protein ingestion during training and fatigue

K

Karky

2
So getting some BCAAs during training can improve performance, probably through reducing central fatigue. I found this pretty interesting, and I've been noticing I'm feeling way less fatigued when I ingest protein and carbs during my workout (of course, for me, there is no way of separating between the effects of the carbs on my muscles and the BCAAs on central fatigue)

The theory is like this:
the amino acid tryptophan is the precussor to a neurotransmitter, 5-HT (serotonin) and BCAAs inhibit the brains uptake of tryptophan from the blood.
Apparently, 5-HT in the extracellular fluid supresses nerves (1)

The theory seems pretty sound, though the evidence I've seen where BCAAs have been supplemented during training have not been so convincing, but still, it's pretty facinating if you ask me! And just because it's the BCAAs that might have this effect, doesn't mean you actually need to take BCAA supplements. There is a lot of BCAAs in regular whey and casein protein powders.. last time I calculated, it was cheaper to get the same amount of BCAAs from whey than from BCAA only supplements, and with the whey you get a lot of other amino acids aswell ;)

1.

Anyone else find this interesting or am I the only true nerd here?
 
Bcaa's

Oh great wise and powerful Karky I find all of your sage advice and endless pearls of wisdom to be provocative and informative on the road to fitness enlightenment. That being said, I must admit I have no idea what you have just said. Regardless I will follow your teachings knowing all good comes from the fountain of knowledge. Buy Whey--Buy Whey--Buy Whey--Aummmm;)
 
CFS Fatigue

Ok I just read the link and now I'm clear. I was surprised to read that the researchers found that CFS Fatigue was different than muscular exertion fatigue and implied that this was something new and undiscovered. I assume anyone who pumps iron has known this since the beginning. What's your take.:rolleyes:
 
World B said:
Ok I just read the link and now I'm clear. I was surprised to read that the researchers found that CFS Fatigue was different than muscular exertion fatigue and implied that this was something new and undiscovered. I assume anyone who pumps iron has known this since the beginning. What's your take.:rolleyes:
Click to expand...

Yeah, they say that CFS fatigue is different from physical fatigue. But they do say that physical activity can cause central fatigue.. but the central fatigue from exercise and that of CFS might be different. I don't think researchers actually know what the mechanisms of CFS are.. and I know what fatigue from exercise is still debated and not completely understood.. so if there are any similarities between exercise induced fatigue (both the central and the peripheral) and CFS, we probably wouldn't know about it :p

I have myself observed people with CFS (I know 2 who have had/have it) and it's definately more serious than the fatigue I get when I'm done with a workout. They basically lie in bed for a year before they feel better.. some even longer.

they say in the article that CFS fatigue is not accompanied by physical fatigue.. I don't quite get that.. I mean surely people with CFS would have a reduced work capacity when it comes to training? Or does he mean physical fatigue as in peripheral fatigue (like protons accumilating in muscles making them more acidic and thus interfering with enzyme reactions, etc) and that the reason they can't exercise hard is because they can't recruit a lot of motor units due to things happening in the brain?.. The article should have defined physical fatigue better, IMO.
 
No idea, it's not very long though. At least not for glucose, maltodextrin and whey. It would probably be pretty easy to find with google scholar..
 
the point this proves IMO is that eating correctly for training,is as important as the training itself,and im not talking about supps just good diet in general.

No idea, it's not very long though. At least not for glucose, maltodextrin and whey. It would probably be pretty easy to find with google scholar..
Click to expand...
it can take the gut hours to actualy release protein,then it can take as long as 72hrs to actualy digest/absorbe something like a steak.
 
but that's a steak. Also, won't the fact that you're exercising play into how long the gut keeps the protein and carbs to itself? I'm trying to find some studies, but none of them mention any time.
 
dont think the gut knows the difference between training and just doing daily activitys.

also as far as steak goes its still a source of protien same as whey etc,and as long as you eat enough protein/carbs/fats they should still be in your system all day.
 
Karky said:
but that's a steak. Also, won't the fact that you're exercising play into how long the gut keeps the protein and carbs to itself? I'm trying to find some studies, but none of them mention any time.
Click to expand...

