The purpose of this study was to explore the association of the MCT1 gene Glu490Asp polymorphism (rs1049434) with athletic status and performance of endurance athletes. A total of 1,208 Brazilians (318 endurance athletes and 890 non-athletes) and 867 Europeans (315 endurance athletes and 552 non-athletes) were evaluated in a case–control approach. Brazilian participants were classified based on self-declared ethnicity to test whether the polymorphism was different between Caucasians and Afro-descendants. Moreover, 66 Hungarian athletes underwent an incremental test until exhaustion to assess blood lactate levels, while 46 Russian athletes had their maximum oxygen uptake ( ) compared between genotypes. In the Brazilian cohort, the major T-allele was more frequent in Caucasian top-level competitors compared to their counterparts of lower competitive level (P = 0.039), and in Afro-descendant athletes compared to non-athletes (P = 0.015). Similarly, the T-allele was more frequent in European athletes (P = 0.029). Meta-analysis of the Brazilian and European cohorts confirmed that the T-allele is over-represented in endurance athletes (OR: 1.48, P = 0.03), especially when Afro-descendant athletes were included in the meta-analysis (OR: 1.58, P = 0.005). Furthermore, carriers of the T/T genotype accumulated less blood lactate in response to intense effort (P < 0.01) and exhibited higher (P = 0.04) . In conclusion, the Glu490Asp polymorphism was associated with endurance athletic status and performance. Our findings suggest that, although ethnic differences may exist, the presence of the major T-allele (i.e., the Glu-490 allele) favours endurance performance more than the mutant A-allele (i.e., the 490-Asp allele).

Background: Continuously rising performances in elite adolescent athletes requires increasing training loads. This training overload without professional monitoring, could lead to overtraining in these adolescents. Methods: 31 elite adolescent athletes (boys: n = 19, 16 yrs; girls: n = 12, 15 yrs) participated in a field-test which contained a unified warm-up and a 200 m maximal freestyle swimming test. Saliva samples for testosterone (T) in boys, estradiol (E) in girls and cortisol (C) in both genders were collected pre-, post- and 30 min post-exercise. Lactate levels were obtained pre- and post-exercise. Brunel Mood Scale, Perceived Stress Scale and psychosomatic symptoms questionnaires were filled out post-exercise. Results: Lactate levels differed between genders (boys: pre: 1.01 ± 0.26; post: 8.19 ± 3.24; girls: pre: 0.74 ± 0.23; post: 5.83 ± 2.48 mmol/L). C levels increased significantly in boys: pre- vs. post- (p = 0.009), pre- vs. 30 min post-exercise (p = 0.003). The T level (p = 0.0164) and T/C ratio (p = 0.0004) decreased after field test which draws attention to the possibility of overtraining. Maximal and resting heart rates did not differ between genders; however, heart rate recovery did (boys: 29.22 ± 7.4; girls: 40.58 ± 14.50 beats/min; p = 0.008). Conclusions: Our models can be used to explain the hormonal ratio changes (37.5–89.8%). Based on the results this method can induce hormonal response in elite adolescent athletes and can be used to notice irregularities with repeated measurements.

Apelin, as a cardiokine/myokine, is emerging as an important regulator of cardiac and skeletal muscle homeostasis. Loss of apelin signaling results in premature cardiac aging and sarcopenia. However, the contribution of apelin to peak athletic performance remains largely elusive. In this paper, we assessed the impact of maximal cardiorespiratory exercise testing on the plasma apelin levels of 58 male professional soccer players. Circulating apelin-13 and apelin-36, on average, increased transiently after a single bout of treadmill exercise; however, apelin responses (Δapelin = peak − baseline values) showed a striking interindividual variability. Baseline apelin-13 levels were inversely correlated with those of Δapelin-13 and Δapelin-36. Δapelin-13 showed a positive correlation with the maximal metabolic equivalent, relative maximal O2 consumption, and peak circulatory power, whereas such an association in the case of Δapelin-36 could not be detected. In conclusion, we observed a pronounced individual-to-individual variation in exercise-induced changes in the plasma levels of apelin-13 and apelin-36. Since changes in plasma apelin-13 levels correlated with the indicators of physical performance, whole-body oxygen consumption and pumping capability of the heart, apelin, as a novel exerkine, may be a determinant of peak athletic performance.

Athletes are often exposed to extreme physical stress during training or competitions. The consequent activation of the hypothalamus–hypophysis–adrenal (HPA) axis results in intensified steroid hormone production in the adrenal cortex. We determined the impact of an acute extreme physical stress on adrenal and gonadal steroidogenesis in healthy male professional athletes (n = 40). The subjects underwent an extreme physical load test until total voluntary fatigue between 14:00 and 18:00 when the hormone levels are relatively stable. Blood was taken before the start (baseline), at the peak load (peak), and 30 min following completion of the exercise (recovery). The vital parameters, lactate levels, and blood levels of the 14 steroid hormones were recorded. The multivariate statistical analysis of the results revealed that all monitored hormone levels increased upon stress. Significant changes in steroid concentrations were detected at peak versus baseline, peak versus recovery, and at baseline versus recovery. The mineralocorticoid (including aldosterone and corticosterone), glucocorticoid (11-deoxycortisol and cortisol), and androgen (androstenedione, dehydroepiandrosterone, and dehydroepiandrosterone sulfate) pathways, as well as gonadal testosterone synthesis are activated simultaneously under extreme physical load. The profiling of adrenal and gonadal steroid biosynthesis in athletes may help the characterization of their loading capacity.

No abstract