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Study aim: The aim of the study was to analyse the lifespan of Polish male Olympic medallists in comparison to the general male population.

An athlete's training aims to achieve the highest possible sports results by improving physical dispositions which lead to cardiac adaptive changes. The annual training cycle is divided into periods. The preparatory period begins with gradually increasing training intensity and volume until the competitive period occurs, when the athlete's maximum performance is expected. Finally, the athlete enters a phase of loss of fitness, which is called detraining. Detraining is a time of resting both physically and mentally from the training regime and usually lasts about 4 weeks for endurance athletes. We collected data from much research on athletes' detraining. According to these data, the earliest change after detraining seems to be a decrease in left ventricular wall thickness and left ventricular mass, followed by decreased performance parameters, diastolic diameter of the left ventricle and size of the left atrium. A reversal of adaptive changes affects the left heart chamber first, then the right atrium and, finally, the right ventricle. Training reduction is often proposed as a method of differentiating an athlete's heart from cardiomyopathies. The aim of this study is to consider the diagnostic value of detraining in differentiating athletes' hearts from cardiomyopathies. We suggest that detraining cannot be conclusive in differentiating the disease from adaptive changes. Although a withdrawal of the characteristic morphological, functional and electrocardiographic changes occurs in healthy athletes during detraining, it can also concern individuals with cardiomyopathies due to the lower expression of abnormal features after decreased training loads. Therefore, a quick diagnosis and individual assessments using imaging and genetic tests are essential to recommend a proper type of activity. [ABSTRACT FROM AUTHOR]

In recent years, numerous prognostic models have been developed to predict VO2max. Nevertheless, their accuracy in endurance athletes (EA) stays mostly unvalidated. This study aimed to compare predicted VO2max (pVO2max) with directly measured VO2max by assessing the transferability of the currently available prediction models based on their R2, calibration-in-the-large, and calibration slope. 5,260 healthy adult EA underwent a maximal exertion cardiopulmonary exercise test (CPET) (84.76% male; age 34.6±9.5 yrs.; VO2max 52.97±7.39 mL·min-1·kg-1, BMI 23.59±2.73 kg·m-2). 13 models have been selected to establish pVO2max. Participants were classified into four endurance subgroups (high-, recreational-, low- trained, and "transition") and four age subgroups (18–30, 31–45, 46–60, and ≥61 yrs.). Validation was performed according to TRIPOD guidelines. pVO2max was low-to-moderately associated with direct CPET measurements (p>0.05). Models with the highest accuracy were for males on a cycle ergometer (CE) (Kokkinos R2 = 0.64), females on CE (Kokkinos R2 = 0.65), males on a treadmill (TE) (Wasserman R2 = 0.26), females on TE (Wasserman R2 = 0.30). However, selected models underestimated pVO2max for younger and higher trained EA and overestimated for older and lower trained EA. All equations demonstrated merely moderate accuracy and should only be used as a supplemental method for physicians to estimate CRF in EA. It is necessary to derive new models on EA populations to include routinely in clinical practice and sports diagnostic. [ABSTRACT FROM AUTHOR]

Background. Cytokines soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and interleukin 6 (IL-6) are involved in immune response, proliferation, apoptosis, and cardiovascular pathologies. We have previously confirmed that changes of their platelet or plasma contents are associated with pulmonary arterial hypertension (PAH). The positron emission tomography/magnetic resonance imaging (PET/MRI) hybrid imaging provides detailed insight into right ventricle (RV) hemodynamic and metabolic function. Objectives. To evaluate the relationship between RV parameters obtained using PET/MRI and concentrations of plasma and platelet sTWEAK and IL-6 in stable PAH patients. Materials and methods. Eighteen stable PAH patients (48.44 ±16.7 years) had simultaneous PET/MRI scans with 18F-fluorodeoxyglucose (18F-FDG) performed. Its uptake was presented as a standardized uptake value (SUV) for RV and left ventricle (LV). Cytokines concentrations were measured in platelet-poor plasma and platelet lysate. Follow-up time of this study was 58 months; the combined endpoint (CEP) was defined as death or clinical deterioration. Results. We observed significant correlations between platelet sTWEAK levels, plasma IL-6 and PET parameter SUVRV/LV (r = -0.57, p = 0.011; r = 0.50, p = 0.032, respectively). In logistic regression, platelet sTWEAK and IL-6 were both prognostic factors for unfavorable ratio of SUVRV/LV higher than 1 (hazard ratio (HR) = 0.44, 95% confidence interval (95% CI): [0.23; 0.84], p = 0.017; and HR = 3.62, 95% CI: [1.21; 10.17], p = 0.011, respectively). Furthermore, their concentrations were related with prognostically important higher late gadolinium enhancement mass index (LGEMI) and RV global longitudinal strain/systolic pulmonary artery pressure (RV GLS/sPAP) values. Patients who had CEP in follow-up (n = 13) had significantly lower platelet sTWEAK content and higher plasma IL-6 at baseline than stable patients. Lower platelet sTWEAK was related to a worse prognosis in log-rank test (p = 0.006). Platelet sTWEAK and plasma IL-6 together with RV GLS/sPAP, RV ejection fraction (RVEF), mean pulmonary arterial pressure (mPAP), and SUVRV/LV were significantly associated with time to CEP in univariate Cox analysis. Conclusions. The sTWEAK and IL-6 concentrations in PAH patients are linked with metabolic and functional changes of RV visualized in PET/MRI, and both sTWEAK and IL-6 predict clinical deterioration. [ABSTRACT FROM AUTHOR]