We sought to investigate the correlation between speckle-tracking echocardiography (STE)-derived myocardial work (MW) and invasively measured contractility in a rat model of athlete's heart. We also assessed MW in elite athletes and explored its association with cardiopulmonary exercise test (CPET)-derived aerobic capacity. Sixteen rats underwent a 12-week swim training program and were compared to controls (n = 16). STE was performed to assess global longitudinal strain (GLS), which was followed by invasive pressure-volume analysis to measure contractility [slope of end-systolic pressure–volume relationship (ESPVR)]. Global MW index (GMWI) was calculated from GLS curves and left ventricular (LV) pressure recordings. In the human investigations, 20 elite swimmers and 20 healthy sedentary controls were enrolled. GMWI was calculated through the simultaneous evaluation of GLS and non-invasively approximated LV pressure curves at rest. All subjects underwent CPET to determine peak oxygen uptake (VO₂/kg). Exercised rats exhibited higher values of GLS, GMWI, and ESPVR than controls (−20.9 ± 1.7 vs. −17.6 ± 1.9%, 2745 ± 280 vs. 2119 ± 272 mmHg·%, 3.72 ± 0.72 vs. 2.61 ± 0.40 mmHg/μL, all P_Exercise < 0.001). GMWI correlated robustly with ESPVR (r = 0.764, P < 0.001). In humans, regular exercise training was associated with decreased GLS (−17.6 ± 1.5 vs. −18.8 ± 0.9%, P_Exercise = 0.002) but increased values of GMWI at rest (1899 ± 136 vs. 1755 ± 234 mmHg·%, P_Exercise = 0.025). GMWI exhibited a positive correlation with VO₂/kg (r = 0.527, P < 0.001). GMWI precisely reflected LV contractility in a rat model of exercise-induced LV hypertrophy and captured the supernormal systolic performance in human athletes even at rest. Our findings endorse the utilization of MW analysis in the evaluation of the athlete’s heart. ESPVR, slope of end-systolic pressure–volume relationship (i.e. the slope of the curve connecting the end-systolic points of the pressure–volume loops recorded during the transient occlusion of inferior vena cava); GLS, global longitudinal strain; GMWI, global myocardial work index; LV, left ventricular; VO₂/kg, peak oxygen uptake.

While left ventricular (LV) adaptation to regular, intense exercise has been thoroughly studied, data concerning the right ventricular (RV) mechanical changes and their continuum with athletic performance are scarce. The aim of this study was to characterize biventricular morphology and function and their relation to sex, age, and sports classes in a large cohort of elite athletes using three-dimensional (3D) echocardiography. Elite, competitive athletes (n = 422) and healthy, sedentary volunteers (n = 55) were enrolled. Left ventricular and RV end-diastolic volumes (EDVi) and ejection fractions (EFs) were measured. To characterize biventricular mechanics, LV and RV global longitudinal (GLS) and circumferential strains (GCS) were quantified. All subjects underwent cardiopulmonary exercise testing to determine peak oxygen uptake (VO₂/kg). Athletes had significantly higher LV and RV EDVi compared with controls (athletes vs. controls; LV EDVi: 81 ± 13 vs. 62 ± 11 mL/m², RV EDVi: 82 ± 14 vs. 63 ± 11 mL/m²; P < 0.001). Concerning biventricular systolic function, athletes had significantly lower resting LV and RV EF (LV EF: 57 ± 4 vs. 61 ± 5%; RV EF: 55 ± 5 vs. 59 ± 5%; P < 0.001). The exercise-induced relative decrease in LV GLS (9.5 ± 10.7%) and LV GCS (10.7 ± 9.8%) was similar; however, the decrement in RV GCS (14.8 ± 17.8%) was disproportionately larger compared with RV GLS (1.7 ± 15.4%, P < 0.01). Right ventricular EDVi was found to be the strongest independent predictor of VO₂/kg by multivariable linear regression. Resting LV mechanics of the athlete’s heart is characterized by a balanced decrement in GLS and GCS; however, RV GCS decreases disproportionately compared with RV GLS. Moreover, this mechanical pattern is associated with better exercise capacity.

