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

It has been hypothesized that fatigue and prolactin (PRL) changes during endurance exercise are influenced by serotonin synthesis, and in turn, release. Such a change is thought to occur through an increase in blood free tryptophan (TRP) and a concomitant decrease in those large neutral amino acids (LNAA) which compete with free TRP for entry into the brain. For further investigation, 10 healthy athletes were randomly subjected to three test units (TU), each consisting of a treadmill run for 90 min. The speed was adjusted to a blood lactate level of 2 mmol/l. During the first 30 min of exercise infusions of 500 ml saline (TU I), 500 ml saline with amino acids (TU II) or 500 ml saline with 30 U heparin/kg following an oral soy oil solution given 1 h before (TU III) were administered. Rate of perceived exertion (RPE), heart rate and running speed were recorded during exercise. Venous blood samples were taken after a 10 h fast, at rest, after 10, 50 and 90 min of exercise as well as 10 and 30 min post-exercise. PRL, insulin, glucose, ammonia, lactate, triglycerides (TG), free fatty acids (FFA) and amino acids were determined in each sample. No significant differences were found in RPE. PRL increased (p < 0.01) in all TU. TG and heparin administration resulted in an increase (p <0.01) in FFA, which correlated (p < 0.01) with free TRP and the ratio of free TRP/TRP. Artificial increase in free TRP in TU III did not affect plasma PRL level. The amino acid infusion in TU II induced an increase in LNAA but had no significant effect on PRL. PRL and ammonia peaked at the end of exercise. We conclude that neither exercise-induced PRL secretion nor RPE are affected by changes in circulating free TRP and LNAA under the present conditions.
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PMID:Alterations in plasma free tryptophan and large neutral amino acids do not affect perceived exertion and prolactin during 90 min of treadmill exercise. 883 6

The causes of fatigue during muscular exercise include factors that reside in the brain (central mechanisms) as well as the muscles themselves (peripheral mechanisms). Central fatigue is largely unexplored, but there is increasing evidence that increased brain serotonin (5-HT) can lead to central (mental) fatigue, thereby causing a deterioration in sport and exercise performance. Although there are also strong theoretical grounds for a beneficial role of nutrition in delaying central fatigue, the data are much more tenuous. Dietary supplementation with branched-chain amino acids (BCAA) in low doses produces small and probably inconsequential effects on peripheral markers of brain 5-HT synthesis (plasma free tryptophan/BCAA), whereas larger doses are likely to be unpalatable, reduce the absorption of water in the gut, and may increase potentially toxic ammonia concentrations in the plasma. Alternatively, carbohydrate supplementation results in large reductions in plasma free tryptophan/BCAA and exercise time to fatigue is significantly longer, but it is difficult to distinguish between the effects of carbohydrate feedings on central fatigue mechanisms and the well-established beneficial effects of carbohydrate supplements on the contracting muscle. These data support the exciting possibility that relationships exist among nutrition, brain neurochemistry and sport performance. However, while the evidence is intriguing and makes good intuitive sense, our knowledge in this area is rudimentary at best.
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PMID:Central and peripheral factors in fatigue. 889 20

This study was designed to determine the effect of ingesting three preexercise meals on energy metabolism during exercise and recovery and to relate metabolic perturbations to subjective and objective measurements associated with central fatigue. Twelve subjects consumed isoenergetic meals consisting of oat, wheat, or corn cereals 90 min before cycling. A fasting trial served as the control. Blood samples and cognitive function, perceived hunger, and sleepiness measurements were obtained before and after feeding and during recovery when self-selected food intake was also measured. After meal ingestion, plasma insulin was lower for oat than for wheat or corn whereas the ratio of tryptophan to large neutral amino acids (LNAAs) for corn was less than for all others. During exercise, the tryptophan-LNAA ratio increased from preexercise values for the fasting and wheat trials, but exercise performance was unaffected. During recovery, tryptophan:LNAA increased from postexercise values in fasting trials. Also, hunger and fatigue ratings were greater in fasted subjects, but self-selected food intake measured at the end of the recovery period was not different among groups. We conclude that preexercise meal consumption affected tryptophan:LNAA before, during, and after exercise, but these changes were not sufficient to alter physical and cognitive performance.
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PMID:Preexercise meal composition alters plasma large neutral amino acid responses during exercise and recovery. 890 1

