Aims To determine the prevalence and characteristics of bicuspid aortic valve (BAV) among elite athletes and to analyse the effect of long-term exercise training on their aortas. Methods and results Consecutive BAV and tricuspid aortic valve (TAV) elite athletes from a population of 5136 athletes evaluated at the Sports Medicine Center of the Spanish National Sports Council were identified using echocardiography. A total of 41 BAV elite athletes were matched with 41 TAV elite athletes, and 41 BAV non-athletic patients from three Spanish tertiary hospitals. Sixteen BAV elite athletes who had undergone at least two cardiac evaluations separated by more than 3 years were selected to assess their clinical course. The prevalence of BAV in elite athletes was 0.8%. The proximal ascending aorta was larger for both BAV groups in comparison to TAV athletes (P = 0.001). No differences in aortic diameters were found between BAV athletes and BAV non-athletes. In BAV elite athletes, the annual growth rates for aortic annulus, sinuses of Valsalva, sinotubular junction, and proximal ascending aorta were 0.04 ± 0.24, 0.11 ± 0.59, 0.14 ± 0.38, and 0.21 ± 0.44 mm/year, respectively. Aortic regurgitation was the only functional abnormality, but no significant progression was found. Conclusion High-intensity training and sports competition may not aggravate BAV condition during elite athletes’ careers. BAV elite athletes with mild-to-moderately dilated aortas may engage in high dynamic cardiovascular exercise without adverse consequences, although an echocardiographic follow-up is recommended.

Endothelial shear stress (ESS) has a possible effect on regulation of gene expression in the protection against atherosclerosis. During exercise, ESS should increase as systolic blood pressure and heart rate (HR) increase too; however, it is hard to determine ESS changes during exercise. Imaging ultrasound assessment of the brachial and the carotid arterial blood flow during exercise might help to estimate exercise-induced ESS. We present here the methodology at the Clinical Applied Physiology Laboratory to estimate exercise-induced ESS. We normally perform 2 exercise tests in 2 different visits. First, a cardiopulmonary exercise test with serial microblood sampling to determine blood lactate (La) levels on a stationary cycle ergometer to determine maximal oxygen consumption, maximal exercising HR, and lactate threshold curve. The second exercise test includes three 5-min steady state stages determined by La levels from test 1 (La <2 mmol/L, La 2–4 mmol/L, and La >4 mmol/L). During the second test, we position an ultrasound probe holder on either the arm or neck to image the brachial or carotid arteries, respectively. We obtain images and blood flow velocities through Doppler at each exercise stage and then we analyze the images using edge detection software to determine artery diameters. With these data, we are able to estimate ESS, flow direction, and the presence of turbulent flow.

Premenopausal females have a lower cardiovascular risk than males. Sex differences on exercise‐induced endothelial shear stress (ESS) and blood flow patterns may explain part of this risk reduction. The purpose of this cross‐sectional study was to determine the differences in brachial artery exercise‐induced ESS and blood flow patterns between males and females. Thirty subjects (13 females) were recruited to perform a three‐workload steady‐state exercise test based on blood lactate levels (i.e. <2.0, 2.0–4.0, >4.0 mmol/l). ESS and blood flow patterns were estimated at rest and during each workload using Womersley's approximation and Reynolds number, respectively. Both males and females showed an exercise intensity‐dependent increase in antegrade and retrograde ESS. There was no significant sex effect or interaction for antegrade ESS (F(1, 30) = 0.715, p = 0.405 and F(1·672, 60) = 1.511, p = 0.232, respectively) or retrograde ESS (F(1, 30) = 0.794, p = 0.380 and F(1·810, 60) = 1.022, p = 0.361, respectively). Additionally, antegrade blood flow was turbulent during all bouts of exercise while retrograde blood flow became disturbed at moderate and high exercise intensities in both groups. There are no differences in exercise‐induced ESS and blood flow patterns between males and females when the exercise load is equivalent. This suggests that the vascular benefits of exercise training are similar in both sexes from a haemodynamic standpoint.

Summary Introduction Endothelial dysfunction is considered the first step in the development of atherosclerosis. Flow‐mediated dilation (FMD) has been the most common assessment of endothelial function in research but it has failed in obtaining a widespread use in clinical settings due to a lack of standardization and a large inter‐subject variability. Normalization of FMD to endothelial shear stress (ESS) has been proposed to solve its technical limitations. However, studies have not considered the characteristic of the blood flow during FMD under pulsatile conditions in their ESS estimations. Methods A total of 26 young healthy subjects (15 females and 11 males) underwent FMD testing. Microhematocrit measurement was used to determine blood viscosity (μ). ESS was calculated by Womersley's approximation, ESS = μ*2K*Velocity/Diameter, where K is a function of Womersley's parameter (α). Blood flow patterns were determined by critical Reynolds number. Statistical analysis included repeated measures ANOVA to detect ESS differences during FMD until peak dilation. Significance was established at P≤0.05. Results The mean (SD) FMD% and time to peak dilation were 7·4 (3·1) % and 35 (9·3) seconds, respectively. ESS was significantly reduced during FMD until peak dilation (P<0·001). Turbulent blood flow was the only pattern observed until peak dilation in 96·15% of the sample. Conclusion Peak FMD dilation in a young healthy population is triggered mostly by high‐ESS under turbulent flow conditions. Due to the pulsatile nature of blood flow and the appearance of a turbulent pattern during FMD, ESS should be estimated by Womersley's approximation rather than Poiseuille's law.

No abstract