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SARS-CoV-2 may affect the cardiovascular system and vascular impairment has been reported in healthy young adults recovering from COVID-19. However, the impact of SARS-CoV-2 infection on the vascular function of elite athletes is unknown. We examined 30 healthy male elite athletes (age 25.8 ± 4.6 years) pre-season and at a 6-month follow-up (182 ± 10 days). Vascular function and central blood pressure were calculated using transfer function-based analysis of peripheral arterial waveforms obtained by oscillometry. We performed a two-way repeated-measures ANOVA on the biomarker data, with SARS-CoV-2 status as the between-groups factor and time as the within-groups factor. Subjects who tested positive for SARS-CoV-2 were studied 18 ± 4 days after their positive testing date at follow-up. Of 30 athletes, 15 tested positive for SARS-CoV-2 after the first examination and prior to the follow-up. None had severe COVID-19 or reported any persisting symptoms. The results of the two-way repeated measures ANOVA revealed that there was no significant main effect of COVID-19 on any of the investigated biomarkers. However, there was a significant interaction between the effects of SARS-CoV-2 exposure and time on augmentation index (Aix) ( p  = 0.006) and augmentation index normalized to a heart rate of 75 beats per minute (Aix@75), ( p  = 0.0018). The observation of an interaction effect on Aix and Aix@75 in the absence of any main effect indicates a cross-over interaction. Significant vascular alterations in male elite athletes recovering from COVID-19 were observed that suggest vascular impairment. Whether these alterations affect athletic performance should be evaluated in future studies.

PurposeSex differences in blood pressure (BP) regulation at rest have been attributed to differences in vascular function. Further, arterial stiffness predicts an exaggerated blood pressure response to exercise (BPR) in healthy young adults. However, the relationship of vascular function to the workload-indexed BPR and potential sex differences in athletes are unknown.MethodsWe examined 47 male (21.6 ± 1.7 years) and 25 female (21.1 ± 2 years) athletes in this single-center pilot study. We assessed vascular function at rest, including systolic blood pressure (SBP). Further, we determined the SBP/W slope, the SBP/MET slope, and the SBP/W ratio at peak exercise during cycling ergometry.ResultsMale athletes had a lower central diastolic blood pressure (57 ± 9.5 vs. 67 ± 9.5 mmHg, p < 0.001) but a higher central pulse pressure (37 ± 6.5 vs. 29 ± 4.7 mmHg, p < 0.001), maximum SBP (202 ± 20 vs. 177 ± 15 mmHg, p < 0.001), and ΔSBP (78 ± 19 vs. 58 ± 14 mmHg, p < 0.001) than females. Total vascular resistance (1293 ± 318 vs. 1218 ± 341 dyn*s/cm5, p = 0.369), pulse wave velocity (6.2 ± 0.85 vs. 5.9 ± 0.58 m/s, p = 0.079), BP at rest (125 ± 10/76 ± 7 vs. 120 ± 11/73.5 ± 8 mmHg, p > 0.05), and the SBP/MET slope (5.7 ± 1.8 vs. 5.1 ± 1.6 mmHg/MET, p = 0.158) were not different. The SBP/W slope (0.34 ± 0.12 vs. 0.53 ± 0.19 mmHg/W) and the peak SBP/W ratio (0.61 ± 0.12 vs. 0.95 ± 0.17 mmHg/W) were markedly lower in males than in females (p < 0.001).ConclusionMale athletes displayed a lower SBP/W slope and peak SBP/W ratio than females, whereas the SBP/MET slope was not different between the sexes. Vascular functional parameters were not able to predict the workload-indexed BPR in males and females.

