c'est un gros facteur limitant de la progression et on n'a peu de suppléments qui adresse se problème.
Là, les BCAA réduisent la sécrétion de sérotonine (ce qui est bien) et de noradrénaline (ce qui n'est pas bien)
la tyrosine réduit ce problème
on a là un stack booster si on rajoute de la caféine
Branched-Chain Amino Acid Administration Reduces Both Serotonin and Catecholamine Synthesis Rates in Rat Brain
Medicine & Science in Sports & Exercise:Volume 40(5) Supplement 1May 2008p S299
Fernstrom, John D.; DiSilvio, Briana; Choi, SuJean; Fernstrom, Madelyn H.
University of Pittsburgh School of Medicine, Pittsburgh, PA.
Email: fernstromjd@upmc.edu
(J.D. Fernstrom, The sponsor of this research, Amino Vital Sports Science Foundation, is supported by Ajiinomoto USA, for which I am an occasional consultant, Consulting Fee.)
Branched-chain amino acid (BCAA) administration is thought to reduce "central fatigue" during exercise by reducing brain tryptophan (TRP) uptake & serotonin (5HT) synthesis (& neuronal release). However, this treatment may also reduce tyrosine (TYR) uptake into brain & catecholamine (CAM; dopamine & norepinephrine) synthesis/release, because (a) elevating blood BCAA levels retards TYR uptake into brain, just as it does TRP uptake, and (b) catecholamine (CAM) synthesis & neuronal release are linked to the supply of TYR, the CAM precursor. Reduced CAM synthesis/ release would be expected to promote fatigue.
PURPOSE: To determine if oral BCAA administration to rats reduces TYR levels and catecholamine synthesis rate in brain.
METHODS: Groups of 10 sedentary, fasting, adult male rats received vehicle or a mixture of BCAA, glutamine and arginine (BCAA dose = 268 mg/kg) by stomach tube (dose based on Smriga M et al., Nutritional Neuroscience 5: 189, 2002), followed 30 minutes later by m-hydroxybenzylhydrazine (NSD-1015, 100 mg/kg ip, an inhibitor of aromatic L-amino acid decarboxylase, to allow 5-hydroxytryptophan (5HTP) & dihydroxyphenylalanine (DOPA) levels to accumulate). They were killed 30 minutes later, & blood & brain samples were collected. Blood & brain samples were assayed for TRP, TYR, the BCAA, 5HTP & DOPA by HPLC/electrochemical detection. 5HTP & DOPA accumulate linearly for 30 minutes after NSD-1015, and provide good in vivo indices of 5HT & CAM synthesis rates, respectively (Carlsson A et al., Naunyn Schmiedbergs Arch Pharmacol 303: 157, 1978).
RESULTS: BCAA intubation markedly raised serum BCAA levels, & reduced brain levels of TRP (vehicle, 8.1 ± 0.6; BCAA, 4.1 ± 0.4 nmol/gram, mean ± sem, P < 0.01, t-test) and TYR (vehicle, 54.6 ± 1.4; BCAA, 28.4 ± 2.0 nmol/gram, P < 0.01). BCAA treatment also reduced both 5HT synthesis (vehicle, 90 ± 6; BCAA, 36 ± 2 ng/g, P < 0.01) & CAM synthesis (vehicle, 351 ± 35; BCAA, 219 ± 23 ng/g, P < 0.01) rates in brain. Similar results were obtained in exercising rats.
CONCLUSIONS: Because CAM synthesis rate is linked to CAM release, BCAA may reduce neuronal CAM release in brain, as it does 5HT release. While reduced 5HT release may improve central fatigue, reduced CAM release should promote central fatigue. The addition of TYR to oral BCAA mixtures may prevent CAM reductions.