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Introduction: Age-related stiffening of the large elastic arteries (e.g., common carotid artery [CCA]) may impair wall dynamics (i.e., strain) and amplify transmission of pulsatile blood flow into the brain with large increases in pressure that occur during maximal resistance exercise (RE). The purpose of this study was to compare CCA arterial wall dynamics, central hemodynamics, and cerebral blood velocity responses during maximal RE between young and older adults., Methods: Thirty-one young (YA; 26 ± 5 yrs; 23.8 ± 3.3 kg/m 2 ) and 25 older adults (OA; 60 ± 6 yrs; 30.0 ± 5.5 kg/m 2 ) performed a unilateral maximal isokinetic knee flexion/extension exercise protocol (i.e., maximal RE). All measures were recorded at baseline and during the last 10 s of maximal RE. Common carotid artery strain, CCA strain time to peak, and CCA strain rate (i.e., variables of arterial wall dynamics) were analyzed using 2D speckle tracking software from circumferential ultrasound images. Transcranial Doppler was used to measure right middle cerebral artery (MCA) blood velocity. Non-invasive arterial blood pressure measurements were obtained using finger photoplethysmography., Results: Older adults had greater reductions in CCA strain time to peak from baseline to maximal RE (345 ± 39 to 242 ± 52 ms) than YA (308 ± 35 to 247 ± 42 ms; interaction effect, p < 0.01). MCA velocity was similar between YA and OA during maximal RE (p = 0.48), despite a greater arterial pressor response in OA (p < 0.01)., Conclusion: These data suggest cerebral blood velocity responds similarly during maximal RE among OA compared to YA, despite subtle age-related differences in the pressor and extracranial vascular response during maximal RE., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Introduction: There are well-established sex differences in central hemodynamic and cardiac adaptations to endurance exercise; however, controversial evidence suggests that excessive endurance exercise may be related to detrimental cardiovascular adaptations in marathoners., Purpose: To examine left ventricle (LV) structure, LV function, 24-h central hemodynamics and ventricular-vascular coupling in male and female marathoners and recreationally active adults., Methods: 52 marathoners (41 ± 5 years, n = 28 female, completed 6 ± 1 marathons/3 years) and 49 recreationally active controls (42 ± 5 years, n = 25 female) participated in the study. Three-Dimensional Echocardiography (3DE) was used to measure LV mass index and LV longitudinal (LS) circumferential (CS), area (AS), and radial strain (RS). An ambulatory blood pressure (BP) cuff was used to measure 24-h central hemodynamics (BP, pulse wave velocity, PWV, wave reflection index, RIx). Hemodynamic and 3DE measures were combined to derive the ratio of arterial elastance (Ea) to ventricular elastance (Elv) as a global measure of ventricular-vascular coupling., Results: There were no sex or group differences in LS, CS, AS, and RS (p > 0.05). Females marathoners had similar aortic BP (116 ± 9 vs. 113 ± 1 mmHg), and PWV (5.9 ± 0.5 vs. 5.9 ± 1.1 m/s) compared to female controls but lower aSBP (116 ± 9 vs. 131 ± 10 mmHg) and PWV (5.9 ± 0.5 vs. 6.2 ± 0.5 m/s) compared to male marathoners (p < 0.05). Female marathoners had lower Ea/Elv than female controls (0.67 ± 0.20 vs. 0.93 ± 0.36) and male marathoners (0.67 ± 0.20 vs. 0.85 ± 0.42, p < 0.05)., Conclusions: Women that have completed multiple marathons do not have reduced LV function or increased aortic stiffness and may have better ventricular-vascular coupling compared to male marathoners and their female untrained counterparts., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: Aortic stiffness may affect shear patterns in the peripheral vasculature. This study examined if sprint exercise, which typically increases aortic stiffness is associated with increased peripheral retrograde blood flow and impaired microvascular function., Methods: Twenty participants (10 women; age: 27 ± 5 years) underwent arterial stiffness, shear rate, and microvascular function assessment at three time points: baseline; following time control; ~ 2 min post a 30-s cycle ergometer sprint against 7.0% body mass. Aortic stiffness was assessed using carotid-femoral pulse wave velocity (cfPWV). Superficial femoral artery (SFA) diameter and blood velocity were assessed using Doppler-ultrasound and were used to calculate shear rates and resistance index (RI). SFA wave reflections were obtained via wave intensity analysis. Vastus medialis microvascular function was measured as tissue saturation index reactivity pre-post exercise via near-infrared spectroscopy., Results: cfPWV increased by + 0.8 ± 0.7 m·s -1 following exercise (p < 0.001). Retrograde shear was reduced following exercise compared with time control (- 4.9 ± 3.8 s -1 ; p < 0.001), while tissue saturation index was increased post-exercise from baseline (+ 2.3 ± 4.6%; p = 0.04). Reductions in SFA wave reflections (- 1.70 ± 1.96 aU) and RI (- 0.17 ± 0.13 aU) were also noted following exercise (p < 0.001)., Conclusion: These data suggest sprint exercise-mediated changes in peripheral shear patterns and microvascular function in the exercised vasculature occur independent from increases in aortic stiffness. Exercise-induced reductions in SFA retrograde shear may be related to decreased wave reflections and peripheral vascular resistance.