Yeah. That's what I was alluding to. The blood flow will be directed away from digestion causing what-I'm-going-to-assume to be a longer digesting term. If protein takes a minimum of 2-4 hours to breakdown into its amino form, then what is the point of injesting protein and carbs during training if you're keeping in the scope of things: consuming nutrients an hour to two hours prior to training and your over all kcal consumption.
 
I'm guessing maybe it takes like 30-60 min or something before it's in the blood.

And you can digest stuff while you train, since your minute volume goes through the roof the digestive organs are still getting quite a bit of blood, just not as many % of the minute volume as during rest, since most of the increased minute volume during exercise goes to the muscles.
 
J Nutr. 2006 Feb;136(2):553S-559S.
Exercise, serum free tryptophan, and central fatigue.

Fernstrom JD, Fernstrom MH.

Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh PA 15213, USA. fernstromjd@upmc.edu

Brain tryptophan (TRP) concentrations and serotonin (5HT) synthesis and release increase during running. This increase in 5HT function may promote central fatigue and contribute to suboptimal physical performance. The rise in brain TRP is reputed to result from exercise-induced elevations in serum nonesterified fatty acid (NEFA) concentrations, which dissociate TRP from albumin in blood and increase the serum free TRP pool. But, as discussed in this article, ample evidence exists that the serum free TRP pool does not control brain TRP uptake. The clearest data are dietary, but pharmacologic data in exercising rats also support this conclusion. Changes in the serum levels of amino acids that compete with TRP for brain uptake appear also not to explain the rise in brain TRP. The mechanism is therefore not presently known. The link between the rise in brain TRP and 5HT synthesis/release is not simple: a rise in brain TRP stimulates 5HT synthesis/release in actively firing neurons. Hence, during exercise, only 5HT neurons that are firing should increase 5HT production/release when brain TRP rises. It is not known which 5HT neurons fire during exercise; the 5HT neurons that respond to exercise-induced increases in brain TRP are therefore not known. Hence, it is not possible to conclude which 5HT neurons contribute to the generation of central fatigue. Because some 5HT neurons control specific functions important to physical performance (e.g., respiration), the current understanding of 5HT neuronal function in central fatigue might benefit from the study of specific 5HT pathways during exercise.

Publication Types:
Research Support, Non-U.S. Gov't

PMID: 16424146 [PubMed - indexed for MEDLINE]

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2: J Nutr. 2006 Feb;136(2):544S-547S.
A role for branched-chain amino acids in reducing central fatigue.

Blomstrand E.

Astrand Laboratory, University College of Physical Education and Sports and Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. eva.blomstrand@gih.se

Several factors have been identified to cause peripheral fatigue during exercise, whereas the mechanisms behind central fatigue are less well known. Changes in the brain 5-hydroxytryptamine (5-HT) level is one factor that has been suggested to cause fatigue. The rate-limiting step in the synthesis of 5-HT is the transport of tryptophan across the blood-brain barrier. This transport is influenced by the fraction of tryptophan available for transport into the brain and the concentration of the other large neutral amino acids, including the BCAAs (leucine, isoleucine, and valine), which are transported via the same carrier system. Studies in human subjects have shown that the plasma ratio of free tryptophan (unbound to albumin)/BCAAs increases and that tryptophan is taken up by the brain during endurance exercise, suggesting that this may increase the synthesis of 5-HT in the brain. Ingestion of BCAAs increases their concentration in plasma. This may reduce the uptake of tryptophan by the brain and also 5-HT synthesis and thereby delay fatigue. Accordingly, when BCAAs were supplied to human subjects during a standardized cycle ergometer exercise their ratings of perceived exertion and mental fatigue were reduced, and, during a competitive 30-km cross-country race, their performance on different cognitive tests was improved after the race. In some situations the intake of BCAAs also improves physical performance. The results also suggest that ingestion of carbohydrates during exercise delays a possible effect of BCAAs on fatigue since the brain's uptake of tryptophan is reduced.

