Anna Oue

The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans

Non‐technical summary  The mechanism underlying the plateau or relative decrease in cerebral blood flow during maximal incremental dynamic exercise remains unclear. We show that during graded dynamic exercise, the regulation of internal carotid artery blood flow was limited by a large increase in external carotid artery blood flow, one function of which is thermoregulation during heavy exercise. The mechanism of the plateau or decrease in internal carotid artery blood flow appears to be partly due to exercise‐induced redistribution of arterial blood flow to the head and brain.

Differential blood flow responses to CO2 in human internal and external carotid and vertebral arteries

•  Arterial CO2 serves as a mediator of cerebral blood flow, and its relative influence on the regulation of cerebral blood flow is defined as cerebral CO2 reactivity. •  Because of methodological limitations, almost all previous studies have evaluated the response of blood flow velocity in the middle cerebral artery to changes in CO2 as a measure of CO2 reactivity across the whole brain. •  We found that the vertebral artery has lower CO2 reactivity than the internal carotid artery. Moreover, CO2 reactivity in the external carotid artery was markedly lower than in the cerebral circulation. •  These results demonstrate regional differences in CO2 regulation of blood flow between the internal carotid, external carotid, and vertebro‐basilar circulation.

Dynamic cerebral autoregulation during and after handgrip exercise in humans

The purpose of the present study was to examine the effect of static exercise on dynamic cerebral autoregulation (CA). In nine healthy subjects at rest before, during, and after static handgrip exercise at 30% maximum voluntary contraction, the response to an acute drop in mean arterial blood pressure and middle cerebral artery mean blood velocity was examined. Acute hypotension was induced nonpharmacologically via rapid release of bilateral thigh occlusion cuffs. Subjects were instructed to avoid executing a Valsalva maneuver during handgrip. To quantify dynamic CA, the rate of regulation (RoR) was calculated from the change in cerebral vascular conductance index during the transient fall in blood pressure. There was no significant difference in RoR between rest (mean+/-SE; 0.278+/-0.052/s), exercise (0.333+/-0.053/s), and recovery (0.305+/-0.059/s) conditions (P=0.747). In addition, there was no significant difference in the rate of absolute cerebral vasodilatory response to acute hypotension between three conditions (P=0.737). This finding indicates that static exercise and related elevations in blood pressure do not alter dynamic CA.

Central command contributes to increased blood flow in the noncontracting muscle at the start of one-legged dynamic exercise in humans

Whether neurogenic vasodilatation contributes to exercise hyperemia is still controversial. Blood flow to noncontracting muscle, however, is chiefly regulated by a neural mechanism. Although vasodilatation in the nonexercising limb was shown at the onset of exercise, it was unclear whether central command or muscle mechanoreflex is responsible for the vasodilatation. To clarify this, using voluntary one-legged cycling with the right leg in humans, we measured the relative changes in concentrations of oxygenated-hemoglobin (Oxy-Hb) of the noncontracting vastus lateralis (VL) muscle with near-infrared spectroscopy as an index of tissue blood flow and femoral blood flow to the nonexercising leg. Oxy-Hb in the noncontracting VL and femoral blood flow increased (P < 0.05) at the start period of voluntary one-legged cycling without accompanying a rise in arterial blood pressure. In contrast, no increases in Oxy-Hb and femoral blood flow were detected at the start period of passive one-legged cycling, suggesting that muscle mechanoreflex cannot explain the initial vasodilatation of the noncontracting muscle during voluntary one-legged cycling. Motor imagery of the voluntary one-legged cycling increased Oxy-Hb of not only the right but also the left VL. Furthermore, an increase in Oxy-Hb of the contracting VL, which was observed at the start period of voluntary one-legged cycling, had the same time course and magnitude as the increase in Oxy-Hb of the noncontracting muscle. Thus it is concluded that the centrally induced vasodilator signal is equally transmitted to the bilateral VL muscles, not only during imagery of exercise but also at the start period of voluntary exercise in humans.

Decreased compliance in the deep and superficial conduit veins of the upper arm during prolonged cycling exercise

We examined whether there is a difference in compliance between the deep and superficial conduit veins of the upper arm in response to prolonged exercise. Eight young men performed cycling exercise at 60% of peak oxygen uptake until rectal temperature had been increased by 1.1°C for 38–48 min. The cross‐sectional area (CSA) of the brachial (deep) and basilic (superficial) veins was assessed by ultrasound during a cuff deflation protocol. Compliance (CPL) was calculated as the numerical derivative of the cuff pressure and CSA curve. During prolonged exercise, CPL in both conduit veins was similarly decreased when compared with pre‐exercise values; however, the CSA decreased in the deep vein but increased in the superficial vein. In addition, passive heating caused an analogous change in CSA and CPL of superficial vein when compared with prolonged exercise, but did not change CSA and CPL of deep vein. Cold pressor test induced the decreased CSA of deep and superficial veins without the alteration of CPL of both veins. These results suggest that CPL in the deep and superficial conduit veins adjusts to prolonged exercise via different mechanisms.

