Carbohydrates, Branched-Chain Amino Acids, and Endurances: The Central Fatigue Hypothesis

1995 ◽  
Vol 5 (s1) ◽  
pp. S29-S38 ◽  
Author(s):  
J. Mark Davis
Keyword(s):  
Amino Acids ◽  
Exercise Performance ◽  
Prolonged Exercise ◽  
Central Fatigue ◽  
Branched Chain Amino Acids ◽  
Convincing Evidence ◽  
Free Tryptophan ◽  
Branched Chain ◽  
Sport And Exercise ◽  
Exercise Induced

The mechanisms of central fatigue are largely unexplored, but the central fatigue hypothesis suggests that increased brain serotonin (5-HT) can cause a deterioration in sport and exercise performance. There is now convincing evidence that exercise-induced increases in the plasma free tryptophan (f-TRP)/branched-chain amino acids (BCCA) ratio are associated with increased brain 5-HT and the onset of fatigue during prolonged exercise. Furthermore, when drugs are administered to alter brain 5-HT, they have the predicted effects on exercise performance. The influence of nutritional manipulations of f-TRP/BCCA on performance is less well established. The effects of BCCA supplementation on exercise performance are mixed, and the published studies often suffer from methodological flaws. Alternatively, dramatic reductions in f-TRP/BCCA and enhanced performance accompany carbohydrate feedings during prolonged exercise. However, it is difficult to distinguish between the effects of carbohydrate feedings on mechanisms that reside in the brain versus the muscles themselves.

scholarly journals Mechanisms of the Pellagragenic Effect of Leucine: Stimulation of Hepatic Tryptophan Oxidation by Administration of Branched-Chain Amino Acids to Healthy Human Volunteers and the Role of Plasma Free Tryptophan and Total Kynurenines

2014 ◽  
Vol 7 ◽  
pp. IJTR.S18231 ◽  
Author(s):  
Abdulla A-B Badawy ◽  
Sarah L. Lake ◽  
Donald M. Dougherty
Keyword(s):  
Amino Acids ◽  
Hepatic Uptake ◽  
Branched Chain Amino Acids ◽  
Amino Acid Mixture ◽  
Kynurenine Pathway ◽  
Acid Mixture ◽  
Healthy Human ◽  
Free Tryptophan ◽  
Tryptophan Oxidation ◽  
Branched Chain

The pellagragenic effect of leucine (Leu) has been proposed to involve modulation of L-tryptophan (Trp) metabolism along the hepatic kynurenine pathway. Here, we discuss some of the mechanisms suggested and report the effects in healthy volunteers of single doses of Leu (4.05–6.75 g) administered in a 16-amino acid mixture on concentrations of plasma Trp and its kynurenine metabolites. Flux of Trp through Trp 2,3-dioxygenase (TDO) is dose-dependently enhanced most probably by Leu and can be attributed to TDO activation. Trp oxidation is better expressed using plasma total kynurenines, rather than kynurenine, and free, rather than total, Trp. Increased hepatic Trp oxidation may be an additional mechanism of action of branched-chain amino acids in the acute Trp depletion test. Inhibition of intestinal absorption or hepatic uptake of Trp by Leu can be excluded. Potential mechanisms of the aggravation of pellagra symptoms by Leu are discussed.

Branched chain amino acids chronic treatment and muscular exercise performance in athletes: a study through plasma acetyl-carnitine levels

Amino Acids ◽  
1993 ◽  
Vol 4 (3) ◽  
pp. 255-266 ◽  
Author(s):  
E. F. De Palo ◽  
P. Metus ◽  
R. Gatti ◽  
O. Previti ◽  
L. Bigon ◽  
...  
Keyword(s):  
Amino Acids ◽  
Exercise Performance ◽  
Chronic Treatment ◽  
Branched Chain Amino Acids ◽  
Muscular Exercise ◽  
Branched Chain

scholarly journals Effect of carbohydrate ingestion on central fatigue during prolonged running exercise in moderate hypoxia

2019 ◽  
Vol 126 (1) ◽  
pp. 141-151 ◽  
Author(s):  
Hunter L. Paris ◽  
Timothy J. Fulton ◽  
Robert F. Chapman ◽  
Alyce D. Fly ◽  
David M. Koceja ◽  
...  
Keyword(s):  
Central Fatigue ◽  
Branched Chain Amino Acids ◽  
Peripheral Fatigue ◽  
Carbohydrate Ingestion ◽  
Moderate Hypoxia ◽  
Free Tryptophan ◽  
Fatigue Development ◽  
Branched Chain ◽  
Trained Runners ◽  
Placebo Drink

