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Purpose: Exercise-induced increases in shear rate (SR) across different exercise intensities may differentially affect hypercapnia-induced vasodilation of the internal carotid artery (ICA), a potential index of cerebrovascular function. We aimed to elucidate the effects of exercise intensity on ICA SR during exercise and post-exercise hypercapnia-induced vasodilation of the ICA in young men., Methods: Twelve healthy men completed 30 min of cycling at moderate [MIE; 65 ± 5% of age-predicted maximal heart rate (HR max )] and high (HIE; 85 ± 5% HR max ) intensities. Hypercapnia-induced vasodilation was induced by 3 min of hypercapnia (target end-tidal partial pressure of CO 2  + 10 mmHg) and was assessed at pre-exercise, 5 min and 60 min after exercise. Doppler ultrasound was used to measure ICA diameter and blood velocity during exercise and hypercapnia tests., Results: SR was not altered during either exercise (interaction and main effects of time; both P > 0.05). ICA conductance decreased during HIE from resting values (5.1 ± 1.3 to 3.2 ± 1.0 mL·min -1 ·mmHg -1 ; P < 0.01) but not during MIE (5.0 ± 1.3 to 4.0 ± 0.8 mL·min -1 ·mmHg -1 ; P = 0.11). Consequently, hypercapnia-induced vasodilation declined immediately after HIE (6.9 ± 1.7% to 4.0 ± 1.4%; P < 0.01), but not after MIE (7.2 ± 2.1% to 7.3 ± 1.8%; P > 0.05). Sixty minutes after exercise, hypercapnia-induced vasodilation returned to baseline values in both trials (MIE 8.0 ± 3.1%; HIE 6.4 ± 2.9%; both P > 0.05)., Conclusion: The present study showed blunted hypercapnia-induced vasodilation of the ICA immediately after high-intensity exercise, but not a moderate-intensity exercise in young men. Given that the acute response is partly linked to the adaptive response in the peripheral endothelial function, the effects of aerobic training on cerebrovascular health may vary depending on exercise intensity., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The balance of angiogenic factors, including vascular endothelial growth factor (VEGF), and angiostatic factors, like thrombospondin-1 (TSP-1) and endostatin, controls striated muscle angiogenic responses to exercise training. The effect of age on circulating levels of these factors following a bout of exercise is unclear. The authors hypothesized that older adults would have lower circulating VEGF but higher TSP-1 and endostatin after exercise compared with young adults. Ten young and nine older participants cycled for 45 min at 60% estimated HRmax. Serum [VEGF], [TSP-1], and [endostatin] obtained before (PREX), immediately after (POSTX0), and 3 hr after (POSTX3) exercise were analyzed. [VEGF] increased in older adults only from PREX to POSTX0 (p < .05). [TSP-1] increased in both age groups (p < .05). There was no effect of age or exercise on [endostatin]. In conclusion, immediately after exercise, both groups had a similar increase in [TSP-1], but [VEGF] increased in older adults only.