Publication Types:
Clinical Trial
Research Support, Non-U.S. Gov't

PMID: 16424144 [PubMed - indexed for MEDLINE]

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3: J Nutr. 2006 Jan;136(1 Suppl):274S-6S.
Branched-chain amino acids and central fatigue.

Newsholme EA, Blomstrand E.

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. eva.blomstrand@gih.se

An account of the tryptophan (Trp)-5-hydroxytryptamine (5-HT)-central fatigue theory is provided and an explanation of how oral administration of BCAAs can decrease fatigue on the basis of this theory is given. The rate-limiting step in the synthesis of 5-HT is the transport of Trp across the blood-brain barrier. This transport is influenced by the fraction of Trp available for transport into the brain and the concentration of the other large neutral amino acids, including the BCAAs, which are transported via the same carrier system. During endurance exercise, there is an uptake of Trp by the brain, suggesting that this may increase the synthesis and release of 5-HT in the brain. Oral intake of BCAAs may reduce this uptake and also brain 5-HT synthesis and release, thereby delaying fatigue. Other hypotheses for the effect of BCAAs on central fatigue are included.

Publication Types:
Research Support, Non-U.S. Gov't

PMID: 16365097 [PubMed - indexed for MEDLINE]

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4: J Nutr. 2005 Jun;135(6 Suppl):1539S-46S.
Branched-chain amino acids and brain function.

Fernstrom JD.

Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, PA 15213, USA. fernstromjd@upmc.edu

Branched-chain amino acids (BCAAs) influence brain function by modifying large, neutral amino acid (LNAA) transport at the blood-brain barrier. Transport is shared by several LNAAs, notably the BCAAs and the aromatic amino acids (ArAAs), and is competitive. Consequently, when plasma BCAA concentrations rise, which can occur in response to food ingestion or BCAA administration, or with the onset of certain metabolic diseases (e.g., uncontrolled diabetes), brain BCAA concentrations rise, and ArAA concentrations decline. Such effects occur acutely and chronically. Such reductions in brain ArAA concentrations have functional consequences: biochemically, they reduce the synthesis and the release of neurotransmitters derived from ArAAs, notably serotonin (from tryptophan) and catecholamines (from tyrosine and phenylalanine). The functional effects of such neurochemical changes include altered hormonal function, blood pressure, and affective state. Although the BCAAs thus have biochemical and functional effects in the brain, few attempts have been made to characterize time-course or dose-response relations for such effects. And, no studies have attempted to identify levels of BCAA intake that might produce adverse effects on the brain. The only "model" of very high BCAA exposure is a very rare genetic disorder, maple syrup urine disease, a feature of which is substantial brain dysfunction but that probably cannot serve as a useful model for excessive BCAA intake by normal individuals. Given the known biochemical and functional effects of the BCAAs, it should be a straightforward exercise to design studies to assess dose-response relations for biochemical and functional effects and, in this context, to explore for adverse effect thresholds.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 15930466 [PubMed - indexed for MEDLINE]

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5: Am J Clin Nutr. 2000 Aug;72(2 Suppl):573S-8S.

Serotonin and central nervous system fatigue: nutritional considerations.

Davis JM, Alderson NL, Welsh RS.

Department of Exercise Science, School of Public Health, University of South Carolina, Columbia, SC 29208, USA.

Fatigue from voluntary muscular effort is a complex phenomenon involving the central nervous system (CNS) and muscle. An understanding of the mechanisms within muscle that cause fatigue has led to the development of nutritional strategies to enhance performance. Until recently, little was known about CNS mechanisms of fatigue, even though the inability or unwillingness to generate and maintain central activation of muscle is the most likely explanation of fatigue for most people during normal daily activities. A possible role of nutrition in central fatigue is receiving more attention with the development of theories that provide a clue to its biological mechanisms. The focus is on the neurotransmitter serotonin [5-hydroxytryptamine (5-HT)] because of its role in depression, sensory perception, sleepiness, and mood. Nutritional strategies have been designed to alter the metabolism of brain 5-HT by affecting the availability of its amino acid precursor. Increases in brain 5-HT concentration and overall activity have been associated with increased physical and perhaps mental fatigue during endurance exercise. Carbohydrate (CHO) or branched-chain amino acid (BCAA) feedings may attenuate increases in 5-HT and improve performance. However, it is difficult to distinguish between the effects of CHO on the brain and those on the muscles themselves, and most studies involving BCAA show no performance benefits. It appears that important relations exist between brain 5-HT and central fatigue. Good theoretical rationale and data exist to support a beneficial role of CHO and BCAA on brain 5-HT and central fatigue, but the strength of evidence is presently weak.

