BCAAs reduce the levels of circulating free fatty-acids (FFA) in the blood. FFAs compete for binding sites on albumin with tryptophan, and when levels of FFAs in the blood are decreased, levels of free tryptophan also decrease as more is bound by albumin. During exercise, levels of free tryptophan entering the brain are increased, causing an increase in 5-hydroxytryptamine (5-HT, aka serotonin), a contributor to the sensation of fatigue. Through their reduction in levels of FFAs in the blood, BCAAs can help to reduce the levels of free tryptophan entering the brain, and help to reduce the sensation of fatigue as a result of exertion. The reduction in tryptophan uptake in the brain leads to a reduction in serotonin synthesis and release (in rats.) The reduction in serotonin can be as great as 90%; low levels of serotonin decrease sensations of fatigue, but also leads to a lack of focus, poor impulse control, aggressive behavior and poor planning. BCAA also inhibits tyrosine uptake in the brain (tyrosine being another aromatic amino acid, like tryptophan); the reduced uptake depresses catecholamine synthesis and release in the brain. Catecholamines are associated with enhanced physical performance. The simultaneous reductions in both catecholamine and serotonin synthesis may account for the relatively neutral effect of BCAA on physical performance. BCAAs are also found to reduce the increase in serum levels of ammonia that occurs during exercise. This is done by increasing the amount of ammonia used in glutamine synthesis, preventing an over-accumulation of ammonia in the blood. Increased levels of ammonia in the brain result in lower levels of GABA and glutamate, causing an increase in central fatigue. Increased levels of ammonia in the muscle tissue also increase phosphofructokinase activity (PFK), leading to an increase in lactic acid, a major contributor to muscle fatigue. In addition, BCAA supplementation has been shown to decrease levels of creatine kinase in muscle cells post exercise. Creatine kinase is an indicator of muscle damage, and is responsible for transferring a phosphate group from ATP to create a phosphocreatine molecule. BCAA supplementation has been shown to decrease levels of creatine kinase, leading to higher levels of intracellular ATP and a lessened sense of fatigue. See also DOMS. See also Branched-chain alpha-keto acid dehydrogenase complex Maple syrup urine disease - excessive accumulation of BCAA in the organism BCKDK deficiency - insufficient levels of BCAA in the organism References External links Branched-chain amino