Interval exercise has been determined to be more effective than continuous exercise for achieving improvement in the cardiovascular function of individuals suffering from cardiovascular disease. However, whether interval exercise improves the cerebrovascular function remains unclear. As per our hypothesis, interval exercise induces a higher cerebrovascular shear rate (SR) than continuous exercise. In this study, 11 adult men randomly performed continuous exercise for 12 min or work-equivalent (57.6 kJ/exercise session) interval exercise of semi-recumbent cycling. The SR in the internal carotid artery (ICA) represents an index of the cerebrovascular SR, which was measured during both the exercises using Doppler ultrasonography. Both the aerobic exercise modes increased the ICA SR. Moreover, the average ICA SR of the interval exercise for the final 4 min of exercise or 2 min of recovery was significantly higher than that for continuous exercise (exercise, 351 ± 75 vs. 330 ± 61/s, p = .038; recovery, 327 ± 86 vs. 290 ± 56/s, p = .014). To our knowledge, this is the first study to show that aerobic interval exercise increased the ICA SR more than equivalent work volume of aerobic continuous exercise. Thus, aerobic interval exercise may be more effective at stimulating the cerebrovasculature, resulting in greater improvements in cerebrovascular function as compared to continuous aerobic exercise in healthy adult men. These findings provide some important information that would help enhance exercise therapy programs for patients with arteriosclerosis, especially in the cerebral circulation., (© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Consumption of a single, sugar-sweetened beverage (SSB) impairs vascular endothelial function. Regular aerobic exercise improves endothelium-dependent vasodilation; however, it is unknown whether these beneficial effects persist with frequent SSB consumption. Therefore, the purpose of this study was twofold; we studied the effects of repetitive SSB consumption (75 g d-glucose, 3 times/day) for 1 wk (Glu, n = 13, 23 ± 4 yr, 23.5 ± 3.4 kg/m 2 ) on endothelium-dependent vasodilation (FMD). Then, in a separate cohort, we investigated whether 45 min of moderate-intensity aerobic exercise on five separate days offset the hypothesized decrease in FMD during the Glu protocol (Glu+Ex, n = 11, 21 ± 3 yr, 23.8 ± 2.4 kg/m 2 ). Baseline, fasting [glucose] ( P = 0.15), [insulin] ( P = 0.25), %FMD ( P = 0.48), absolute FMD ( P = 0.66), and shear rate area under the curve (SR AUC ; P = 0.82) were similar between groups. Following the interventions, fasting [glucose] (Glu: 94 ± 6 to 92 ± 6 mg/dL, Glu+Ex: 89 ± 8 to 87 ± 6 mg/dL, P = 0.74) and [insulin] (Glu: 11.3 ± 6.2 to 11.8 ± 8.9 μU/mL, Glu+Ex: 8.7 ± 2.9 to 9.4 ± 3.2 μU/mL, P = 0.89) were unchanged. %FMD was reduced in Glu (6.1 ± 2.2 to 5.1 ± 1.3%) and increased in Glu+Ex (6.6 ± 2.2 to 7.8 ± 2.4%, P < 0.05 for both). SR AUC increased similarly in both Glu [17,715 ± 8,275 to 22,922 ± 4,808 arbitrary units (A.U.)] and Glu+Ex (18,216 ± 4,516 to 21,666 ± 5,392 A.U., main effect of time P < 0.05). When %FMD was adjusted for SR AUC , attenuation was observed in Glu (0.41 ± 0.18 to 0.23 ± 0.08%/s × 103, P < 0.05) but not Glu+Ex (0.38 ± 0.14 to 0.38 ± 0.13%/s × 103, P = 0.88). Despite unchanged fasting [glucose] and [insulin], repeated consumption of SSBs impaired conduit artery vascular endothelial function. Additionally, subjects who engaged in regular moderate-intensity aerobic exercise did not demonstrate the same SSB-induced endothelial dysfunction. Collectively, these data suggest aerobic exercise may offset the deleterious effects of repetitive SSB consumption.