Acute eosinophilia-myalgia syndrome (EMS) due to contaminated L-tryptophan (LT) exposure is an inflammatory microangiopathy of the dermis, fascia, and muscle. Select individuals evolve from acute EMS to have persistence of myalgia, fatigue, cramps, and skin changes for years. Many develop memory dysfunction and confusion. The objective of this study is to delineate the pathology in individuals with chronic EMS. Seventeen patients with ongoing symptoms representing chronic EMS are studied by skin, fascia, and muscle biopsies four to five years after exposure to contaminated LT and initial onset of EMS. All have microvascular disease. Most have lymphocytic inflammatory infiltrates. Several have dermal sclerosis. The findings indicate that persistent microvascular disease is present in chronic EMS. The pathologic changes are similar to those of acute EMS but with notable differences. Tissue eosinophil infiltration is rare in the chronic state as compared to acute EMS. The persistence of endothelial pathology indicates continuing microvascular dysfunction.
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PMID:Persistent microvasculopathy in chronic eosinophilia-myalgia syndrome. 890 89

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 concentrations of albumin, free tryptophan, total tryptophan, and BCAA were measured before and after major surgery in nine elderly and nine coronary artery bypass graft (CABG) patients. In both the elderly and the CABG patients plasma free tryptophan concentrations were increased after surgery, compared with baseline levels; the plasma free tryptophan/BCAA concentration ratio was also increased significantly after surgery. Plasma albumin concentrations were decreased significantly after surgery in both the elderly and the CABG patients. Plasma BCAA concentrations were not affected by surgery in either group. The effect of exercising to exhaustion on 5-HT and tryptophan were investigated in Nagase analbuminemic rats (NAR). The intrasynaptosomal concentration of tryptophan, 5-hydroxy-tryptophan, and 5-HT was increased by fatigue after exercise. In addition, running time to exhaustion was shortened in NAR. These data suggest that free tryptophan uptake and 5-HT synthesis were enhanced in the nerve terminal. A decrease in plasma albumin may account for the increase in plasma-free tryptophan levels. An increase in plasma free tryptophan, resulting in an enhanced plasma concentration ratio of free tryptophan/BCAA, may lead to a higher 5-HT concentration in some parts of the brain and, consequently, to central fatigue. It is suggested that provision of BCAA as a dietary supplement may counteract the increase in plasma free tryptophan and thus improve the status of some patients after major surgery.
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PMID:Changes in the albumin binding of tryptophan during postoperative recovery: a possible link with central fatigue? 920 93

The major symptoms of overtraining including decreased exercise performance, altered mood states, and depleted muscle glycogen stores closely resemble the effects of brain serotonin, the level of which is dependent on the plasma ratio of tryptophan to branched-chain amino acids (BCAA). To examine the relation between plasma amino acids and overtraining, ten highly-trained endurance runners underwent two weeks of base training (normal training) before increasing their training volume by 40% for two weeks to achieve a state of short-term overtraining (or overreaching). The overtraining period was followed by two weeks of recovery in which training volume was reduced by 41% of the base training. For the whole group, no significant changes were observed in running economy and maximum oxygen uptake. There were no changes in resting heart rate, blood pressure, resting metabolic rate, and serum cortisol level in response to the changes in training volume. The runners experienced a significant increase (p < 0.05) in fatigue score for the profile of mood states when the training volume was increased. The elevated fatigue score returned to baseline when the training volume was reduced. Plasma free or total tryptophan, BCAA, and the tryptophan/BCAA ratio were not significantly altered throughout the course of this study. We concluded that proposed physiological markers of overtraining, including plasma tryptophan and BCAA levels, were unchanged despite a 40% increase in training volume.
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PMID:Changes in plasma tryptophan/branched chain amino acid ratio in responses to training volume variation. 923 43

Effects of a serotonin re-uptake inhibitor and oral amino acid supplementations on physical and mental performance as well as neuroendocrine variables were investigated. 10 male subjects cycled in four trials until exhaustion. Participants ingested a placebo in trial (T) I, 20 mg paroxetine in T II, 21 g branched-chain amino acids (BCAA) in T III and 20g tyrosine (TYR) in T IV. Heart rate, capillary lactate, plasma insulin, free fatty acids, glucose, serotonin and beta-endorphin did not differ in trials. Plasma ammonia increments during exercise were higher in T III. Plasma BCAA in T III and plasma TYR in T IV were increased after 30 min of exercise according to the supplemented substances. In contrast to all other trials, the ratio of plasma free TRP/BCAA did not increase in T III. Plasma TYR/BCAA was augmented in T IV and decreased in T III after 30 min of exercise, whereas it did not change in T I and II. Plasma prolactin (PRL), growth hormone, cortisol, adrenocorticotropic hormone, norepinephrine and epinephrine increased during all trials. Plasma PRL increments were higher in T IV. Exhaustion was reached earlier in T II. No significant differences were found between other trials. Drive during psychometric testing subsequent to exercise was improved in T III and IV. The results indicate that fatigue during endurance exercise was increased by pharmacological augmentation of the brain serotonergic activity. However, a reduction of 5-HT synthesis via BCAA supplementation did not affect physical fatigue. TYR administration did not alter physical performance either although plasma PRL increments suggest that changes in the monoaminergic system were induced. Precaution is necessary before assuming an ergogenic value of amino acids.
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PMID:Influence of paroxetine, branched-chain amino acids and tyrosine on neuroendocrine system responses and fatigue in humans. 962 32

