Jonas Haferanke

Resting antioxidant enzyme activity in youth athletes may reflect stable individual redox characteristics and developmentally modulated plasticity. This 12-month longitudinal analysis from the MuCAYA^plus study examined the tracking of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in 69 trained athletes aged 10–17 years. Participants underwent repeated assessments of antioxidant enzyme activity, training exposure, body composition, and hematological parameters. Longitudinal tracking was evaluated using Pearson correlation and intraclass correlation coefficients, while change-score regression models tested whether changes in training exposure, growth-related variables, sex interactions, and hematological parameters predicted changes in SOD or GPX. In exploratory analyses, cluster-based redox phenotype stability was assessed using agreement statistics. Over 12 months, SOD decreased whereas GPX increased. GPX showed substantial tracking (r = 0.714, p < 0.001; ICC = 0.683), while SOD showed no meaningful tracking (r = 0.057, p = 0.644; ICC = 0.053). No statistically supported associations were detected between changes in training-exposure or growth-related measures and enzyme changes. Exploratory erythrocyte-related associations were observed for SOD, whereas leukocyte and platelet changes were unrelated. Cluster-based SOD/GPX phenotype analyses were not robust. These findings are compatible with a comparatively stronger trait-like component for GPX and greater state-like variability for SOD.

Adolescence is a critical window for cardiovascular (CV) development, yet the molecular drivers of vascular adaptation to regular exercise in youth remain poorly understood. This cross-sectional study assessed vascular structure and function alongside endothelial, metabolic, and lipoprotein biomarkers in 203 healthy young athletes (aged 10–16). Vascular phenotyping included carotid intima-media thickness (IMT), pulse wave velocity, and carotid deformation indices (strain, strain rate). Circulating nitric oxide (NO), endothelin-1, free triiodothyronine (fT3), leptin, low-density lipoprotein, and high-density lipoprotein were analyzed. Associations were examined using hierarchically adjusted multivariable linear regression, mediation and moderation were tested and sex-stratified/matched analyses were conducted. While training volume was not associated with endothelial markers, leptin was correlated positively with NO and negatively with diastolic strain rate, suggesting dual vascular actions. fT3 was inversely associated with IMT, indicating a potential protective role in vascular remodeling. Lipoprotein profiles showed no independent associations with vascular parameters. Hemodynamic load, particularly systolic blood pressure, emerged as the dominant determinant of arterial stiffness. Sex-specific differences across biomarkers and vascular indices support a multifactorial model: in active youth, vascular phenotype reflects hemodynamics, body composition, and endocrine–metabolic signals more than training; longitudinal mechanistic studies should clarify causal pathways and guide individualized cardiovascular risk profiling.

Maximal aerobic power (V̇O₂peak) in youth depends on hemoglobin (Hb)—mediated oxygen transport. While sex- and age-specific patterns are established in untrained cohorts, further research is needed in competitive adolescent athletes. We studied 124 young athletes matched by age and sex (62 boys, 62 girls; 10–16 years). Hb was measured from fasting blood samples, and V̇O₂peak was determined via cardiopulmonary exercise testing (CPET). Boys showed higher Hb than girls (14.43 ± 0.85 g/dL vs. 13.6 ± 0.74 g/dL; p < 0.001) and a significant age-related increase (B = 0.29, p < 0.001), whereas girls remained stable. V̇O₂peak was also higher in boys (50.03 ± 6.18 mL/min/kg, p < 0.001). Regression analysis identified Hb as a strong predictor of V̇O₂peak (β = 0.40, p < 0.001). These findings demonstrate that classical developmental Hb trajectories persist in highly trained youth and confirm Hb as a key determinant of aerobic power. Monitoring hematological status, particularly in female athletes, is essential for optimizing performance and development.