Publication Types:
Review

PMID: 10919962 [PubMed - indexed for MEDLINE]

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6: Eur J Appl Physiol Occup Physiol. 1999 Mar;79(4):318-24.
Effect of acute and chronic exercise on plasma amino acids and prolactin concentrations and on [3H]ketanserin binding to serotonin2A receptors on human platelets.

Strüder HK, Hollmann W, Platen P, Wöstmann R, Weicker H, Molderings GJ.

Institute of Sports Games, German Sport University, Cologne.

The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) has been shown to modulate various physiological and psychological functions such as fatigue. Altered regulation of the serotonergic system has been suggested to play a role in response to exercise stress. In the present study, the influence was investigated of acute endurance exercise and short-term increase in the amount of training on the concentrations of the 5-HT precursor tryptophan (TRP), of prolactin (PRL) and of branched-chain amino acids (BCAA) in the blood, as well as on the binding of [3H]ketanserin to the serotonin-2A (5-HT2A) receptors on platelets. Nine healthy endurance-trained men were tested the day before (I) and after (II) a 9-day training programme. Samples of venous blood were drawn after an overnight fast and following 5 h of cycling. Fasted and post-exercise plasma concentrations of free TRP, BCAA and free TRP:BCAA ratio did not differ between I and II. A significant decrease of plasma BCAA (P < 0.01) and significant augmentations of plasma free TRP, free TRP:BCAA ratio and PRL (P < 0.01) were found post-exercise. The increase in plasma PRL was smaller in II compared with I. Acute endurance exercise reduced the density of platelet 5-HT2A receptor [3H]ketanserin binding sites at I and II (P < 0.05). The basal density of the binding sites and the affinity of [3H]ketanserin for these binding sites were unaffected by an increase in the amount of training. The present results support the hypothesis that acute endurance exercise may increase 5-HT availability. This was reflected in the periphery by increased concentration of the 5-HT precursor free TRP, by increased plasma PRL concentration, and by a reduction of 5-HT2A receptors on platelets. It remains to be resolved whether these alterations in the periphery occur in parallel with an increase in the availability of 5-HT in the brain.

Publication Types:
Research Support, Non-U.S. Gov't

PMID: 10090630 [PubMed - indexed for MEDLINE]

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7: Adv Exp Med Biol. 1999;467:697-704.
The role of tryptophan in fatigue in different conditions of stress.

Castell LM, Yamamoto T, Phoenix J, Newsholme EA.

University Department of Biochemistry, Oxford, UK. cat@bioch.ox.ac.uk

Tryptophan is the precursor for the neurotransmitter 5-hydroxytryptamine (5-HT), which is involved in fatigue and sleep. It is present in bound and free from in the blood, where the concentration is controlled by albumin binding to tryptophan. An increase in plasma free tryptophan leads to an increased rate of entry of tryptophan into the brain. This should lead to a higher level of 5-HT which may cause central fatigue. Central fatigue is implicated in clinical conditions such as chronic fatigue syndrome and post-operative fatigue. Increased plasma free tryptophan leads to an increase in the plasma concentration ratio of free tryptophan to the branched chain amino acids (BCAA) which compete with tryptophan for entry into the brain across the blood-brain barrier. The plasma concentrations of these amino acids were measured in chronic fatigue syndrome patients (CFS) before and after exercise (Castell et al., 1998), and in patients undergoing major surgery (Yamamoto et al., 1997). In the CFS patients, the pre-exercise concentration of plasma free tryptophan was higher than in controls (p < 0.05) but did not change during or after exercise. This might indicate an abnormally high level of brain 5-HT in CFS patients leading to persistent fatigue. In the control group, plasma free tryptophan was increased after maximal exercise (p < 0.001), returning towards baseline levels 60 min later. The apparent failure of the CFS patients to change the plasma free tryptophan concentration or the free tryptophan/BCAA ratio during exercise may indicate increased sensitivity of brain 5-HT receptors, as has been demonstrated in other studies (Cleare et al., 1995). In post-operative recovery after major surgery plasma free tryptophan concentrations were markedly increased compared with baseline levels; the plasma free tryptophan/BCAA concentration ratio was also increased after surgery. Plasma albumin concentrations were decreased after surgery: this may account for the increase in plasma free tryptophan levels. Provision of BCAA has improved mental performance in athletes after endurance exercise (Blomstrand et al., 1995, 1997). It is suggested that BCAA supplementation may help to counteract the effects of an increase in plasma free tryptophan, and may thus improve the status of patients during or after some clinically stressful conditions.

