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Context: The incidence of injury for elite youth and professional adult soccer players is an important concern, but the risk factors for these groups are different. Objective: To summarize and compare the injury incidences and injury characteristics of male professional adult and elite youth soccer players. Data Sources: We searched MEDLINE and Web of Science using the search terms elite , international , European , soccer , football , injury , injuries , epidemiology , incidence , prevalence , not female , not American football , and not rugby . We also used the search terms professional for studies on professional adult soccer players and high-level , soccer academy , youth , adolescent , and young for studies on elite youth soccer players. Study Selection: Eligible studies were published in English, had a prospective cohort design, and had a minimum study period of 6 months. To ensure that injury data were assessed in relationship to the athlete's individual exposure, we included only studies that reported on injuries and documented exposure volume. Data Extraction: Two independent reviewers applied the selection criteria and assessed the quality of the studies. Data Synthesis: A total of 676 studies were retrieved from the literature search. Eighteen articles met the inclusion criteria: 6 for elite youth and 12 for professional adult soccer players. Conclusions: Injury rates were higher for matches than for training for both youth and adult players. Youth players had a higher incidence of training injuries than professionals. Efforts must be made to reduce the overall injury rate in matches. Therefore, preventive interventions, such as adequately enforcing rules and focusing on fair play, must be analyzed and developed to reduce match-related injury incidences. Reducing training injuries should be a particular focus for youth soccer players.

Attempts to establish a biomarker reflecting individual player load in intermittent sports such as football have failed so far. Increases in circulating DNA (cfDNA) have been demonstrated in various endurance sports settings. While it has been proposed that cfDNA could be a suitable marker for player load in intermittent sports, the effects on cfDNA of repeated sprinting as an essential feature in intermittent sports are unknown. For the first time, we assessed both alterations of cfDNA due to repeated maximal sprints and due to a professional football game. Nine participants were subjected to a standardised sprint training session with cross-over design of five maximal sprints of 40 meters with either \"short\" (1 minute) or \"long\" pauses (5 minutes). Capillary cfDNA and lactate were measured after every sprint and venous cfDNA before and after each series of sprints. Moreover, capillary cfDNA and lactate values were taken in 23 professional football players before and after incremental exercise testing, during the course of a training week at rest (baseline) and in all 17 enrolled players following a season game. Lactate and venous cfDNA increased more pronounced during \"short\" compared to \"long\" (1.4-fold, p = 0.032 and 1.7-fold, p = 0.016) and cfDNA correlated significantly with lactate (r = 0.69; p<0.001). Incremental exercise testing increased cfDNA 7.0-fold (p<0.001). The season game increased cfDNA 22.7-fold (p<0.0001), while lactate showed a 2.0-fold (p = 0.09) increase compared to baseline. Fold-changes in cfDNA correlated with distance covered during game (spearman's r = 0.87, p = 0.0012), while no correlation between lactate and the tracking data could be found. We show for the first time that cfDNA could be an objective marker for distance covered in elite intermittent sports. In contrast to the potential of more established blood-based markers like IL-6, CK, or CRP, cfDNA shows by far the strongest fold-change and a high correlation with a particular load related aspect in professional football.

Background Doping in sports compromises fair play and endangers health. To deter doping among elite athletes, the World Anti-Doping Agency (WADA) oversees testing of several hundred thousand athletic blood and urine samples annually, of which 1–2% test positive. Measures using the Athlete Biological Passport suggest a higher mean prevalence of about 14% positive tests. Biological testing, however, likely fails to detect many cutting-edge doping techniques, and thus the true prevalence of doping remains unknown. Methods We surveyed 2167 athletes at two sporting events: the 13th International Association of Athletics Federations Word Championships in Athletics (WCA) in Daegu, South Korea in August 2011 and the 12th Quadrennial Pan-Arab Games (PAG) in Doha, Qatar in December 2011. To estimate the prevalence of doping, we utilized a “randomized response technique,” which guarantees anonymity for individuals when answering a sensitive question. We also administered a control question at PAG assessing past-year use of supplements. Results The estimated prevalence of past-year doping was 43.6% (95% confidence interval 39.4–47.9) at WCA and 57.1% (52.4–61.8) at PAG. The estimated prevalence of past-year supplement use at PAG was 70.1% (65.6–74.7%). Sensitivity analyses, assessing the robustness of these estimates under numerous hypothetical scenarios of intentional or unintentional noncompliance by respondents, suggested that we were unlikely to have overestimated the true prevalence of doping. Conclusions Doping appears remarkably widespread among elite athletes, and remains largely unchecked despite current biological testing. The survey technique presented here will allow future investigators to generate continued reference estimates of the prevalence of doping.