To determine whether acute exposure to moderate hypoxia alters central and peripheral fatigue and to test whether carbohydrate ingestion impacts fatigue characteristics, 12 trained runners completed three running trials lasting 1 h each at 65% of normoxic maximum oxygen uptake. The first trial was performed in normoxia [inspired O2 fraction ([Formula: see text]) = 0.21], and the last two trials were completed in hypoxia ([Formula: see text] = 0.15). Participants ingested a placebo drink in normoxia (NORM-PLA), a placebo drink in hypoxia (HYP-PLA), or a carbohydrate solution in hypoxia (HYP-CHO). HYP conditions were randomized. Peripheral [change in potentiated quadriceps twitch force (ΔQtw,pot)] and central [change in voluntary activation (ΔVA)] fatigue were assessed via preexercise-to-postexercise changes in magnetically evoked quadriceps twitch. In HYP, blood was drawn to determine the ratio of free-tryptophan (f-TRP) to branched-chain amino acids (BCAA). After exercise, peripheral fatigue was reduced to a similar degree in normoxia and hypoxia (ΔQtw,pot = −4.5 ± 1.3% and −4.0 ± 1.5% in NORM-PLA and HYP-PLA, respectively; P = 0.61). Central fatigue was present after normoxic and hypoxic exercise but to a greater degree in HYP-PLA compared with NORM-PLA (ΔVA: −4.7 ± 0.9% vs. −1.9 ± 0.7%; P < 0.01). Carbohydrate ingestion did not influence central fatigue (ΔVA in HYP-CHO: −5.7 ± 1.2%; P = 0.51 vs. HYP-PLA). After exercise, no differences were observed in the ratio of f-TRP to BCAA between HYP-PLA and HYP-CHO ( P = 0.67). Central fatigue increased during prolonged running exercise in moderate hypoxia although the ratio of f-TRP to BCAA remained unchanged. Ingesting carbohydrates while running in hypoxia did not influence fatigue development. NEW & NOTEWORTHY Hypoxic exposure influences the origin of exercise-induced fatigue and the rate of fatigue development depending on the severity of hypoxia. Our data suggest that moderate hypoxia increases central, but not peripheral, fatigue in trained runners exercising at 65% of normoxic maximum oxygen uptake. The increase in central fatigue was unaffected by carbohydrate intake and occurred although the ratio of free tryptophan to branched-chain amino acids remained unchanged.

Changes in plasma concentration of kynurenine following intake of branched-chain amino acids are not caused by alterations in muscle kynurenine metabolism

2021 ◽  
Author(s):  
William O Jonsson ◽  
Jonathan Ponette ◽  
Oscar Horwath ◽  
Tomas Rydenstam ◽  
Karin Söderlund ◽  
...  
Keyword(s):  
Amino Acids ◽  
Plasma Concentration ◽  
Kynurenic Acid ◽  
Aromatic Amino Acids ◽  
Random Order ◽  
Fold Increase ◽  
Branched Chain Amino Acids ◽  
Kynurenine Metabolism ◽  
Branched Chain ◽  
Exercise Induced

Administration of branched-chain amino acids (BCAA) has been suggested to enhance mitochondrial biogenesis, including levels of PGC-1α, which may, in turn, alter kynurenine metabolism. Ten healthy subjects performed 60 min of dynamic one-leg exercise at ~70% of Wmax on two occasions. They were in random order supplied either a mixture of BCAA or flavored water (placebo) during the experiment. Blood samples were collected during exercise and recovery, and muscle biopsies were taken from both legs before, after and 90 and 180 min following exercise. Ingestion of BCAA doubled their concentration in both plasma and muscle while causing a 30-40% reduction (P<0.05 vs. placebo) in levels of aromatic amino acids in both resting and exercising muscle during 3-h recovery. The muscle concentration of kynurenine decreased by 25% (P<0.05) during recovery, similar in both resting and exercising leg and with both supplements, although plasma concentration of kynurenine during recovery was 10% lower (P<0.05) when BCAA were ingested. Ingestion of BCAA reduced the plasma concentration of kynurenic acid by 60% (P<0.01) during exercise and recovery, while the level remained unchanged with placebo. Exercise induced a 3-4-fold increase (P<0.05) in muscle content of PGC-1a1 mRNA after 90 min of recovery under both conditions, whereas levels of KAT4 mRNA and protein were unaffected by exercise or supplement. In conclusion, the reduction of plasma levels of kynurenine and kynurenic acid caused by BCAA were not associated with any changes in the level of muscle kynurenine, suggesting that kynurenine metabolism was altered in tissues other than muscle.

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