A number of peripheral indices of serotonergic function were examined in endurance-trained (ET) and sedentary males using the blood platelet as a model of the serotonergic neurone. The aim of the study was to investigate possible involvement and adaptation of the central serotonergic system in exercise-induced fatigue. The [3H] paroxetine-defined density of platelet serotonin transporters, platelet serotonin content and the plasma concentration of amino acids were determined in 10 ET and eight sedentary males. The mean (standard deviation) density of the serotonin transporter in the platelet membranes of the ET subjects was greater [1237 (182) fmol mg protein-1] than that of the sedentary subjects [910 (119) fmol mg protein-1; P = 0.013]. No difference (P = 0.51) could be seen between the median (range) platelet serotonin content of the ET subjects [0.98 (0.37-3.04) nmol platelet-10] and that of the sedentary subjects [0.82 (0.18-1.49) nmol platelet-10]. The platelet poor plasma concentrations of tryptophan and tyrosine were lower in the ET subjects (P = 0.028 and 0.015, respectively). The present study suggests that the platelet membrane of the ET subjects has a greater density of the serotonin transporter and that this is inversely related to the circulating concentration of the serotonin precursor, tryptophan. It remains to be resolved whether the increase in serotonin transporter density in the platelet membrane of ET subjects is reflected centrally and whether the ET platelet population may be sufficiently different from that of sedentary individuals to alter serotonin transporter density.
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PMID:Platelet serotonin transporter density and related parameters in endurance-trained and sedentary male subjects. 964 35

The purpose of this review was to give an answer to the question whether there are convincing data to support the hypothesis of an amino acid imbalance as one possible mechanism to explain overtraining syndrome. Animal studies point to an enhanced synthesis of the neurotransmitter 5-hydroxytryptamine through an amino acid imbalance at the blood-brain barrier with a preferable tryptophan uptake into the brain, resulting in premature fatigue. Human studies, however, show contradictory results, mainly because of nonstandardized methodology, so that a final conclusion cannot be made at present. BCAA supplementation in addition to standard carbohydrate ingestion during sustained exercise seems to be of no eminent advantage to delay fatigue. The overall results concerning the BCAA hypothesis to explain overtraining are inconclusive and require more controlled experimental research.
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PMID:Overtraining and the BCAA hypothesis. 966 92

We hypothesized that central fatigue may have a role in limiting the endurance capacity of horses. Therefore, we tested the effect of infusing tryptophan and/or glucose on endurance time and plasma concentrations of free tryptophan and other substrates thought to affect tryptophan uptake into the brain of seven mares (3-4 yr of age, 353-435 kg) that ran on a treadmill at 50% of maximal O2 consumption to fatigue. With use of a counterbalanced crossover design, the horses were infused with tryptophan (100 mg/kg in saline solution) or a similar volume of saline solution (placebo) before exercise. During exercise, horses received infusions of glucose (2 g/min, 50% wt/vol) or a similar volume of saline. Thus the treatments were 1) tryptophan and glucose (T & G), 2) tryptophan and placebo (T & P), 3) placebo and glucose (P & G), and 4) placebo and placebo (P & P). Mean heart rate, hematocrit, and concentration of plasma total solids before and during exercise were similar for all trials. Mean time to exhaustion was reduced (P < 0.05) for T & P and T & G compared with P & P [86.1 +/- 6.9 and 87.1 +/- 6.8 vs. 102.3 +/- 10.3 (SE) min], whereas endurance for P & G (122.4 +/- 11.9 min) was greater than for all other trials (P < 0.05). Compared with nontryptophan trials, during the tryptophan trials plasma prolactin increased (P < 0.05) nearly threefold before exercise and almost twofold early in exercise. Muscle glycogen concentrations were reduced (P < 0.05) below preexercise values in the P & G and P & P trials only. However, glucose infusions (P & G) did not affect (P > 0.05) concentrations of plasma free fatty acids or ratios of branched-chain amino acids to free tryptophan. In conclusion, tryptophan infusion reduced endurance time, which was consistent with the central fatigue hypothesis. The failure of glucose infusion to alleviate the effects of tryptophan and the absence of significant muscle glycogen reduction in the tryptophan trials suggest that the early onset of fatigue in the tryptophan trials is not due to a lack of readily available substrate.
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PMID:Effect of tryptophan and of glucose on exercise capacity of horses. 972 51


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