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Background Preparticipation examinations (PPE) are frequently used to evaluate eligibility for competitive sports in adolescent athletes. Nevertheless, the effectiveness of these examinations is under debate since costs are high and its validity is discussed controversial. Purpose To analyse medical findings and consequences in adolescent athletes prior to admission to a sports school. Methods In 733 adolescent athletes (318 girls, 415 boys, age 12.3±0.4, 16 sports disciplines), history and clinical examination (musculoskeletal, cardiovascular, general medicine) was performed to evaluate eligibility. PPE was completed by determination of blood parameters, ECG at rest and during ergometry, echocardiography and x-rays and ultrasonography if indicated. Eligibility was either approved or rated with restriction. Recommendations for therapy and/or prevention were given to the athletes and their parents. Results Historical (h) and clinical (c) findings (eg, pain, verified pathologies) were more frequent regarding the musculoskeletal system (h:120, 16.4%; c:247, 33.7%) compared to cardiovascular (h:9, 1.2%; c:23, 3.1%) or general medicine findings (h:116, 15.8%; c:71, 9.7%). ECG at rest was moderately abnormal in 46 (6.3%) and severely abnormal in 25 athletes (3.4%). Exercise ECG was suspicious in 25 athletes (3.4%). Relevant echocardiographic abnormalities were found in 17 athletes (2.3%). In 52 of 358 cases (14.5%), x-rays led to diagnosis (eg, Spondylolisthesis). Eligibility was temporarily restricted in 41 athletes (5.6%). Three athletes (0.4%) had to be excluded from competitive sports. Therapy (eg, physiotherapy, medication) and/or prevention (sensorimotor training, vaccination) recommendations were deduced due to musculoskeletal (t:n=76,10.3%;p: n=71,9.8%) and general medicine findings (t:n=80, 10.9%; p:n=104, 14.1%). Conclusion Eligibility for competitive sports is restricted in only 5.5% of adolescent athletes at age 12. Eligibility refusals are rare. However, recommendations for therapy and prevention are frequent, mainly regarding the musculoskeletal system. In spite of time and cost consumption, adolescent preparticipation before entering a career in high-performance sports is supported. [ABSTRACT FROM AUTHOR]

Objectives: The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. Methods: During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l*min-1 oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg*m-2 VO2peak 51.3-62.1 ml*min-1*kg-1). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. Results: In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l*min-1) compared with the first test. Conclusions: For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms. [ABSTRACT FROM AUTHOR]

Objective: To investigate if the exercise-induced immune response contributes to the exercise-induced increase in brain natriuretic peptide (BNP) in healthy athletes. This has previously been speculated, as elevated concentrations of BNP or N-terminal pro brain natriuretic peptide (NT-proBNP) in cardiovascular patients were found to be related to immune reactions and elevations in inflammatory cytokines such as interleukin 6 (IL-6). Methods: Stored serum samples were analysed for NT- proBNP concentrations of 14 healthy endurance athletes (mean age: 25 (SD 5) years; VO2peak 67 (SD 6) ml/min/kg), who had been examined previously for exercise-induced immune reactions and their dependence on carbohydrate supplementation (6 or 12% carbohydrate vs placebo beverages) after three bouts of 4 h cycling at a given workload of 70% of the individual anaerobic threshold. Venous blood samples were taken before, immediately after, and 1 h and 1 day after exercise. Leucocyte subpopulations were determined immediately after blood sampling by flow cytometry. Serum samples for posterior analysis of C-reactive protein (CRP), IL-6, cortisol and NT- proBNP were stored at -80°C. Results: The exercise-induced increases in NT-proBNP (p<0.001 ) were not related to the exercise-induced immune response, although exercise induced marked (CHOS-dependent) increases in IL-6, CAP, cortisol, leucocytes, neutrophils, monocytes and natural killer cells. Conclusion: It is unlikely that the exercise-induced increases in NT-proBNP or BNP in healthy athletes are caused by the exercise-induced immune response. Therefore, exercise-induced increases in NT-proBNP or BNP in healthy athletes have to be differentiated from increases in cardiovascular patients with systemic inflammation. [ABSTRACT FROM AUTHOR]

