology to interpret and to obtain clinical insight into the metabolic alterations that underlie an epileptogenic process. In this review some of these basic neurochemical and electrophysiological mechanisms are discussed. In addition, certain adjuncts to established antiepileptic drug therapy are suggested in the hope that over the long term they may help in correcting the primary metabolic deficits.
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PMID:Metabolic parameters of epilepsy: adjuncts to established antiepileptic drug therapy. 1260 9

Pesticides, such as parathion, are metabolized by cytochrome p-450 system to paraoxon, which is a potent cholinesterase inhibitor. Paraoxonase (PON) catalyzes the hydrolysis of these toxic metabolites and protects against pesticide toxicity. A glutamine/arginine (Gln/Arg) polymorphism at amino acid position 192 of PON has been described. The Arg/Arg genotype is associated with higher serum paraoxonase activity compared to Gln/Gln. The Arg/Gln genotype is associated with intermediate serum PON activity. The potential association between PON genotype and symptoms of chronic pesticide toxicity was examined among 100 farm workers. As part of a cross-sectional study of pesticide toxicity among mixed-race farm workers in the Western Cape. South Africa, 100 farm workers were genotyped for polymorphism of the paraoxonase gene at amino acid position 192. Subjects with two or more of the following symptoms were considered to have evidence of chronic toxicity: abdominal pain, nausea, rhinorrhea, dizziness, headache, somnolence, fatigue, gait disturbance, limb numbness, paresthesias, limb pain, or limb weakness. In multivariable logistic regression analysis, the independent predictors of chronic toxicity were previous history of head trauma resulting in loss of consciousness (OR 2.8, 95% CI = 1.7-6.7), having worked as a pesticide applicator (OR 5.4, 95% CI = 3.2-8.9), and having one of the two "slow metabolism" (Gln/Gln or Gln/Arg) genotypes (OR 2.9, 95% CI = 1.7-6.9). Furthermore, the prevalence of chronic toxicity increased in a stepwise fashion from 15% among pesticide nonapplicators with a "fast metabolism" (Arg/Arg) genotype, to 42.9% among pesticide nonapplicators with "slow metabolism" (Gln/Gln or Gln/Arg) genotypes, to 58.8% among pesticide applicators with "fast metabolism" genotype, and 75.0% among pesticide applicators with "slow metabolism" genotypes (P = 0.001). Age, number of years on the job, smoking history, alcohol history, education level, plasma or red blood cell cholinesterase level, or previous history of acute organophosphate poisoning were not statistically significant predictors of chronic toxicity. The PON genotype is an important determinant of a farmworker's susceptibility to chronic pesticide poisoning.
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PMID:Association between human paraoxonase gene polymorphism and chronic symptoms in pesticide-exposed workers. 1262 27

Oral glutamine supplementation during and after exercise abolishes exercise-induced decreases in plasma glutamine concentration but does not affect secretory IgA (sIgA) salivary output. Whether chronic glutamine supplementation during high-intensity interval training influences salivary and nasal sIgA concentration is unknown. The purpose of this study was examine the effects of chronic glutamine supplementation on sIgA during intense running training. Runners (n = 13, body mass 69.9 +/- 2.8 kg, peak whole body oxygen uptake 55.5 +/- 2 ml.kg(-1).min(-1), age 29.1 +/- 2.8 yr) participated in twice-daily interval training for 9-9.5 days, followed by recovery (5-7 days). Oral glutamine supplement (0.1 g/kg) or placebo was given four times daily for the first 14 days. After an overnight fast, venous blood, nasal washes, and stimulated saliva were collected at baseline (T1), midtraining (T2), posttraining (T3), and after recovery (T4). Mood states were assessed by using Profile of Mood States (POMS) inventories. We found that glutamine concentration in resting subjects decreased from T1 to T4 (P < 0.05) and was not altered by supplementation. Salivary IgA concentration and output were unchanged by training or supplementation. Mean nasal IgA across the study period was greater in runners receiving glutamine (264.7 +/- 35.0 microg/mg protein) vs. placebo (172.4 +/- 33.7 microg/mg protein; P < 0.05). POMS analyses indicated that vigor was lower at T3 vs. T1 (P < 0.05) and fatigue was higher at T2 vs. T1 and T4 (P < 0.05). We conclude that chronic glutamine supplementation during interval training results in higher nasal IgA than placebo but does not affect salivary IgA concentration or output.
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PMID:Chronic glutamine supplementation increases nasal but not salivary IgA during 9 days of interval training. 1510 13