Heat stress redistributes blood flow in arteries of the brain during dynamic exercise

We hypothesized that heat stress would decrease anterior and posterior cerebral blood flow (CBF) during exercise, and the reduction in anterior CBF would be partly associated with large increase in extracranial blood flow (BF). Nine subjects performed 40 min of semirecumbent cycling at 60% of the peak oxygen uptake in hot (35°C; Heat) and thermoneutral environments (25°C; Control). We evaluated BF and conductance (COND) in the external carotid artery (ECA), internal carotid artery (ICA), and vertebral artery (VA) using ultrasonography. During the Heat condition, ICA and VA BF were significantly increased 10 min after the start of exercise (P < 0.05) and thereafter gradually decreased. ICA COND was significantly decreased (P < 0.05), whereas VA COND remained unchanged throughout Heat. Compared with the Control, either BF or COND of ICA and VA at the end of Heat tended to be lower, but not significantly. In contrast, ECA BF and COND at the end of Heat were both higher than levels in the Control condition (P < 0.01). During Heat, a reduction in ICA BF appears to be associated with a decline in end-tidal CO2 tension (r = 0.84), whereas VA BF appears to be affected by a change in cardiac output (r = 0.87). In addition, a change in ECA BF during Heat was negatively correlated with a change in ICA BF (r = -0.75). Heat stress resulted in modification of the vascular response of head and brain arteries to exercise, which resulted in an alteration in the distribution of cardiac output. Moreover, a hyperthermia-induced increase in extracranial BF might compromise anterior CBF during exercise with heat stress.

Compliance in the deep and superficial conduit veins of the nonexercising arm is unaffected by short‐term exercise

The effects of short‐term dynamic and static exercise on compliance (CPL) in a single conduit vein in the nonexercising limb are not fully understood, although prolonged cycling exercise was found to produce a significant reduction of CPL in the veins. In this study, we investigated the cross‐sectional area (CSA) and CPL in the brachial (deep) and basilic (superficial) veins of the nonexercising arm in 14 participants who performed a 5‐min cycling exercise at 35% and 70% of peak oxygen uptake (study 1) and in 11 participants who performed a 2‐min static handgrip exercise at 30% of maximal voluntary contraction (study 2). The CSA in the deep and superficial veins at rest and during the final minute of exercise was measured by high‐resolution ultrasonography during a short‐duration cuff deflation protocol. The CPL in each vein was calculated as the numerical derivative of the cuff pressure and CSA curve. During short‐term dynamic and static exercise, there was no change in CPL in either vein, but there was a decrease in CSA in both veins. The simultaneous findings of unchanged CPL and decreased CSA suggest that CPL during short‐term exercise are independently controlled by the mechanisms responsible for exercise‐induced sympathoexcitation in both single veins. Thus, short‐term exercise does not alter CPL in both conduit superficial and deep veins in nonexercising upper arm.

Relationship between cerebral arterial inflow and venous outflow during dynamic supine exercise

The regulation of cerebral venous outflow during exercise has not been studied systematically. To identify relations between cerebral arterial inflow and venous outflow, we assessed the blood flow (BF) of the cerebral arteries (internal carotid artery: ICA and vertebral artery: VA) and veins (internal jugular vein: IJV and vertebral vein: VV) during dynamic exercise using ultrasonography. Nine subjects performed a cycling exercise in supine position at a light and moderate workload. Similar to the ICA BF, the IJV BF increased from baseline during light exercise (P < 0.05). However, the IJV BF decreased below baseline levels during moderate exercise, whereas the ICA BF returned near resting levels. In contrast, BF of the VA and VV increased with the workload (P < 0.05). The change in the ICA or VA BF from baseline to exercise was significantly correlated with the change in the IJV (r = 0.73, P = 0.001) or VV BF (r = 0.52, P = 0.028), respectively. These findings suggest that dynamic supine exercise modifies the cerebral venous outflow, and there is coupling between regulations of arterial inflow and venous outflow in both anterior and posterior cerebral circulation. However, it remains unclear whether changes in cerebral venous outflow influence on the regulation of cerebral arterial inflow during exercise.