Oxidative stress is a key driver of endothelial dysfunction and early cardiovascular risk. Antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPX) are vital for vascular protection, especially during growth. While exercise-induced redox adaptations are well established in adults, data in pediatric athletes are limited. This cross-sectional study examined associations between training load and systemic antioxidant enzyme activity in 203 youth athletes aged 10–16 years, also considering sex, age, sports discipline, and redox phenotypes. Physical activity was assessed via validated questionnaires and expressed as weekly hours and MET-hours. Fasting blood samples were analyzed for SOD and GPX. Statistical tests included t-test, ANOVA, regression, and k-means clustering. Antioxidant enzyme levels were stable across training volumes, sports disciplines, and age groups. Boys showed significantly higher SOD than girls (259.43 ± 54.02 U/mL vs. 226.93 ± 48.22 U/mL, p < 0.001); GPX levels were similar between sexes. Cluster analysis identified three distinct redox profiles with differing training and sex distributions. No linear association was observed between training load and enzyme activity. Findings suggest that youth athletes exhibit robust antioxidant defenses, with individual and sex-related factors playing a more prominent role than training volume. These results highlight the value of regular physical activity for vascular health during development and the need for longitudinal studies to track redox adaptation.

Vasoactive molecules are central regulators of vascular tone, angiogenesis and inflammation. Key molecular agents include nitric oxide (NO), endothelin-1 (ET-1), prostacyclin, free triiodothyronine (fT3), leptin, low-density lipoprotein (LDL), high-density lipoprotein (HDL), superoxide dismutase (SOD), and glutathione peroxidase (GPX). Dysregulation of these compounds can lead to endothelial dysfunction, an early predictor of atherosclerosis and cardiovascular diseases (CVD). Maintaining endothelial health is thus essential for vascular homeostasis and cardiovascular risk prevention. Regular exercise serves as a vital protective measure against CVD and the risk of cardiovascular conditions. However, young athletes often significantly exceed recommended levels of training load, engaging in highly intensive training that leads to substantial physiological adaptations. Despite this, research on the impact of exercise on vasoactive substances in children and adolescents, particularly young athletes, is limited and inconsistent. Most studies focus on those with pre-existing conditions, like obesity or diabetes mellitus. Existing findings suggest exercise may favorably affect vascular biomarkers in youth, but methodological variations hinder consistent conclusions. This literature review examines 68 studies on the effects of exercise on vascular molecules in children and adolescents, young athletes, and children and adolescents with pre-existing conditions, offering deeper insights into how exercise may influence vascular health at the molecular level.

Background: Exercise has beneficial effects on cancer and its treatment, but the underlying mechanisms are poorly understood. Some studies have linked the positive impact of exercise to catecholamine signaling. In contrast, cancer stress studies have typically reported that catecholamines worsen cancer hallmarks and outcomes. Here, we aimed to investigate whether adrenergic receptor isoform expression can explain the contradictory effects of catecholamines in cancer. Methods: We cultured two pediatric sarcoma cancer cell lines that either express (A673 cell line) or do not express (RD cell line) adrenergic receptors. The cells were treated with a 5× dilution series of noradrenaline to assess the effects of noradrenaline on cell numbers. After these dose-finding experiments, we treated both cancer cell lines with 60 μM noradrenaline to examine its effect on cell proliferation and migration and cAMP signaling. Results: Treatment with 60 μM noradrenaline significantly decreased the cell numbers by 61.89% ± 10.36 (p ≤ 0.001), decreased cell proliferation by 15.88% ± 6.76 (p ≤ 0.05), decreased cell migration after 24 h (p ≤ 0.001), and increased cAMP concentrations 38-fold (p ≤ 0.001) in the A673 cells, which express adrenergic receptors, but not in the RD cells, which do not express adrenergic receptors. Conclusions: Our results indicate, as a proof of principle, that the effects of catecholamines on cancer progression and metastasis might depend on the expressions of the nine adrenergic receptor isoforms. As cancers express adrenergic and other receptors differentially, this has implications for the response of cancers to exercise, stress, and medication and may help to further personalize cancer treatments.