Changes in Plasma Free Amino Acid Profile in Endurance Athletes over a 9-Month Training Cycle.
Krzysztof KusyMonika Ciekot-SołtysiakLeszek PawelczykAgnieszka KlupczynskaSzymon PlewaEwa Anna ZarębskaZenon J KokotPaweł DerezińskiJacek ZielinskiPublished in: Metabolites (2024)
We aimed to evaluate long-term changes in proteinogenic and non-proteinogenic plasma free amino acids (PFAA). Eleven male endurance triathletes participated in a 9-month study. Blood was collected at rest, immediately after exhaustive exercise, and during 30-min recovery, in four consecutive training phases: transition, general, specific, and competition. Twenty proteinogenic and 22 non-proteinogenic PFAAs were assayed using the LC-ESI-MS/MS technique. The structured training modified the patterns of exercise-induced PFAA response, with the competition phase being the most distinct from the others. Branched-chain amino acids ( p = 0.002; η 2 = 0.216), phenylalanine ( p = 0.015; η 2 = 0.153), methionine ( p = 0.002; η 2 = 0.206), and lysine ( p = 0.006; η 2 = 0.196) declined more rapidly between rest and exhaustion in the competition phase. Glutamine ( p = 0.008; η 2 = 0.255), glutamate ( p = 0.006; η 2 = 0.265), tyrosine ( p = 0.001; η 2 = 0.195), cystine ( p = 0.042; η 2 = 0.183), and serine ( p < 0.001; η 2 = 0.346) levels were reduced in the competition phase. Arginine ( p = 0.046; η 2 = 0.138) and aspartate ( p = 0.011; η 2 = 0.171) levels were highest during exercise in the transition phase. During the competition phase, α-aminoadipic acid ( p = 0.023; η 2 = 0.145), β-aminoisobutyric acid ( p = 0.007; η 2 = 0.167), β-alanine ( p < 0.001; η 2 = 0.473), and sarcosine ( p = 0.017; η 2 = 0.150) levels increased, whereas phosphoethanolamine ( p = 0.037; η 2 = 0.189) and taurine ( p = 0.008; η 2 = 0.251) concentrations decreased. Overtraining indicators were not elevated. The altered PFAA profile suggests adaptations within energy metabolic pathways such as the tricarboxylic acid cycle, oxidative phosphorylation, ammonia neutralization, the purine nucleotide cycle, and buffering of intracellular H + ions. The changes seem to reflect normal adaptations.