Essential amino acid supplements ingestion has a positive effect on executive function after moderate-intensity aerobic exercise.

Aerobic exercise acutely improves cognitive function (e.g., executive function (EF); memory recognition (MR)) and increases circulating brain-derived neurotrophic factor (BDNF). In addition, branched-chain amino acids (BCAA) ingestion acutely shortens the choice reaction time and increases brain BDNF. We examined whether the ingestion of essential amino acid (EAA) supplements (mainly composed of BCAA) would positively impact on cognitive function and circulating BDNF after moderate-intensity aerobic exercise. Twenty-two healthy young men received either an EAA supplements or the placebo (PL) 30 min before undergoing aerobic exercise. The participants performed a cycling exercise at 60% of peak oxygen uptake for 30 min. EF after aerobic exercise was better after the EAA treatment than after the PL treatment (P = 0.02). MR (P = 0.38 for response accuracy; P = 0.15 for reaction time) and circulating BDNF (P = 0.59) were not altered by EAA supplements. EF improvement was correlated with increases in some amino acids (leucine, isoleucine, valine, lysine, phenylalanine; all Ps < 0.05) that are potential substrates for synthesizing neurotransmitters in the brain. These results suggest that EAA supplements ingestion had a positive effect on EF after moderate-intensity aerobic exercise, while MR and BDNF were not altered.

Effects of Five Amino Acids (Serine, Alanine, Glutamate, Aspartate, and Tyrosine) on Mental Health in Healthy Office Workers: A Randomized, Double-Blind, Placebo-Controlled Exploratory Trial.

BACKGROUND: The importance of maintaining good mental health with overall well-being has recently drawn attention from various spheres of academics and the working population. Amino acid intake has been reported to reduce depression symptoms and other mental health problems. However, the effectiveness of amino acid intake (i.e., single or combined) remains unknown. In this study, we assessed a combination of five amino acids (serine, alanine, glutamate, aspartate, and tyrosine; SAGAT) reported to regulate mental health. METHODS: A randomized, double-blind, placebo-controlled exploratory trial was conducted. Participants, aged between 20 and 65 years with fatigue sensation, were randomized to receive either SAGAT or the placebo and ingested them for four weeks. A transient mental work was loaded at day 0 and after four weeks of intervention. As the primary outcomes, the fatigue sensation was assessed. The mood status, cognitive function, work efficiency, and blood marker were also measured as secondary outcomes. RESULTS: The number of participants analyzed for the efficacy evaluation were 20 in SAGAT and 22 in the placebo. There were no significant differences in the primary outcomes. However, as the secondary outcomes, the SAGAT group showed a significant improvement in motivation and cognitive function in the recovery period after mental work loaded in a four-week intervention compared to the placebo. CONCLUSION: The current findings suggest that SAGAT contributes to maintaining proper motivation and cognitive function. CLINICAL TRIAL REGISTRATION: University Hospital Medical Information Network Clinical Trial Registry (ID: UMIN 000041221).

Neurodegenerative processes accelerated by protein malnutrition and decelerated by essential amino acids in a tauopathy mouse model.

Protein malnutrition is epidemiologically suggested as a potential risk factor for senile dementia, although molecular mechanisms linking dietary proteins and amino acids to neurodegeneration remain unknown. Here, we show that a low-protein diet resulted in down-regulated expression of synaptic components and a modest acceleration of brain atrophy in mice modeling neurodegenerative tauopathies. Notably, these abnormal phenotypes were robustly rescued by the administration of seven selected essential amino acids. The up-regulation of inflammation-associated gene expression and progressive brain atrophy in the tauopathy model were profoundly suppressed by treatment with these essential amino acids without modifications of tau depositions. Moreover, the levels of kynurenine, an initiator of a pathway inducing neuroinflammatory gliosis and neurotoxicity in the brain, were lowered by treatment through inhibition of kynurenine uptake in the brain. Our findings highlight the importance of specific amino acids as systemic mediators of brain homeostasis against neurodegenerative processes.