Introduction: Retrograde shear causes endothelial damage and is pro-atherogenic. The purpose of our study was to examine the impact of vascular remodeling from habitual exercise training on acute changes in retrograde shear and microvascular oxygenation (SMO 2 ) induced via 30 min of external compression., Methods: Participants included 11 exercise trained (ET) men (Division I track athletes; age 20 ± 3 years) and 18 recreationally active (RA) men (age 23 ± 5 years). Near-infrared spectroscopy (NIRS) was used to measure vastus medialis SMO 2 . Doppler-ultrasound was used to assess SFA intima-media thickness, diameter and flow velocity to derive retrograde shear. Vascular measures were made at baseline (BASELINE), during a sham condition (calf compression to 5 mmHg, SHAM) and during the experimental condition (calf compression to 60 mmHg, EXP)., Results: Compared to RA, ET had larger SFA diameters (0.66 ± 0.06 vs 0.58 ± 0.06 cm, p < 0.05) and lower SFA IMT (0.33 ± 0.03 vs 0.36 ± 0.07 mm, p < 0.05). Retrograde shear increased similarly in both groups during EXP (p < 0.05) but ET men had lower overall retrograde shear during the conditions (BASELINE 75.8 ± 26.8 vs EXP 88.2 ± 16.9 s -1 ) compared to RA men (BASELINE 84.4 ± 23.3 vs EXP 106.4 ± 19.6 s -1 p < 0.05). There was a similar increase in SMO 2 from BASELINE to SHAM (ET + 8.1 ± 4.8 vs RA + 6.4 ± 9.7%) and BASELINE to EXP (ET + 8.7 ± 6.4 vs RA + 7.1 ± 9.0%) in both groups., Conclusion: Beneficial vascular remodeling in ET men is associated with lower retrograde shear during external compression. Acute increases in retrograde shear with external compression do not detrimentally impact microvascular oxygenation.

Introduction: While resistance exercise (RE) is known to be beneficial for overall health, one bout of RE acutely increases aortic stiffness and pulse pressure (PP). Increases in aortic stiffness and PP in a setting of aging has been shown to detrimentally impact cognitive function. This study examined whether increased aortic stiffness and PP from an acute bout of RE is associated with cognitive function., Methods: Thirty-five participants (21 ± 2 years) underwent cognitive testing before and after either an acute bout of RE or a non-exercise time-control condition. Cognitive function was assessed as reaction time and accuracy during memory recognition, attention (Flanker) and working memory (N-back) tasks. Aortic stiffness and PP were measured via pulse wave velocity (PWV) and pulse wave analysis, respectively, using a brachial oscillometric device., Results: There were significant increases in aortic PWV and aortic PP following RE (p < 0.05) with no change in PWV or PP following the non-exercise control condition (p > 0.05). There was no change in accuracy metrics (% hits) across conditions for any cognitive task (p > 0.05). There was a condition-by-time interaction for reaction time for the memory task (p < 0.05) driven by a significant decrease in reaction times following RE (p < 0.05) with no change in reaction time following the non-exercise control (p > 0.05)., Conclusion: Functional increases in aortic stiffness and pulse pressure following acute RE occur in the absence of detrimental changes in cognitive function in young, healthy adults.

Purpose: Investigate the effects of acute high-intensity exercise on common carotid artery (CCA) dimensions, stiffness, and wave intensity., Methods: Fifty-five healthy men and women (22 ± 5 year; 24.5 ± 2.7 kg m(-2)) underwent 30 s of high-intensity cycling (HIC; Wingate anaerobic test). CCA diameter, stiffness [β-stiffness, Elastic Modulus (E p)], pulsatility index (PI), forward wave intensities [due to LV contraction (W 1) and LV suction (W 2)], and reflected wave intensity [negative area (NA)] were assessed using a combination of Doppler ultrasound, wave intensity analysis, and applanation tonometry at baseline and immediately post-HIC., Results: CCA β-stiffness, E p, PI and pulse pressure increased significantly immediately post-HIC (p < 0.05). CCA diameter decreased acutely post-HIC (p < 0.05). There were also significant increases in W 1 and NA and a significant decrease in W 2 (p < 0.05). A significant correlation was found between change in W 1 and PI (r = 0.438, p < 0.05), from rest to recovery as well as a significant inverse correlation between W 2 and PI (r = -0.378, p < 0.05). Change in PI was not associated with change in CCA stiffness or NA (p > 0.05)., Conclusions: Acute HIC results in CCA constriction and increases in CCA stiffness along with increases in hemodynamic pulsatility. The increase in pulsatility may be due to a combination of increased forward wave intensity from increased LV contractility into a smaller vessel (i.e. impaired matching of diameter and flow) coupled with reduced LV suction.