PurposeLow vitamin D levels have been associated with elevated blood pressure (BP) in the general population. However, whether there is an association of vitamin D insufficiency with BP changes during maximum exercise in athletes is currently unclear. MethodsA total of 120 male professional indoor athletes (age 26 ± 5 years) were examined. BP was measured at rest and during a graded cycling test. We assessed the BP response (BPR) during maximum exercise and the respective load. BP and BPR (peak-baseline BP) were analysed with respect to 25-OH vitamin D levels, with levels < 30 ng/mL defining vitamin D insufficiency. Results35 athletes were classified as being vitamin D insufficient. BP was not different between sufficient and insufficient vitamin D groups (122 ± 10/75 ± 7 vs. 120 ± 12/77 ± 9 mmHg). At maximum exercise, however, systolic BP (198 ± 17 vs. 189 ± 19, p = 0.026) and the pulse pressure (118 ± 18 vs. 109 ± 21 mmHg, p = 0.021) were higher in the sufficient group; the BPR was not different between groups (76 ± 20/5 ± 6 vs. 69 ± 22/3 ± 6 mmHg, p = 0.103). Athletes with sufficient levels had a higher maximum power output (3.99 ± 0.82 vs. 3.58 ± 0.78 W/kg, p = 0.015) and achieved higher workloads (367 ± 78 vs. 333 ± 80 W, p = 0.003). The workload-adjusted BPR (maximum systolic BP/MPO) was not different between athletes with sufficient and insufficient vitamin D levels (51 ± 10 vs. 56 ± 14 mmHg × kg/W, p = 0.079). ConclusionAthletes with sufficient vitamin D achieved a higher maximum systolic BP and a higher maximum power output. The workload-adjusted BPR was not different between groups, which suggests that this finding reflects a better performance of athletes with sufficient vitamin D.

Background Cardiovascular and diabetic disease are the leading and preventable causes of death worldwide. The currently prognosticated dramatic increase in disease burden over the next two decades, however, bespeaks a low confidence in our prevention ability. This conflicts with the almost enthusiastic reporting of study results, which demonstrate substantial risk reductions secondary to simple lifestyle changes. Discussion There is a case to be made for a disregard of the difference between statistical significance and clinical relevance of the reported data. Nevertheless, lifestyle change remains the main weapon in our battle against the epidemic of cardiometabolic disease. But along the way from risk screening to intervention to maintenance the compound inefficiencies of current primary preventive strategies marginalize their impact. Summary Unless we dramatically change the ways in which we deploy preventive interventions we will inevitably lose the battle. In this paper we will argue for three provocative strategy changes, namely (a) the disbanding of screening in favor of population-wide enrollment into preventive interventions, (b) the substitution of the current cost utility analysis for a return-on-investment centered appraisal of interventions, and (c) the replacement of standardized programs modeled around acute care by individualized and perpetual interventions.

PurposeThe systolic blood pressure/workload (SBP/MET) slope was recently reported to be a reliable parameter to identify an exaggerated blood pressure response (eBPR) in the normal population and in athletes. However, it is unclear whether an eBPR correlates with central blood pressure (CBP) and vascular function in elite athletes.MethodsWe examined 618 healthy male elite athletes (age 25.8 ± 5.1 years) of mixed sports with a standardized maximum exercise test. CBP and vascular function were measured non-invasively with a validated oscillometric device. The SBP/MET slope was calculated and the threshold for an eBPR was set at > 6.2 mmHg/MET. Two groups were defined according to ≤ 6.2 and > 6.2 mmHg/MET, and associations of CBP and vascular function with the SBP/MET slope were compared for each group.ResultsAthletes with an eBPR (n = 180, 29%) displayed a significantly higher systolic CBP (102.9 ± 7.5 vs. 100 ± 7.7 mmHg, p = 0.001) but a lower absolute (295 ± 58 vs. 384 ± 68 W, p < 0.001) and relative workload (3.14 ± 0.54 vs. 4.27 ± 1.1 W/kg, p < 0.001) compared with athletes with a normal SBP/MET slope (n = 438, 71%). Systolic CBP was positively associated with the SBP/MET slope (r = 0.243, p < 0.001). In multiple logistic regression analyses, systolic CBP (odds ratio [OR] 1.099, 95% confidence interval [CI] 1.045–1.155, p < 0.001) and left atrial volume index (LAVI) (OR 1.282, CI 1.095–1.501, p = 0.002) were independent predictors of an eBPR.ConclusionSystolic CBP and LAVI were independent predictors of an eBPR. An eBPR was further associated with a lower performance level, highlighting the influence of vascular function on the BPR and performance of male elite athletes.