Habitual aerobic exercise attenuates elevated vasoconstriction during acute exercise (functional sympatholysis) in older men; however, this effect remains unknown in postmenopausal women (PMW). This study tested the hypothesis that PMW who participate in habitual aerobic exercise demonstrate a greater functional sympatholysis compared with their untrained counterparts. Nineteen PMW (untrained n = 9 vs. trained n = 10) performed 5 min of steady-state (SS) forearm exercise at relative [10% and 20% of maximum voluntary contraction (MVC)] and absolute (5 kg) contraction intensities. Lower-body negative pressure (LBNP) was used to increase sympathetic vasoconstriction during rest and forearm exercise. Brachial artery diameter and blood velocities (via Doppler ultrasound) determined forearm blood flow (FBF; ml/min). Forearm muscle oxygen consumption ([Formula: see text]; ml/min) and arteriovenous oxygen difference (a-vO 2diff ) were estimated during SS-exercise and SS-exercise with LBNP. Forearm vascular conductance (FVC; ml·min -1 ·100 mmHg -1 ) was calculated from FBF and mean arterial pressure (MAP; mmHg). Vasoconstrictor responsiveness was determined as the %change in FVC during LBNP. The reduction in FVC (% change FVC) during LBNP was lower in trained compared with untrained PMW at 10% MVC (-7.3 ± 1.2% vs. -13.0 ± 1.1%; P < 0.05), 20% MVC (-4.4 ± 0.8% vs. -8.6 ± 1.4%; P < 0.05), and 5 kg (-5.3 ± 0.8% vs. -8.9 ± 1.4%; P < 0.05) conditions, whereas there were no differences at rest (-32.7 ± 4.4% vs. -33.7 ± 4.0%). Peripheral (FVC, FBF, and [Formula: see text]) and the magnitude change in systemic hemodynamics (heart rate and MAP) did not differ between groups during exercise. Collectively, the findings present the first evidence suggesting that PMW who participate in aerobic exercise demonstrate a greater functional sympatholysis compared with untrained PMW during mild to moderate forearm exercise. NEW & NOTEWORTHY Habitual aerobic exercise attenuates the elevated sympathetic nervous system-induced vasoconstriction during an acute bout of exercise (improved functional sympatholysis) in aging men; however, this effect remains unknown in postmenopausal women (PMW). The novel findings of this study suggest that habitual aerobic exercise results in an enhanced functional sympatholysis in PMW. Conversely, habitual aerobic exercise does not alter blood flow and oxygen utilization during acute forearm exercise compared with PMW who do not habitually exercise.

Purpose: Modulation of vascular function follows an exercise intensity-dependent pattern in young adults. This study aimed to investigate the potential intensity-dependent effects of an acute bout of exercise on conduit and resistance artery function in healthy older adults., Methods: Eleven healthy older adults (five males/six females, 66 ± 1 yr) completed 30 min of recumbent cycling at 50%-55% (low intensity) and 75%-80% (high intensity) of their age-predicted HRmax on two separate study visits. Doppler ultrasound measures of brachial artery flow-mediated dilation (FMD) and reactive hyperemia were taken at baseline, 10 min postexercise, and 1 h postexercise. In addition, cardiovascular hemodynamics and brachial shear rate were measured every 5 min during exercise., Results: Brachial artery FMD was enhanced 10 min after high-intensity exercise (4.8% ± 0.2% to 9.1% ± 0.3%, P < 0.01), but not low-intensity (4.7% ± 0.2% to 6.2% ± 0.3%, P = 0.54) exercise. Peak and total (area under the curve) blood flow during reactive hyperemia (measures of resistance artery function) were enhanced 10 min postexercise for both intensities (peak low intensity, 372 ± 31 to 444 ± 37 mL·min; peak high intensity, 391 ± 30 to 455 ± 28 mL·min; total low intensity, 142 ± 16 to 205 ± 20 mL; total high intensity, 158 ± 14 to 240 ± 25 mL; main effect of time for both, P < 0.05). However, the magnitude of change in peak and the total blood flow were not different between exercise intensities (interaction effect; P = 0.56 and P = 0.97, respectively). Independent of exercise intensity, FMD returned to baseline 1 h after exercise (high, 5.9% ± 0.3%; low, 5.1% ± 0.1%; both P > 0.05)., Conclusion: Our data indicate that high-intensity exercise acutely enhances conduit artery function in healthy older adults. In addition, an acute bout of exercise enhances resistance artery function independent of intensity.