Reproducible animal models to recapitulate the pathophysiology of non-alcoholic fatty liver disease (NAFLD) are urgently required to improve the understanding of the mechanisms of liver injury and to explore novel therapeutic options. Current guidelines recommend life-style interventions as first-line therapy for NAFLD and these types of intervention are considered standard-of-care. The current study establishes a reproducible mouse model of a life-style intervention in NAFLD using voluntary wheel running (VWR). Male C57BL/6J mice were fed a high-fat, high-carbohydrate diet (HFD) to induce NAFLD or a corresponding control diet for 12 weeks. Starting at week 9 of the obesogenic NAFLD diet, mice were randomized to either free access to a running wheel or being single caged resembling a sedentary (SED) life-style. VWR induced a transient weight reduction in HFD-fed mice up until week 10. In contrast to the SED mice, VWR mice exhibited normal ALT at the end of the intervention, while the metabolic alterations including elevated fasting glucose, insulin, triglyceride, and total cholesterol levels remained almost unchanged. Additionally, VWR prevented HFD-induced hepatic steatosis by alterations in key liver metabolic processes including the induction of fatty acid β-oxidation and lipogenesis inhibition following increased AMP-activated protein kinase (AMPK)-α activity. Phosphorylation of the serine kinase Akt in hepatic tissue was enhanced following VWR. Furthermore, VWR mice were protected from HFD-induced expression of pro-inflammatory cytokines, chemokines and liver macrophage infiltration. The SED/HFD group exhibited increasing activity of hepatic nuclear factor (NF)-κB p65, which was absent following exercise in the VWR/HFD group. In summary, in an obesogenic mouse model of NAFLD physical exercise improves fatty acid and glucose homeostasis and protects from macrophage-associated hepatic inflammation.

Circulating cell-free DNA (cfDNA) has been investigated as a screening tool for many diseases. To avoid expensive and time-consuming DNA isolation, direct quantification PCR assays can be established. However, rigorous validation is required to provide reliable data in the clinical and non-clinical context. Considering the International Organization for Standardization, as well as bioanalytical method validation guidelines, we provide a comprehensive procedure to validate assays for cfDNA quantification from blood plasma without DNA isolation. A 90 and 222 bp assay was validated to study the kinetics of cfDNA after exercise in patients with systemic lupus erythematosus (SLE). The assays showed ultra-low limit of quantification (LOQ) with 0.47 and 0.69 ng/ml, repeatability ≤ 11.6% (95% CI 8.1–20.3), and intermediate precision ≤ 12.1% (95% CI 9.2–17.7). Incurred sample reanalysis confirmed the precision of the procedure. The additional consideration of pre-analytical factors shows that centrifugation speed and temperature do not change cfDNA concentrations. In SLE patients cfDNA increases ~ twofold after a walking exercise, normalizing after 60 min of rest. The established assays allow reliable and cost-efficient quantification of cfDNA in minute amounts of plasma in the clinical setting. Additionally, the assay can be used as a tool to determine the impact of pre-analytical factors and validate cfDNA quantity and quality of isolated samples.

