11 research outputs found

    CD3+/CD56+ NKT-like Cells Show Imbalanced Control Immediately after Exercise in Delayed-Onset Muscle Soreness

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    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−/CD56dim+ 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

    Is cardiac involvement prevalent in highly trained athletes after SARS-CoV-2 infection? A cardiac magnetic resonance study using sex-matched and age-matched controls

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    ObjectivesTo investigate the cardiovascular consequences of SARS-CoV-2 infection in highly trained, otherwise healthy athletes using cardiac magnetic resonance (CMR) imaging and to compare our results with sex-matched and age-matched athletes and less active controls.MethodsSARS-CoV-2 infection was diagnosed by PCR on swab tests or serum immunoglobulin G antibody tests prior to a comprehensive CMR examination. The CMR protocol contained sequences to assess structural, functional and tissue-specific data.ResultsOne hundred forty-seven athletes (94 male, median 23, IQR 20–28 years) after SARS-CoV-2 infection were included. Overall, 4.7% (n=7) of the athletes had alterations in their CMR as follows: late gadolinium enhancement (LGE) showing a non-ischaemic pattern with or without T2 elevation (n=3), slightly elevated native T1 values with or without elevated T2 values without pathological LGE (n=3) and pericardial involvement (n=1). Only two (1.4%) athletes presented with definite signs of myocarditis. We found pronounced sport adaptation in both athletes after SARS-CoV-2 infection and athlete controls. There was no difference between CMR parameters, including native T1 and T2 mapping, between athletes after SARS-CoV-2 infection and the matched athletic groups. Comparing athletes with different symptom severities showed that athletes with moderate symptoms had slightly greater T1 values than athletes with asymptomatic and mildly symptomatic infections (p<0.05). However, T1 mapping values remained below the cut-off point for most patients.ConclusionAmong 147 highly trained athletes after SARS-CoV-2 infection, cardiac involvement on CMR showed a modest frequency (4.7%), with definite signs of myocarditis present in only 1.4%. Comparing athletes after SARS-CoV-2 infection and healthy sex-matched and age-matched athletes showed no difference between CMR parameters, including native T1 and T2 values

    Frequent Constriction-Like Echocardiographic Findings in Elite Athletes Following Mild COVID-19: A Propensity Score-Matched Analysis

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    Background: The cardiovascular effects of SARS-CoV-2 in elite athletes are still a matter of debate. Accordingly, we sought to perform a comprehensive echocardiographic characterization of post-COVID athletes by comparing them to a non-COVID athlete cohort. Methods: 107 elite athletes with COVID-19 were prospectively enrolled (P-CA; 23 ± 6 years, 23% female) 107 healthy athletes were selected as a control group using propensity score matching (N-CA). All athletes underwent 2D and 3D echocardiography. Left (LV) and right ventricular (RV) end-diastolic volumes (EDVi) and ejection fractions (EF) were quantified. To characterize LV longitudinal deformation, 2D global longitudinal strain (GLS) and the ratio of free wall vs. septal longitudinal strain (FWLS/SLS) were also measured. To describe septal flattening (SF—frequently seen in P-CA), LV eccentricity index (EI) was calculated. Results: P-CA and N-CA athletes had comparable LV and RVEDVi (P-CA vs. N-CA; 77 ± 12 vs. 78 ± 13mL/m2; 79 ± 16 vs. 80 ± 14mL/m2). P-CA had significantly higher LVEF (58 ± 4 vs. 56 ± 4%, p < 0.001), while LVGLS values did not differ between P-CA and N-CA (−19.0 ± 1.9 vs. −18.8 ± 2.2%). EI was significantly higher in P-CA (1.13 ± 0.16 vs. 1.01 ± 0.05, p < 0.001), which was attributable to a distinct subgroup of P-CA with a prominent SF (n = 35, 33%), further provoked by inspiration. In this subgroup, the EI was markedly higher compared to the rest of the P-CA (1.29 ± 0.15 vs. 1.04 ± 0.08, p < 0.001), LVEDVi was also significantly higher (80 ± 14 vs. 75 ± 11 mL/m2, p < 0.001), while RVEDVi did not differ (82 ± 16 vs. 78 ± 15mL/m2). Moreover, the FWLS/SLS ratio was significantly lower in the SF subgroup (91.7 ± 8.6 vs. 97.3 ± 8.2, p < 0.01). P-CA with SF experienced symptoms less frequently (1.4 ± 1.3 vs. 2.1 ± 1.5 symptom during the infection, p = 0.01). Conclusions: Elite athletes following COVID-19 showed distinct morphological and functional cardiac changes compared to a propensity score-matched control athlete group. These results are mainly driven by a subgroup, which presented with some echocardiographic features characteristic of constrictive pericarditis

    Orthostasis Is Impaired Due to Fatiguing Intensive Acute Concentric Exercise Succeeded by Isometric Weight-Loaded Wall-Sit in Delayed-Onset Muscle Soreness: A Pilot Study

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    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

    The Impact of COVID-19 on the Preparation for the Tokyo Olympics: A Comprehensive Performance Assessment of Top Swimmers

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    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

    Novel insights into the athlete’s heart: is myocardial work the new champion of systolic function?

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    AIMS: 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. METHODS AND RESULTS: 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 (VO(2)/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 VO(2)/kg (r = 0.527, P < 0.001). CONCLUSIONS: 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
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