Publication Types:
Review

PMID: 10721121 [PubMed - indexed for MEDLINE]

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8: Med Sci Sports Exerc. 1997 Jan;29(1):58-62.
Effects of acute physical exercise on central serotonergic systems.

Chaouloff F.

Génétique du Stress, INSERM CJF 94-05, Université Bordeaux II, France.

This paper reviews data concerning the effects of acute physical exercise (treadmill running) in trained rats. Works from the 1980's have established that acute running increases brain serotonin (5-hydroxytryptamine: 5-HT) synthesis in two ways. Lipolysis-elicited release of free fatty acids in the blood compartment displaces the binding of the essential amino acid tryptophan to albumin, thereby increasing the concentration of the so-called "free tryptophan" portion, and because exercise increases the ratio of circulating free tryptophan to the sum of the concentrations of the amino acids that compete with tryptophan for uptake at the blood-brain barrier level, tryptophan enters markedly in the brain compartment. However, this marked increase in central tryptophan levels increases only to a low extent brain 5-HT synthesis, as assessed by the analysis of 5-hydroxyindoleacetic acid levels, thereby suggesting that exercise promotes feedback regulatory mechanisms. Indirect indices of 5-HT functions open the possibility that acute exercise-induced increases in 5-HT biosynthesis are associated with (or lead to) increases in 5-HT release. Lastly, the hypothesis that training and/or acute exercise triggers changes in 5-HT receptors has been examined in several studies; actually, both positive and negative results have been reached. Taken together, all these data support the need for future studies on the functional effects of exercise on 5-HT, including those related to the hypothesis that the positive mood effects of exercise rely (partly or totally) on central serotonergic systems.

Publication Types:
Review

PMID: 9000156 [PubMed - indexed for MEDLINE]

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9: J Physiol. 1995 Aug 1;486 ( Pt 3):789-94.
Ingestion of branched-chain amino acids and tryptophan during sustained exercise in man: failure to affect performance.

van Hall G, Raaymakers JS, Saris WH, Wagenmakers AJ.

Department of Human Biology, University of Limburg, Maastricht, The Netherlands.

1. An increased uptake of tryptophan in the brain may increase serotoninergic activity and recently has been suggested to be a cause of fatigue during prolonged exercise. The present study, therefore, investigates whether ingestion of tryptophan or the competing branched-chain amino acids (BCAAs) affect performance. Ten endurance-trained male athletes were studied during cycle exercise at 70-75% maximal power output, while ingesting, ad random and double-blind, drinks that contained 6% sucrose (control) or 6% sucrose supplemented with (1) tryptophan (3 g l-1), (2) a low dose of BCAA (6 g l-1) or (3) a high dose of BCAA (18 g l-1). 2. These treatments greatly increased the plasma concentration of the respective amino acids. Using the kinetic parameters of transport of human brain capillaries, BCAA supplements were estimated to reduce brain tryptophan uptake at exhaustion by 8-12%, while tryptophan ingestion caused a 7- to 20-fold increase. Exercise time to exhaustion was not different between treatments (122 +/- 3 min). 3. The data suggest that manipulation of tryptophan supply to the brain either has no additional effect upon serotoninergic activity during prolonged exhaustive exercise or that manipulation of serotoninergic activity functionally does not contribute to mechanisms of fatigue.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 7473239 [PubMed - indexed for MEDLINE]
PMCID: PMC1156566


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10: J Sports Sci. 1995 Summer;13 Spec No:S49-53.Related Articles, Links
Central and peripheral factors in fatigue.

