Oral Branched-Chain Amino Acid Supplements That Reduce Brain Serotonin During Exercise in Rats Also Lower Brain Catecholamines

Exercise raises brain serotonin release and is postulated to cause fatigue in athletes; ingestion of branched-chain amino acids (BCAA), by competitively inhibiting tryptophan transport into brain, lowers brain tryptophan uptake and serotonin synthesis and release in rats, and reputedly in humans prevents exercise-induced increases in serotonin and fatigue. This latter effect in humans is disputed. But BCAA also competitively inhibit tyrosine uptake into brain, and thus catecholamine synthesis and release. Since increasing brain catecholamines enhances physical performance, BCAA ingestion could lower catecholamines, reduce performance and thus negate any serotonin-linked benefit. We therefore examined in rats whether BCAA would reduce both brain tryptophan and tyrosine concentrations and serotonin and catecholamine synthesis. Sedentary and exercising rats received BCAA or vehicle orally; tryptophan and tyrosine concentrations and serotonin and catecholamine synthesis rates were measured 1 h later in brain. BCAA reduced brain tryptophan and tyrosine concentrations, and serotonin and catecholamine synthesis. These reductions in tyrosine concentrations and catecholamine synthesis, but not tryptophan or serotonin synthesis, could be prevented by co-administering tyrosine with BCAA. Complete essential amino acid mixtures, used to maintain or build muscle mass, were also studied, and produced different effects on brain tryptophan and tyrosine concentrations and serotonin and catecholamine synthesis. Since pharmacologically increasing brain catecholamine function improves physical performance, the finding that BCAA reduce catecholamine synthesis may explain why this treatment does not enhance physical performance in humans, despite reducing serotonin synthesis. If so, adding tyrosine to BCAA supplements might allow a positive action on performance to emerge

Mechanisms for Sweetness123

A remarkable amount of information has emerged in the past decade regarding sweet taste physiology. This article reviews these data, with a particular focus on the elucidation of the sweet taste receptor, its location and actions in taste transduction in the mouth, its nontaste functions in the gastrointestinal tract (e.g., in enteroendocrine cells), and the brain circuitry involved in the sensory processing of sweet taste. Complications in the use of rodents to model human sweet taste perception and responses are also considered. In addition, information relating to low-calorie sweeteners (LCS) is discussed in the context of these issues. Particular consideration is given to the known effects of LCS on enteroendocrine cell function

The ingestion of different dietary proteins by humans induces large changes in the plasma tryptophan ratio, a predictor of brain tryptophan uptake and serotonin synthesis.

Background & aimsThe ingestion by rats of different proteins causes large differences in the plasma ratio of tryptophan to other large neutral amino acids, which predicts brain tryptophan uptake and serotonin synthesis. We evaluated in humans whether ingesting these proteins also produces large excursions in the tryptophan ratio.MethodsFasting males (n = 6) ingested V-8 Juice containing 40 g of α-lactalbumin, gluten, zein or starch. Blood was drawn before and at 30 min intervals after ingestion for 4 h; tryptophan and other large neutral amino acids were quantitated.ResultsPre-meal plasma tryptophan was ~50 nmol/ml; the tryptophan ratio was ~0.010. α-Lactalbumin increased plasma tryptophan (3-fold) and the tryptophan ratio (50%); starch did not change either tryptophan variable, while gluten caused a modest (25%) and zein a large reduction (50%) in plasma tryptophan. Gluten and zein reduced the tryptophan ratio. The maximal difference in the tryptophan ratio occurred between α-lactalbumin and zein and was large (~3-fold).ConclusionSince the plasma tryptophan ratio predicts brain tryptophan uptake and serotonin synthesis in rats, the differences in the ratio produced in humans by these proteins may modify serotonin synthesis, and perhaps elicit serotonin-linked changes in behavior

The ingestion of different dietary proteins by humans induces large changes in the plasma tryptophan ratio, a predictor of brain tryptophan uptake and serotonin synthesis.

Background & aimsThe ingestion by rats of different proteins causes large differences in the plasma ratio of tryptophan to other large neutral amino acids, which predicts brain tryptophan uptake and serotonin synthesis. We evaluated in humans whether ingesting these proteins also produces large excursions in the tryptophan ratio.MethodsFasting males (n = 6) ingested V-8 Juice containing 40 g of α-lactalbumin, gluten, zein or starch. Blood was drawn before and at 30 min intervals after ingestion for 4 h; tryptophan and other large neutral amino acids were quantitated.ResultsPre-meal plasma tryptophan was ~50 nmol/ml; the tryptophan ratio was ~0.010. α-Lactalbumin increased plasma tryptophan (3-fold) and the tryptophan ratio (50%); starch did not change either tryptophan variable, while gluten caused a modest (25%) and zein a large reduction (50%) in plasma tryptophan. Gluten and zein reduced the tryptophan ratio. The maximal difference in the tryptophan ratio occurred between α-lactalbumin and zein and was large (~3-fold).ConclusionSince the plasma tryptophan ratio predicts brain tryptophan uptake and serotonin synthesis in rats, the differences in the ratio produced in humans by these proteins may modify serotonin synthesis, and perhaps elicit serotonin-linked changes in behavior