Background: The Olympic preparation of athletes has been highly influenced by COVID and post-COVID syndrome. As the complex screening of athletes is essential for safe and successful sports, we aimed to repeat the 2019-year sports cardiology screening of the Olympic Swim Team before the Olympics and to compare the results of COVID and non-COVID athletes. Methods: Patient history, electrocardiogram, laboratory tests, body composition analysis, echocardiography, cardiopulmonary exercise test (CPET) were performed. We used time-ranking points to compare swimming performance. Results: From April 2019, we examined 46 elite swimmers (24 ± 4 years). Fourteen swimmers had COVID infection; all cases were mild. During CPET there was no difference in the performance of COVID (male: VO₂ max 55 ± 4 vs. 56.5 ± 5 mL/kg/min, p = 0.53; female: VO₂ max 54.6 ± 4 vs. 56 ± 5.5 mL/kg/min, p = 0.86) vs. non-COVID athletes (male VO₂ max 56.7 ± 5 vs. 55.5 ± 4.5 mL/kg/min, p = 0.50; female 49.6 ± 3 vs. 50.7 ± 2.6 mL/kg/min, p = 0.47) between 2019 and 2021. When comparing the time results of the National Championships, 54.8% of the athletes showed an improvement (p = 0.75). Conclusions: COVID infection with short-term detraining did not affect the performance of well-trained swimmers. According to our results, the COVID pandemic did not impair the effectiveness of the preparation for the Tokyo Olympics.

The purpose of the study was to carry out an immunophenotypical characterization with a special focus on natural killer cells of junior swimmers from the Hungarian National Swim Team before and after an intensive acute exercise. Nineteen swimmers, ten females and nine males, completed the exercise protocol. Sixteen swimmers experienced delayed-onset muscle soreness. Most of our findings substantiated earlier results, such as the increase in the percentage of the CD3⁻/CD56⁺ natural killer cells and the CD3⁻/CD56^dim+ NK cells, and the decrease in the percentage of CD3⁺ T cells among lymphocytes after the exercise protocol. The drop of natural killer cell activity back to the pre-exercise level was in line with earlier findings. Interestingly, the percentage of CD3⁺/CD56⁺ NKT-like cells did not change significantly in those three swimmers who did not report delayed-onset muscle soreness. On the contrary, the percentage of CD3⁺/CD56⁺ NKT-like cells among lymphocytes increased in fourteen and decreased in two swimmers reporting delayed-onset muscle soreness. This study for the first time demonstrated a link between the delayed-onset muscle soreness and the imbalanced control of CD3⁺/CD56⁺ NKT-like cells among lymphocytes. However, validation of this association in a larger sample size study will be necessary.

The aim of the study was to investigate any indication of diminished orthostatic tolerance as a result of fatiguing intensive acute concentric exercise with a successive isometric wall-sit followed by an orthostatic stress test, with a special focus on any distinguishable alterations due to a delayed-onset muscle soreness effect. The exercise protocol was carried out among nineteen (10 female, 9 male) junior swimmers from the Hungarian National Swim Team. All athletes showed a positive orthostatic stress test right after our exercise protocol. The diastolic blood pressure was significantly lower due to the delayed-onset muscle soreness effect in the standing position after the supine position of the orthostatic stress test, in contrast to the athletes who did not experience delayed-onset muscle soreness. Furthermore, the heart rate was dysregulated in athletes with a delayed-onset muscle soreness effect when they assumed a supine position after the sustained standing position during the orthostatic stress test, in contrast to the athletes without delayed-onset muscle soreness. Interesting to note is that, in three subjects, the sustained standing position decreased the heart rate below the level of the initial supine position and six athletes experienced dizziness in the standing position, and all of these athletes were from the group that experienced delayed-onset muscle soreness. Accordingly, this study, for the first time, demonstrated that delayed-onset muscle soreness impairs orthostasis after unaccustomed fatiguing intensive acute concentric exercise with a successive isometric weight-loaded wall-sit; however, validation of this association should be investigated in a larger sample size.

At the pandemic's beginning, significant concern has risen about the prevalence of myocardial involvement after SARS‐CoV‐2 infection. We assessed the cardiovascular burden of SARS‐CoV‐2 in a large cohort of athletes and identified factors that might affect the disease course. We included 633 athletes in our study on whom we performed extensive cardiology examinations after recovering from SARS‐CoV‐2 infection. More than half of the athletes (n = 322) returned for a follow‐up examination median of 107 days after the commencement of their infection. Troponin T positivity was as low as 1.4% of the athletes, where the subsequently performed examinations did not show definitive, ongoing myocardial injury. Altogether, 31% of the athletes' rapid training rebuild was hindered by persistent or reoccurring symptoms. Female athletes reported a higher prevalence of return to play (RTP) symptoms than their male counterparts (34% vs. 19%, p = 0.005). The development of long COVID symptoms was independently predicted by increasing age and acute symptoms' severity in a multiple regression model (AUC 0.75, CI 0.685–0.801). Athletes presenting with either or both cough and ferritin levels higher than >150 μg/L had a 4.1x (CI 1.78–9.6, p = 0.001) higher odds ratio of developing persistent symptoms. While SARS‐CoV‐2 rarely affects the myocardium in athletes, about one in three of them experience symptoms beyond the acute phase. Identifying those athletes with a predisposition to developing long‐standing symptoms may aid clinicians and trainers in finding the optimal return‐to‐play timing and training load rebuild pace.