A significant increase in circulating cell‐free DNA (cfDNA) occurs with physical exercise, which depends on the type of exertion and the duration. The aims of this study were as follows: (1) to investigate the time course of cfDNA and conventional markers of muscle damage from immediately after to 96 h after muscle‐damaging exercise; and (2) to investigate the relationship between cfDNA and indicators of primary (low‐frequency fatigue and maximal voluntary isometric contraction) and secondary (creatine kinase and delayed‐onset muscle soreness) muscle damage in young healthy males. Fourteen participants (age, 22 ± 2 years; weight, 84.4 ± 11.2 kg; height, 184.0 ± 7.4 cm) performed 50 intermittent drop jumps at 20 s intervals. We measured cfDNA and creatine kinase concentrations, maximal voluntary isometric contraction torque, low‐frequency fatigue and delayed‐onset muscle soreness before and at several time points up to 96 h after exercise. Plasma cfDNA levels increased from immediately postexercise until 72 h postexercise (P < 0.01). Elevation of postexercise cfDNA was correlated with both more pronounced low‐frequency fatigue (r = −0.52, P = 3.4 × 10−11) and delayed‐onset muscle soreness (r = 0.32, P = 0.00019). Levels of cfDNA change in response to severe primary and secondary muscle damage after exercise. Levels of cfDNA exhibit a stronger correlation with variables related to primary muscle damage than to secondary muscle damage, suggesting that cfDNA is a more sensitive marker of acute loss of muscle function than of secondary inflammation or damaged muscle fibres. What is the central question of this study? How do plasma cell‐free DNA (cfDNA) levels change in response to primary and secondary muscle damage when muscle‐damaging exercise is performed without metabolic stress? What is the main finding and its importance? In this study, we found that cfDNA concentration increases following severe primary and secondary muscle damage after 50 drop jumps. However, acute postexercise increases in cfDNA were higher than following secondary muscle damage and were more correlated with variables related to primary muscle damage (low‐frequency fatigue). This suggests that muscle‐damaging exercise causing no accumulation of metabolites can lead to acute and delayed increases in cfDNA levels. However, they are more sensitive to primary muscle damage.

Cell-free DNA (cfDNA) in body tissues or fluids is extensively investigated in clinical medicine and other research fields. In this article we provide a direct quantitative real-time PCR (qPCR) as a sensitive tool for the measurement of cfDNA from plasma without previous DNA extraction, which is known to be accompanied by a reduction of DNA yield. The primer sets were designed to amplify a 90 and 222 bp multi-locus L1PA2 sequence. In the first module, cfDNA concentrations in unpurified plasma were compared to cfDNA concentrations in the eluate and the flow-through of the QIAamp DNA Blood Mini Kit and in the eluate of a phenol-chloroform isoamyl (PCI) based DNA extraction, to elucidate the DNA losses during extraction. The analyses revealed 2.79-fold higher cfDNA concentrations in unpurified plasma compared to the eluate of the QIAamp DNA Blood Mini Kit, while 36.7% of the total cfDNA were found in the flow-through. The PCI procedure only performed well on samples with high cfDNA concentrations, showing 87.4% of the concentrations measured in plasma. The DNA integrity strongly depended on the sample treatment. Further qualitative analyses indicated differing fractions of cfDNA fragment lengths in the eluate of both extraction methods. In the second module, cfDNA concentrations in the plasma of 74 coronary heart disease patients were compared to cfDNA concentrations of 74 healthy controls, using the direct L1PA2 qPCR for cfDNA quantification. The patient collective showed significantly higher cfDNA levels (mean (SD) 20.1 (23.8) ng/ml; range 5.1-183.0 ng/ml) compared to the healthy controls (9.7 (4.2) ng/ml; range 1.6-23.7 ng/ml). With our direct qPCR, we recommend a simple, economic and sensitive procedure for the quantification of cfDNA concentrations from plasma that might find broad applicability, if cfDNA became an established marker in the assessment of pathophysiological conditions.

