Ewa Anna Zarębska

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.

Background/Objectives: A high level of specific metabolic capacity is essential for maximal sprinting in both male and female athletes. Various factors dictate sex differences in maximal power production and energy utilization. This study aims to compare the contribution of energy systems between male and female athletes with similar sport-specific physiological adaptations during a 15-s sprint exercise. Methods: The endurance group consisted of 17 males (23 ± 7 y) and 17 females (20 ± 2 y). The speed-power group included 14 males (21.1 ± 2.6 y) and 14 females (20 ± 3 y). The contribution of phosphagen, glycolytic, and aerobic systems was determined using the three-component PCr-LA-O₂ method. Results: Significant differences were observed in the energy expenditure for all systems and total energy expenditure between males and females in both groups (p = 0.001–0.013). The energy expenditure in kJ for individual systems (phosphagen–glycolytic–aerobic) was 35:25:7 vs. 20:16:5 in endurance males vs. female athletes, respectively. In the speed-power group, male athletes expended 33:37:6 kJ and female athletes expended 21:25:4 kJ, respectively. The percentage proportions did not differ between males and females in any system. The contribution of the phosphagen–glycolytic–aerobic systems was 52:37:11 vs. 48:39:13 in endurance male and female athletes, respectively. For speed-power males vs. female athletes, the proportions were 42:50:8 vs. 41:50:9, respectively. Conclusions: Despite the differences in body composition, mechanical output, and absolute energy expenditure, the energy system contribution appears to have a similar metabolic effect between male and female athletes engaged in sprint exercises with similar sport-related adaptations. The magnitude and profile of sex differences are related to sports discipline.

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; η² = 0.216), phenylalanine (p = 0.015; η² = 0.153), methionine (p = 0.002; η² = 0.206), and lysine (p = 0.006; η² = 0.196) declined more rapidly between rest and exhaustion in the competition phase. Glutamine (p = 0.008; η² = 0.255), glutamate (p = 0.006; η² = 0.265), tyrosine (p = 0.001; η² = 0.195), cystine (p = 0.042; η² = 0.183), and serine (p < 0.001; η² = 0.346) levels were reduced in the competition phase. Arginine (p = 0.046; η² = 0.138) and aspartate (p = 0.011; η² = 0.171) levels were highest during exercise in the transition phase. During the competition phase, α-aminoadipic acid (p = 0.023; η² = 0.145), β-aminoisobutyric acid (p = 0.007; η² = 0.167), β-alanine (p < 0.001; η² = 0.473), and sarcosine (p = 0.017; η² = 0.150) levels increased, whereas phosphoethanolamine (p = 0.037; η² = 0.189) and taurine (p = 0.008; η² = 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.

This study aimed to assess the effect of training loads on plasma adenosine triphosphate responsiveness in highly trained athletes in a 1 y cycle. Highly trained futsal players (11 men, age range 20–31 y), endurance athletes (11 men, age range 18–31 y), sprinters (11 men, age range 21–30 y), and control group (11 men, age range 22–34 y) were examined across four characteristic training phases in response to an incremental treadmill test until exhaustion. A considerably higher exercise and post-exercise plasma adenosine triphosphate concentrations were observed in consecutive training phases in highly trained athletes, with the highest values reached after the competitive period. No differences in plasma adenosine triphosphate concentrations were found in the control group during the 1 y cycle. Sprinters showed a higher absolute and net increase in plasma adenosine triphosphate concentration by 60–114% during exercise in consecutive training phases than futsal players (63–101%) and endurance athletes (64–95%). In this study, we demonstrated that exercise-induced adenosine triphosphate concentration significantly changes in highly trained athletes over an annual training cycle. The obtained results showed that high-intensity but not low- to moderate-intensity training leads to an increased adenosine triphosphate response to exercise, suggesting an important role of ATP for vascular plasticity.

Summary: Study aim: To compare the blood ammonia and lactate concentrations in sprinters and triathletes during an incremental treadmill exercise test and in the 30 minutes of recovery. Material and methods: The study included 10 male sprinters and 14 male triathletes who compete at the national and international level. A treadmill test until exhaustion was administered. Blood samples for ammonia and lactate were obtained when the athletes were at rest, during and immediately after exercise, and between 5 and 30 min after exercise. Results: The ammonia concentration and time course were similar in the sprinters and triathletes (F = 1.81, p ≥ 0.05, η2 = 0.08). An exercise-related increase in blood ammonia was almost linear, regardless of the exercise intensity. In the case of lactate, the interactions between the concentrations measured in the sprinters and triathletes were statistically significant (F = 5.78, p ≤ 0.001, η2 = 0.21). Post-hoc tests revealed that the lactate concentrations differed significantly between the sprinters and triathletes in the 18th min (p ≤ 0.01) and the 21st min (p ≤ 0.001) of the exercise test. The blood lactate increased in a nonlinear manner (slowly at lower intensities and rapidly at higher intensities). During the 30 min recovery period, both the ammonia and lactate levels decreased linearly. However, in the sprinters, the peak values were maintained in the first stage of recovery (5 min post-exercise). Conclusions: The study showed that the blood ammonia concentration may be a useful marker of exercise-related metabolic responses in sprint-trained as well as in endurance-trained competitive athletes. Blood ammonia levels were more intensity-sensitive across the whole intensity range during the incremental exercise when compared to the blood lactate levels.