BackgroundReference values for right ventricular function and pulmonary circulation coupling were recently established for the general population. However, normative values for elite athletes are missing, even though exercise-related right ventricular enlargement is frequent in competitive athletes.MethodsWe examined 497 healthy male elite athletes (age 26.1 ± 5.2 years) of mixed sports with a standardized transthoracic echocardiographic examination. Tricuspid annular plane excursion (TAPSE) and systolic pulmonary artery pressure (SPAP) were measured. Pulmonary circulation coupling was calculated as TAPSE/SPAP ratio. Two age groups were defined (18–29 years and 30–39 years) and associations of clinical parameters with the TAPSE/SPAP ratio were determined and compared for each group.ResultsAthletes aged 18–29 (n = 349, 23.8 ± 3.5 years) displayed a significantly lower TAPSE/SPAP ratio (1.23 ± 0.3 vs. 1.31 ± 0.33 mm/mmHg, p = 0.039), TAPSE/SPAP to body surface area (BSA) ratio (0.56 ± 0.14 vs. 0.6 ± 0.16 mm*m2/mmHg, p = 0.017), diastolic blood pressure (75.6 ± 7.9 vs. 78.8 ± 10.7 mmHg, p < 0.001), septal wall thickness (10.2 ± 1.1 vs. 10.7 ± 1.1 mm, p = 0.013) and left atrial volume index (27.5 ± 4.5 vs. 30.8 ± 4.1 ml/m2, p < 0.001), but a higher SPAP (24.2 ± 4.5 vs. 23.2 ± 4.4 mmHg, p = 0.035) compared to athletes aged 30–39 (n = 148, 33.1 ± 3.4 years). TAPSE was not different between the age groups. The TAPSE/SPAP ratio was positively correlated with left ventricular stroke volume (r = 0.133, p = 0.018) and training amount per week (r = 0.154, p = 0.001) and negatively correlated with E/E′ lat. (r = −0.152, p = 0.005).ConclusionThe reference values for pulmonary circulation coupling determined in this study could be used to interpret and distinguish physiological from pathological cardiac remodeling in male elite athletes.

Objective Evaluation of diagnostic accuracy of an oscillometry-based device (VascAssist) combining fully automated ankle-brachial index (ABI) and pulse-wave velocity (PWV) assessment for detection of peripheral arterial disease (PAD). Subjects and methods 110 consecutive subjects including symptomatic PAD patients ( n  = 41) and healthy PAD-free participants ( n  = 69) were recruited. All subjects underwent standard manual Doppler-based ABI (sABI) and oscillometry-based automated ABI (aABI) measurements (VascAssist). Oscillometry by the VascAssist included central and peripheral PWV assessment. Additionally, arterial stiffness (AS) was evaluated by flow-mediated vasodilation (FMD) of the brachial artery in all patients. All symptomatic PAD patients underwent catheter angiography for endovascular intervention and post-interventional acquisition of sABI, aABI, PWV and FMD. Results Sensitivity, specificity, PPV and NPV of aABI for detecting PAD was 73%, 100%, 100%, and 86% as compared to 80%, 96%, 92%, and 89% for sABI. Pearson-correlation for diabetics was r  = 0.81; ( P  < .001) and for non-diabetics r  = 0.77; ( P  < .001). Bland–Altman-analysis revealed a difference (95% CI) for diabetics of 0.09 (−0.22–0.4] and non-diabetics 0.022 [−0.25–0.295]. Weak correlation exists for FMD/AS analysis (pre-interventional R  = 0.386, P  = .043; post-interventional R  = −0.06; P  = .76) and significant increase of pre-/post-interventional PWV analysis ( P  < .001). Conclusion Combined automatic ABI and PWV acquisition with the VascAssist device showed excellent diagnostic accuracy for detection of PAD. Compared to FMD, AS analysis may serve as an investigator-independent (screening) tool for determination of functional vascular damage in atherosclerosis.