Purpose: This study aimed to elucidate the effects of hypoxia on the pattern of oscillatory blood flow in the inactive limb during constant-load dynamic exercise. We hypothesised that retrograde blood flow in the brachial artery of the inactive limb would increase during constant-load leg cycling under hypoxic conditions., Methods: Three maximal exercise tests were conducted in eight healthy males on a semi-recumbent cycle ergometer while the subjects breathed a normoxic [inspired oxygen fraction (FIO2) = 0.209] or two hypoxic gas mixtures (FIO2 = 0.155 and 0.120). Subjects then performed submaximal exercise at the same relative exercise intensity of 60 % peak oxygen uptake under normoxic or the two hypoxic conditions for 30 min. Brachial artery blood velocity and diameter were recorded simultaneously during submaximal exercise using Doppler ultrasonography., Results: Antegrade blood flow gradually increased during exercise, with no significant differences among the three trials. Retrograde blood flow showed a biphasic response, with an initial increase followed by a gradual decrease during normoxic exercise. In contrast, retrograde blood flow significantly increased during moderate and severe hypoxic exercise, and remained elevated above normoxic conditions during exercise. At 30 min of exercise, the magnitude of the change in retrograde blood flow during exercise was greater as the level of hypoxia increased (normoxia: -18.7 ± 23.5 ml min(-1); moderate hypoxia: -39.3 ± 21.4 ml min(-1); severe hypoxia: -64.0 ± 36.3 ml min(-1))., Conclusion: These results indicate that moderate and severe hypoxia augment retrograde blood flow in the inactive limb during constant-load dynamic leg exercise.

The purpose of the present study was to clarify the influence of inspiratory resistive breathing during exercise under hypoxic conditions on muscle sympathetic nerve activity (MSNA) and blood pressure (BP). Six healthy males completed this study. The subjects performed a submaximal exercise test using a cycle ergometer in a semirecumbent position under normoxic [inspired oxygen fraction (FiO2) = 0.21] and hypoxic (FiO2 = 0.12-0.13) conditions. The subjects carried out two 10-min exercises at 40% peak oxygen uptake [spontaneous breathing for 5 min and voluntary breathing with inspiratory resistance for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 s each)]. MSNA was recorded via microneurography of the right median nerve at the elbow. A progressive increase in MSNA burst frequency (BF) during leg-cycling exercise with inspiratory resistance in normoxia and hypoxia were accompanied by an augmentation of BP. The increased MSNA BF and mean arterial BP (MBP) during exercise with inspiratory resistive breathing in hypoxia (MSNA BF, 55.7 ± 1.4 bursts/min, MBP, 134.3 ± 6.6 mmHg) were higher than those in normoxia (MSNA BF, 39.2 ± 1.8 bursts/min, MBP, 123.6 ± 4.5 mmHg). These results suggest that an enhancement of inspiratory muscle activity under hypoxic condition leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.

The purpose of this study was to elucidate the influence of inspiratory muscle fatigue on muscle sympathetic nerve activity (MSNA) and blood pressure (BP) response during submaximal exercise. We hypothesized that inspiratory muscle fatigue would elicit increases in sympathetic vasoconstrictor outflow and BP during dynamic leg exercise. The subjects carried out four submaximal exercise tests: two were maximal inspiratory pressure (PI(max)) tests and two were MSNA tests. In the PI(max) tests, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without inspiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each set at 0.5 s)]. Before and immediately after exercise, PI(max) was estimated. In MSNA tests, the subjects performed two 15-min exercises (spontaneous breathing for 5 min, with or without inspiratory resistive breathing for 5 min, and spontaneous breathing for 5 min). MSNA was recorded via microneurography of the right median nerve at the elbow. PI(max) decreased following exercise with resistive breathing, whereas no change was found without resistance. The time-dependent increase in MSNA burst frequency (BF) appeared during exercise with inspiratory resistive breathing, accompanied by an augmentation of diastolic BP (DBP) (with resistance: MSNA, BF +83.4%; DBP, +23.8%; without resistance: MSNA BF, +19.2%; DBP, -0.4%, from spontaneous breathing during exercise). These results suggest that inspiratory muscle fatigue induces increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise at mild intensity.