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Diminished central fatigue by inhibition of the L-system transporter for the uptake of tryptophan.

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Nagase genetically analbuminemic rats (NAR) were run to fatigue. Administration of branched chain amino acids (BCAA) before exhaustive exercise, resulted in a post-fatigue decreased tryptophan uptake (-22%, p < 0.05) and 5-hydroxytryptophan (5-HTP) uptake (-29%, p < 0.01) into the synaptosomes

Tryptophan and kynurenic Acid may produce an amplified effect in central fatigue induced by chronic sleep disorder.

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Tryptophan (TRP) and its neuroactive metabolite, kynurenic acid (KYNA), are thought to play key roles in central fatigue, but the specifics are still unknown. To clarify their roles in the brain, we developed a rat model of central fatigue induced by chronic sleep disorder (CFSD) by disturbing the

The effect of tryptophan deficiency in the brain on rat fatigue levels: a rat model of fatigue reduction.

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The level of tryptophan and 5-hydroxyindoleacetic acid were measured in the brain (striatum) of rats on tryptophan-deficient diet and tryptophan-enriched diet. We measured concentrations of tryptophan and 5-hydroxyindoleacetic acid in striatum by using microdialysis and HPLC methods. The

A placebo controlled investigation of the effects of tryptophan or placebo on subjective and objective measures of fatigue.

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OBJECTIVE To examine the effect of L-tryptophan administration on subjective and objective measures of fatigue in healthy volunteers. METHODS Six healthy volunteers (4M:2F) were recruited from staff and students at the College. METHODS Department of Human Nutrition, St. Bartholomews and the Royal

L-tryptophan supplementation can decrease fatigue perception during an aerobic exercise with supramaximal intercalated anaerobic bouts in young healthy men.

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Physical exercise is often terminated not due to muscle fatigue but because of inadequate neural drive in the serotonergic system. Modifications in activity levels of the serotonergic system, induced by variations in the availability of L-tryptophan (a serotonin precursor) may alter neural drive. We

Tryptophan depletion in chronic fatigue syndrome, a pilot cross-over study.

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BACKGROUND Chronic fatigue syndrome (CFS) is still an enigmatic disorder. CFS can be regarded as a complex disorder with tremendous impact on lives of CFS-patients. Full recovery without treatment is rare. A somatic explanation for the fatigue is lacking. There is clinical and experimental evidence

Heterogeneity of serum tryptophan concentration and availability to the brain in patients with the chronic fatigue syndrome.

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We assessed the serotonin status of patients with the chronic fatigue syndrome (CFS). Tryptophan (Trp) availability to the brain, expressed as the ratio of concentration of serum Trp to the sum of those of its five competitors (CAA), and other parameters of Trp disposition were compared in 23

Decreased tryptophan availability but normal post-synaptic 5-HT2c receptor sensitivity in chronic fatigue syndrome.

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BACKGROUND Chronic fatigue syndrome (CFS) has been associated with increased prolactin (PRL) responses to the serotonin (5-HT) releasing agent fenfluramine. It is not known whether this abnormality is due to increased 5-HT release or heightened sensitivity of post-synaptic 5-HT receptors. METHODS We

Fatigue in patients with lung cancer is related with accelerated tryptophan breakdown.

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BACKGROUND Patients with cancer often suffer from fatigue and decreased quality of life which might be related to the breakdown of essential amino acid tryptophan. METHODS In 50 patients with lung cancer we examined fatigue and the deterioration of quality of life in patients using the Functional

Sex differences in plasma prolactin response to tryptophan in chronic fatigue syndrome patients with and without comorbid fibromyalgia.

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BACKGROUND Some think chronic fatigue syndrome (CFS) and fibromyalgia (FM) are variants of the same illness process. This would imply that CFS patients with and without comorbid FM have similar biological underpinnings. To test this, we compared serotonergic-based responses, plasma prolactin (PRL),

A Brief Historic Overview of Clinical Disorders Associated with Tryptophan: The Relevance to Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM).

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Last century there was a short burst of interest in the tryptophan related disorders of pellagra and related abnormalities that are usually presented in infancy.1,2 Nutritional physiologists recognized that a severe human dietary deficiency of either tryptophan or the B group vitamins could result

Association between the transcriptional levels of Htr-1a and tryptophan hydroxylase-1 in the hippocampus and the antifatigue effects of leucine on rats with postoperative fatigue.

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Leucine (Leu), a branched-chain amino acid (BCAA), is widely used in clinical practice following severe burns, gastrointestinal surgery, trauma and sepsis. In the present study, the antifatigue effects of BCAAs on a postoperative fatigue (POF) rat model, induced by 70% intestinal resection, were

Changes in the albumin binding of tryptophan during postoperative recovery: a possible link with central fatigue?

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Tryptophan is the precursor of the neurotransmitter 5-hydroxytryptamine (5-HT), known to be involved in sleep and fatigue. In the blood, tryptophan binds to albumin, and that which does not, free tryptophan, competes with branched chain amino acids (BCAA) for entry into the brain. The plasma

Inhibition of tryptophan hydroxylase abolishes fatigue induced by central tryptophan in exercising rats.

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Fatigue during prolonged exercise is related to brain monoamines concentrations, but the mechanisms underlying this relationship have not been fully elucidated. We investigated the effects of increased central tryptophan (TRP) availability on physical performance and thermoregulation in running rats

Hydrocortisone Affects Fatigue and Physical Functioning Through Metabolism of Tryptophan: A Randomized Controlled Trial.

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UNASSIGNED Hydrocortisone (HC) treatment influences health-related quality of life (HRQOL) in secondary adrenal insufficiency (AI). Glucocorticoids regulate tryptophan metabolism through the kynurenine pathway, which modulates mood and energy homeostasis. UNASSIGNED This study investigated whether

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