PurposeLow vitamin D levels have been associated with elevated blood pressure in the general population. Prospective studies, however, have produced conflicting evidence about the blood pressure-lowering effects of vitamin D supplementation. Cardiorespiratory fitness may modulate the vitamin D–blood pressure association. We therefore examined this association in professional athletes, whose high training load serves as a biological control for physical fitness.Methods50 male professional handball players (age 26 ± 5 years) were examined. We assessed the central aortic pressure parameters using transfer function-based analysis of oscillometrically obtained peripheral arterial waveforms. Serum 25-OH vitamin D concentrations were determined by chemiluminescent immunoassay. The threshold for insufficiency was set at values of < 30 ng/mL.ResultsCentral blood pressure (cBP) was 98 ± 7/60 ± 10 mmHg. The aortic pulse wave velocity (PWV) was 6.3 ± 1.0 m/s. Nine athletes (18%) displayed insufficient 25-OH vitamin D levels and had a significantly (p < 0.01) higher cBP compared with the 41 (82%) athletes with sufficient 25-OH vitamin D levels (106 ± 5/68 ± 8 vs. 97 ± 7/58 ± 9 mmHg). Central systolic blood pressure (cSBP) in vitamin D-sufficient athletes was significantly lower in comparison to the healthy reference population (97 mmHg vs. 103 mmHg, p < 0.001). This significance of difference was lost in vitamin D-insufficient athletes (106 mmHg vs. 103 mmHg, p = 0.12).ConclusionSignificantly raised central systolic and diastolic blood pressure in vitamin D-insufficient elite athletes implicates vitamin D as a potential modifier of vascular functional health.

This study aims to investigate whether a Web-based tool will facilitate the adoption of feedback control over calorie balance in overweight individuals, thereby promoting an increase of physical activity and a reduction of body weight and cardiovascular risk factors. This is a prospective exercise intervention study, commencing with a minimum weekly 3 × 20-min requirement of high-intensity interval training and requirement for Web-based self-monitoring and self-reporting of exercise and body weight. Subjects of this study include 83 overweight, sedentary, otherwise healthy adults aged 26–68 years. Anthropometric parameters, body fat, peak oxygen consumption, self-reported physical activity, frequency of use of the Web-based tool are among the characters measured in this study. This 24-week intervention substantially increased time spent for exercise (mean and median of 135 and 170 min/week, respectively) among the 72 % of participants who had adopted cognitive feedback control vs. no increase in the remaining participants of nonadopters. Adopters witnessed significantly improved peak oxygen consumption of >1 metabolic equivalent vs. no improvement among nonadopters. Adopters also reduced body mass index, body weight, and body fat by 1.6 kg/m 2 , 4.8 kg, and 3.6 kg, respectively vs. 0.4 kg/m 2 , 1.4 kg, and 1.1 kg in the control group. The increase in physical activity came at virtually no intervention effort of the investigators. This study demonstrates for the first time that adoption of cognitive feedback control over energy balance is possible with the help of a simple Web-based tool and that overweight adopters self-regulate exercise volume to significantly reduce body weight and improve biomarkers of fitness and cardiovascular risk.

The use of mesenchymal stromal cells (MSCs) differentiated toward a smooth muscle cell (SMC) phenotype may provide an alternative for investigators interested in regenerating urinary tract organs such as the bladder where autologous smooth muscle cells cannot be used or are unavailable. In this study we measured the effects of good manufacturing practice (GMP)-compliant expansion followed by myogenic differentiation of human MSCs on the expression of a range of contractile (from early to late) myogenic markers in relation to the electrophysiological parameters to assess the functional role of the differentiated MSCs and found that differentiation of MSCs associated with electrophysiological competence comparable to bladder SMCs. Within 1-2 weeks of myogenic differentiation, differentiating MSCs significantly expressed alpha smooth muscle actin (αSMA; ACTA2), transgelin (TAGLN), calponin (CNN1), and smooth muscle myosin heavy chain (SM-MHC; MYH11) according to qRT-PCR and/or immunofluorescence and Western blot. Voltage-gated Na+ current levels also increased within the same time period following myogenic differentiation. In contrast to undifferentiated MSCs, differentiated MSCs and bladder SMCs exhibited elevated cytosolic Ca2+ transients in response to K+-induced depolarization and contracted in response to K+ indicating functional maturation of differentiated MSCs. Depolarization was suppressed by Cd2+, an inhibitor of voltage-gated Ca2+-channels. The expression of Na+-channels was pharmacologically identified as the Nav1.4 subtype, while the K+ and Ca2+ ion channels were identified by gene expression of KCNMA1, CACNA1C and CACNA1H which encode for the large conductance Ca2+-activated K+ channel BKCa channels, Cav1.2 L-type Ca2+ channels and Cav3.2 T-type Ca2+ channels, respectively. This protocol may be used to differentiate adult MSCs into smooth muscle-like cells with an intermediate-to-late SMC contractile phenotype exhibiting voltage-gated ion channel activity comparable to bladder SMCs which may be important for urological regenerative medicine applications.