Acute effects of supramaximal exercise on carotid artery compliance and pulse pressure in young men and women

Abstract

The purpose of this study was to determine the cumulative effects of repeated cycling sprints (Wingate tests) on carotid compliance and blood pressure (BP). Fourteen young, healthy men and women completed this study. Vascular and hemodynamic measurements were taken at rest, 5 min following a first Wingate test, 25 min following the first Wingate test, 5 min following a second Wingate test, and 25 min following the second Wingate test. At each time point, the measurements taken included brachial and carotid pulse pressure (PP), heart rate, carotid artery maximum and minimum diameters, and carotid compliance. Carotid BP was obtained with applanation tonometry. Carotid diameters were obtained using ultrasonography and compliance was calculated from carotid diameters and BP. Carotid and brachial PP increased significantly (P < 0.05) 5 min after each Wingate test and returned to near baseline 25 min after each Wingate test. No cumulative PP effects were seen. A cumulative effect was seen for carotid compliance: 5 min following the second sprint, carotid arterial compliance decreased significantly more than 5 min following the first sprint (P < 0.05). A single cycling sprint reduces carotid artery compliance immediately after exercise. Performance of a second identical cycling sprint further compounds this vascular change, reducing carotid artery compliance beyond levels seen following a single cycling sprint.

The acute effect of maximal exercise on central and peripheral arterial stiffness indices and hemodynamics in children and adults

“…Our data are consistent with these findings and those of Rossow et al (2010). In addition, our results show that the response patterns of central and peripheral blood pressure to exercise are not age-dependent once the values were adjusted for body size.…”

“…effect found, and that the measurement of peripheral blood pressure during exercise recovery provides little insight into the central vascular burden associated with high-intensity dynamic exercise (Rossow et al 2010). Moreover, there was no change in the stiffness index α and β after the exercise bout further supporting the importance of local pressure.…”

“…It is conceivable that examination of the response of the arteries to physical stress, such as acute intense exercise, could offer additional critical information about vascular differences between healthy age groups, with possible clinical implications also for the understanding of the "unhealthy" child response. If changes in arterial stiffness indices following high-intensity exercise in adults are related to changes in blood pressure (Rossow et al 2010), the arterial response may be different in children because they have lower SBP during maximal exercise compared to adults . Whether the change in arterial stiffness indices following high-intensity exercise in children are a function of central or peripheral distending pressure is also unknown.…”

“…However, the varying exercise protocols used in these studies including incremental exercise to exhaustion (Heffernan et al 2007d;Naka et al 2003;Ranadive et al 2012;Yan et al 2014), moderate intensity continuous exercise (Kingwell et al 1997;Mc Clean et al 2007), brief low intensity exercise (Sugawara et al 2004;Sugawara et al 2003) and supramaximal exercise (Rakobowchuk et al 2009;Rossow et al 2010) showed that the effects of exercise in central stiffness are dependent on the intensity of exercise as well. High-intensity sprint exercise for instance, increases central artery stiffness (Rakobowchuk et al 2009) similarly to the response following acute resistance exercise (DeVan et al…”

How Healthy Were the Arteries of Phidippides?

“…4 High-intensity exercise increases arterial stiffness. 16 Following completion of a marathon, there are large reductions in pressure from wave reflections, aortic pulse pressure, and aortic diastolic pressure. 3 This is clinically relevant, as aortic diastolic pressure is a significant determinant of coronary perfusion pressure and subendocardial viability.…”