After severe trauma or disease glutamine (GLN) is mobilised from all muscles, including the heart and smooth muscles. The result is weakness and fatigue which affects recovery. The breakdown of muscle tissue can be counteracted by external GLN supply. There are concerns, however, that increasing the blood glutamine (Blood-GLN) concentration in patients with acute brain diseases is harmful by elevating the CNS interstitial (IS) concentration of glutamate (CNS-GLT), and that this may result in a secondary excitotoxic injury. We therefore studied the IS CNS-GLN and CNS-GLT when a commercially available nutritional amino acid solution was given intravenously. Ten NICU patients were included. The IS concentrations of amino acids in the brain were measured using intracerebral microdialysis. Blood concentrations of amino acids were measured before and after the amino acid infusion. The change in Blood-GLN was 2.14 (median; range 1.34-3.22) times the basal levels and Blood-GLT increased 1.37 (median; range 0.93-3.45) times basal levels. Both changes were statistically significant. The changes in CNS-GLN was 1.21 (median; range 0.72-1.92) and for CNS-GLT 0.96 (median; range 0.45-1.53) times the basal levels. This was statistically significant for CNS-GLN but not for CNS-GLT. A high initial CNS-GLT (55.3 micromol/l) in one patient increased even further to 84.4 micromol/l after infusion of amino acid solution. We submit that nutritional amino acid solutions can be administrated to some patients with acute brain disease without increasing the CNS-GLT values. However, since BBB function was not quantified in our study, further evaluation of this issue is warranted.
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PMID:Cerebral interstitial levels of glutamate and glutamine after intravenous administration of nutritional amino acids in neurointensive care patients. 1589 76

This review discusses some of the beneficial effects of a dietary amino acid supplement on muscle function, fatigue, and recovery in exercising athletes. The supplement, a mixture of amino acids that included the branched-chain amino acids, arginine and glutamine, was studied chronically at several daily dose levels for extended periods of time (10, 30, and 90 d). Outcome variables included physical measures of muscle strength, fatigue and damage, and blood indices of muscle damage and oxygen-carrying capacity. One beneficial effect of the amino acid supplement was a quicker recovery from the muscle fatigue that followed eccentric exercise training. A dose-response study of the amino acid mixture at 2.2, 4.4, and 6.6 g/d for 1 mo showed that at the highest dose, indices of blood oxygen-carrying capacity were increased and those of muscle damage were decreased at the end of the trial. When the amino acid mixture was given for 90 d to elite rugby players during training at a dose of 7.2 g/d, a blood-component analysis indicated improvements in the oxygen-carrying capacity of the blood. Together, the studies suggest that the amino acid supplement contributed to an improvement in training efficiency through positive effects on muscle integrity and hematopoiesis.
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PMID:Amino acid mixture improves training efficiency in athletes. 1642 43

In this article we discuss studies showing that rats are able to regulate their intake of BCAA depending on the level of exercise, and that they will choose a solution of BCAA over water during times of intense exercise. We found that the voluntary intake of a solution made of BCAA, L-arginine and L-glutamine positively correlated with the timing and volume of exercise during the dark (active) period of the circadian rhythm. In the second behavioral protocol in which rats were fed BCAA fortified diet (2.0%, wt:wt), we observed voluntarily increased volume of physical activity beginning from d 4 of feeding on. In the second, neuro-behavioral, part of the study we measured the brain content of 5-hydroxytryptamine (5-HT) as well as plasma amino acid profiles in well-trained exercising rats to test a hypothesis that BCAA may alleviate central aspects of fatigue. A solution made of BCAA, L-arginine, and L-glutamine applied before running elevated the BCAA/tryptophan plasma ratio at the end of and after running, and decreased 5-HT release in the lateral hypothalamus and amygdala after running, when compared with the controls. The exercise-related shift in the fluid preference toward a BCAA-based solution suggests an ergogenic benefit. The forced-running study shows the lateral hypothalamus and possibly amygdala might be the critical brain regions implied in the central effects of a BCAA-based solution.
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PMID:Exercise-dependent preference for a mixture of branched-chain amino acids and homeostatic control of brain serotonin in exercising rats. 1642 45

The overtraining syndrome is characterized by an excessive training that results in several adverse effects the main of which being the decay in performance. Its incidence among elite athletes has been experiencing a significant increase lately, which prompted a rush of interest in the search for efficient measures to prevent and treat this condition. It is necessary, however, to clarify possible mechanisms involved in the development of overtraining. Several hypothesis are being proposed, such as a greater activation of both the autonomic nervous system and the hypothalamic-pituitary-adrenal axis, and suppression of the hypothalamic-pituitary-gonadal axis. On the contrary, some studies suggest that the modulation of such systems is but a consequence of the overtraining syndrome and not its cause. Thus, recent hypothesis related to cytokine release, to central fatigue, to depletion of muscle and liver glycogen, and to a reduction in glutamine availability during physical activity are being raised.
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PMID:[Neuroendocrine and nutritional aspects of overtraining]. 1654 89

Sarcopenia describes the involuntary decline in muscle mass with aging, coupled with fatigue, and loss of force and function. We investigated 113 human muscle biopsy specimens obtained from patients with neuromuscular diseases and controls. We measured 21 amino acids in these muscle biopsies. Age emerged as a significant negative predictor of cytosolic concentration ratio of glutamine to total branched chain amino acids and of glutamine to total aromatic amino acids using stepwise multiple linear regression analysis. This pattern of alteration corresponds well to documented alterations in skeletal muscle of critically ill patients and after immobilization. Additionally, in myositis, citrulline was significantly elevated, while glutamate, lysine and taurine were significantly reduced. Furthermore, in sporadic amyotrophic lateral sclerosis (sALS) the total aromatic amino acids, arginine, glutamate, threonine, and tyrosine were significantly elevated. This study provides evidence, that alteration of glutamine is correlated to aging and might reflect increased proteolysis in aged and diseased human skeletal muscle.
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PMID:Age related profiles of free amino acids in human skeletal muscle. 1664 14


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