Davis JM.

Department of Exercise Science, University of South Carolina, Columbia 29208, USA.

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.

Publication Types:
Review

PMID: 8897320 [PubMed - indexed for MEDLINE]

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11: Int J Sports Med. 1995 Apr;16(3):155-9.
Serum amino acid concentrations in nine athletes before and after the 1993 Colmar ultra triathlon.

Lehmann M, Huonker M, Dimeo F, Heinz N, Gastmann U, Treis N, Steinacker JM, Keul J, Kajewski R, Häussinger D.

Department of Sports and Performance Medicine, University Medical Hospital, Freiburg, Germany.

The amino acid imbalance hypothesis should explain the fatigue originating in the brain during sustained exercise or over-training as a branched-chain (BCAA)/aromatic amino acids (AAA) imbalance with increased brain tryptophan uptake and 5-hydroxytryptamine synthesis. The serum amino acid profile was determined in 9 ultra-triathletes before and after completing the 1993 Colmar ultra-triathlon to additionally analyse the extent of this amino acid imbalance during such an extreme prolonged contest lasting more than 23 hours. The summed serum concentration of 25 amino acids decreased by 18% from 3962 +/- 846 to 3255 +/- 694 umol.l-1 likely reflecting a catabolic state of the organism with a decrease in 18 individual amino acids by 9-56%, an increase in cystine (+38%), methionine (+24%), tyrosine (+10%), phenylalanine (+12%), free tryptophan (+74%), and constant glutamine, leucine and total tryptophan levels. Since plasma volume increased by approximately 7.6% with a 3.3 kg body mass decrease in the athletes during the ultra triathlon, a decrease in intra-cellular water with an extra-cellular fluid increase is hypothesized. This decrease in cellular hydration state is seen as a protein-catabolic signal.

PMID: 7649705 [PubMed - indexed for MEDLINE]

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12: Biochem Biophys Res Commun. 1986 May 29;137(1):149-53.
Effect of sustained exercise on concentrations of plasma aromatic and branched-chain amino acids and brain amines.

Acworth I, Nicholass J, Morgan B, Newsholme EA.

In both trained and untrained rats, exercise increased the plasma concentration ratio of aromatic amino acids to branched-chain amino acids which might favour entry of the aromatic amino acids into the brain. Exercise in trained rats did not change the brain concentration of 5-hydroxytryptamine but increased that of 5-hydroxyindole acetic acid. Exercise in the untrained rat increased the concentration of brain tryptophan and that of 5-hydroxytryptamine but that of 5-hydroxyindole acetic acid was unchanged. The increased concentration of 5-hydroxytryptamine in untrained rats might be involved in central fatigue.
 
Wait...I skimmed through the studies. What does 5-HTP have to do with the conumpstion of BCAAs in combination with fast acting carbs during peri-workout?
 
5-HT is made from tryptophan. Tryptophan is an amino acid "competing" against BCAAs for entry into the brain. The theory is that if your BCAA levels are high then tryptophans entry into the brain (where it can be made into 5-HT) will be slowed down.
 
Karky said:
5-HT is made from tryptophan. Tryptophan is an amino acid "competing" against BCAAs for entry into the brain. The theory is that if your BCAA levels are high then tryptophans entry into the brain (where it can be made into 5-HT) will be slowed down.
Click to expand...

I must've missed something cause I thought we were just discussing BCAAs and carbs during workouts.
 
yeah, but the effect of getting BCAAs during training is that less tryptophan gets transported into the brain. More BCAAs in the blood means more BCAA will be transported into the brain and then less tryptophan (they use the same transport system, so they compete against each other). And when the brain gets less tryptophan it won't synthesise as much 5-HT. All this will, according to the hypothesis, reduce central fatigue. It's far from proven, though.
 
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