Aiming to develop and implement intervention strategies targeting pharmacological neuroenhancement (PN) among university students more specifically, we (1) assessed the prevalence of PN among German university students, (2) identified potential sociodemographic and study-related risk groups, and (3) investigated sociodemographic, psychological, study-related psychosocial, general psychosocial and health behavior related factors predicting the 12-month prevalence of PN. Therefore, a cross-sectional online survey was administered to students of the University of Mainz, Germany. A binary logistic regression with stepwise inclusion of the five variable groups was performed to predict PN. A total number of 4351 students out of 31,213 registered students (13.9%) participated in the survey, of which N  = 3984 answered the question concerning PN. Of these, 10.4% had used one substance for PN at least once in the past 12 months. The regression analysis revealed 13 variables that were significantly related to the 12-month prevalence of PN. Specifically, the group of health behavior related variables showed the strongest relationship with PN. Therefore, an approach to the prevention of PN should be multifactorial so that it addresses social conditions, as well as education on substance use and healthy behaviors in terms of non-pharmacological strategies as alternatives of PN.

Cells secrete extracellular vesicles (EVs) by default and in response to diverse stimuli for the purpose of cell communication and tissue homeostasis. EVs are present in all body fluids including peripheral blood, and their appearance correlates with specific physiological and pathological conditions. Here, we show that physical activity is associated with the release of nano-sized EVs into the circulation. Healthy individuals were subjected to an incremental exercise protocol of cycling or running until exhaustion, and EVs were isolated from blood plasma samples taken before, immediately after and 90 min after exercise. Small EVs with the size of 100-130 nm, that carried proteins characteristic of exosomes, were significantly increased immediately after cycling exercise and declined again within 90 min at rest. In response to treadmill running, elevation of small EVs was moderate but appeared more sustained. To delineate EV release kinetics, plasma samples were additionally taken at the end of each increment of the cycling exercise protocol. Release of small EVs into the circulation was initiated in an early phase of exercise, before the individual anaerobic threshold, which is marked by the rise of lactate. Taken together, our study revealed that exercise triggers a rapid release of EVs with the characteristic size of exosomes into the circulation, initiated in the aerobic phase of exercise. We hypothesize that EVs released during physical activity may participate in cell communication during exercise-mediated adaptation processes that involve signalling across tissues and organs.

Background Cell-free DNA (cfDNA) has emerged as a relevant biomarker reflecting disease severity in hospitalised COVID-19 patients, correlating with respiratory failure and mortality. However, its utility has not yet been evaluated in general practitioner setting. Methods A prospective single-centre, two-arm, parallel, longitudinal cohort study conducted in a German general practice with four doctors between 8/2021 and 4/2022. Participants : Sixty-one outpatients with flu-like symptoms participated: 31 (10 men, 21 women) tested SARS-CoV-2 positive (COVID group); 30 (12 men, 18 women) were controls (control group). The groups were demographically similar. Primary outcome measures : Comparison of cfDNA levels between groups at day 0, 7 and 14. Secondary outcome measures : Correlations between cfDNA levels and laboratory and clinical parameters like blood counts, respiratory rate and oxygen saturation. Results cfDNA levels did not differ significantly between groups (F [1, 59] = 1.538, p  = 0.22): day 0: mean (± standard deviation) = 14.45 (± 6.24) ng/ml (COVID group) vs. 11.32 (± 4.79) ng/ml (control group); day 7: 14.46 (± 6.57) ng/ml vs. 12.53 (± 6.67) ng/ml; day 14: 12.94 (± 6.66) ng/ml vs. 12.93 (± 7.02) ng/ml. However, at t0, the integrity index was significantly lower in the COVID group (t0: 0.30 [±- 0.15] vs. 0.41 [± 0.1]; p  = 0.0127) increasing at t1 (0.38 [± 0.17]; p  = 0.008) and at t2 (0.42 [± 0.22]; p  < 0.001). Conclusion Unlike hospitalised patients, cfDNA levels did not differ significantly between outpatient groups. Therefore, a decision on the need for hospitalisation based on clinical and serological factors is still required. The significantly lower integrity index of the SARS-CoV-2 infected individuals indicates that their DNA kinetics differ from those of individuals infected with other respiratory pathogens. Trial registration : German Clinical Trials Register: DRKS00024722, Registration date: 10 March 2021.