Objective: To investigate the underlying causes and regional patterns of sudden death in football (soccer) players worldwide to inform and improve existing screening and prevention measures., Methods: From 2014 to 2018 cases of sudden cardiac death (SCD), survived sudden cardiac arrest (SCA) and traumatic sudden death were recorded by media monitoring (Meltwater), a confidential web-based data platform and data synchronisation with existing national Sudden Death Registries (n=16). Inclusion criteria were met when sudden death occurred during football-specific activity or up to 1 hour afterwards. Death during other activities was excluded., Results: A total of 617 players (mean age 34±16 years, 96% men) with sudden death were reported from 67 countries; 142 players (23%) survived. A diagnosis by autopsy or definite medical reports was established in 211 cases (34%). The leading cause in players >35 years was coronary artery disease (76%) and in players ≤35 years was sudden unexplained death (SUD, 22%). In players ≤35 years the leading cause of SCD varied by region: cardiomyopathy in South America (42%), coronary artery anomaly in North America (33%) and SUD in Europe (26%). Traumatic sudden death including commotio cordis occurred infrequently (6%). Cardiopulmonary resuscitation (CPR) resulted in a survival rate of 85% with the use of an automated external defibrillator (AED) compared with 35% without., Conclusions: Regional variation in SCD aetiology should be verified by expansion of national registries and uniform autopsy protocols. Immediate access to an AED at training and competition sites, as well as CPR training for players, coaches and staff members, is needed to improve survival from SCA., Competing Interests: Competing interests: TM is chairman of the Medical Committee of the German FA and UEFA. JD is former chairman of F-MARC. All authors declare that they have no competing interests regarding the aims of the study., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Athlete's heart as an adaptation to long-time and intensive endurance training can vary considerably between individuals. Genetic polymorphisms in the cardiological relevant insulin-like growth factor 1 (IGF1) signalling pathway seem to have an essential influence on the extent of physiological hypertrophy., Objective: Analysis of polymorphisms in the genes of IGF1, IGF1 receptor (IGF1R) and the negative regulator of the cardiac IGF1 signalling pathway, myostatin (MSTN), and their relation to left ventricular mass (LVM) of endurance athletes., Methods: In 110 elite endurance athletes or athletes with a high amount of endurance training (75 males and 35 females) and 27 male controls, which were examined by echocardiographic imaging methods and ergometric exercise-testing, the genotypes of a cytosine-adenine repeat polymorphism in the promoter region of the IGF1 gene and a G/A substitution at position 3174 in the IGF1R gene were determined. Additionally, a mutation screen of the MSTN gene was performed., Results: The polymorphisms in the IGF1 and the IGF1R gene showed a significant relation to the LVM for male (IGF1: p=0.003; IGF1R: p=0.01), but not for female athletes. The same applies to a previously unnoticed polymorphism in the 1 intron of the MSTN gene, whose deletion allele (AAA→AA) appears to increase the myostatic effect (p=0.015). Moreover, combinations of the polymorphisms showed significant synergistic effects on the LVM of the male athletes., Conclusions: The authors' results argue for the importance of polymorphisms in the IGF1 signalling pathway in combination with MSTN on the variant degree of physiological hypertrophy of male athletes.

Background: Prolonged exercise may induce temporary immunosuppression with a presumed increased susceptibility for infection. However, there are only few data on immune cell function after prolonged cycling at moderate intensities typical for road cycling training sessions., Methods: The present study examined the influence on immune cell function of 4 h of cycling at a constant intensity of 70% of the individual anaerobic threshold. Interleukin-6 (IL-6) and C-reactive protein (CRP), leukocyte and lymphocyte populations, activities of natural killer (NK), neutrophils, and monocytes were examined before and after exercise, and also on a control day without exercise., Results: Cycling for 4 h induced a moderate acute phase response with increases in IL-6 from 1.0 (SD 0.5) before to 9.6 (5.6) pg/ml 1 h after exercise and CRP from 0.5 (SD 0.4) before to 1.8 (1.3) mg/l 1 day after exercise. Although absolute numbers of circulating NK cells, monocytes, and neutrophils increased during exercise, on a per cell basis NK cell activity, neutrophil and monocyte phagocytosis, and monocyte oxidative burst did not significantly change after exercise. However, a minor effect over time for neutrophil oxidative burst was noted, tending to decrease after exercise., Conclusions: Prolonged cycling at moderate intensities does not seem to seriously alter the function of cells of the first line of defence. Therefore, the influence of a single typical road cycling training session on the immune system is only moderate and appears to be safe from an immunological point of view.