Changes in Plasma Concentration of Free Proteinogenic and Non-Proteinogenic Amino Acids in High-Performance Sprinters over a 6-Month Training Cycle

Background/Objectives: Free amino acids substantially contribute to energy metabolism. Also, their profile may identify (over)training status and effectiveness. The long-term effects of speed-power training on plasma free amino acid (PFAA) profiles are not known. We aimed to observe variations in PFAA levels in high-performance sprinters in a six-month training cycle. Methods: Ten male athletes (24.6 ± 3.3 years) were examined during four training phases: transition (1 month), general preparation (2 months), specific preparation (1 month), and pre-competition/competition (2 months). Venous blood was collected at rest, after exhaustive exercise, and recovery. Forty-two PFAAs were analyzed by the LC-ESI-MS/MS method. Results: Significant decreases in resting concentrations were observed between the transition and competition phases for glutamine (762 ± 117 vs. 623 ± 53 μmol∙L⁻¹; p < 0.001, η² = 0.47) and histidine (89 ± 15 vs. 75 ± 10 μmol∙L⁻¹; p = 0.010, η² = 0.27), whereas β-alanine (30 ± 7 vs. 41 ± 9 μmol∙L⁻¹; p = 0.024, η² = 016) and sarcosine (3.6 ± 0.4 vs. 4.8 ± 0.6 μmol∙L⁻¹; p = 0.006, η² = 0.188) levels increased. Between the specific and competition phases, significant decreases in the resting levels of 1-methylhistidine (22.1 ± 19.4 vs. 9.6 ± 8.8 μmol∙L⁻¹; p = 0.14, η² = 0.19), 3-methylhistidine (7.1 ± 1.5 vs. 6.5 ± 1.6 μmol∙L⁻¹; p = 0.009, η² = 0.18), citrulline (40 ± 10 vs. 29 ± 4 μmol∙L⁻¹; p = 0.05, η² = 0.29), and ornithine (74 ± 15 vs. 56 ± 10 μmol∙L⁻¹; p = 0.015, η² = 185) were noticed. Also, for β-alanine and sarcosine, the pattern of response to exercise strongly changed between the training phases. Blood ammonia levels at exhaustion decreased between the transition and competition phases (32 ± 4 vs. 23 ± 5 μmol∙L⁻¹; p < 0.001, η² = 0.67), while lactate, the phenylalanine–tyrosine ratio, the glutamine–glutamate ratio, hematological parameters, and cardiorespiratory indices remained at similar levels. Conclusions: Speed-power training seems to affect PFAAs involved in skeletal muscle metabolic pathways responsible for neutralizing toxic ammonia (glutamine, arginine, citrulline, ornithine), attenuating the deleterious effects of H⁺ ions (histidine, β-alanine), and reducing exercise-induced protein breakdown (1- and 3-methylhistidine). Our findings suggest that sprint-oriented training supports metabolic pathways that are responsible for the removal of harmful metabolites produced during exercise.