Tomoko Sadamoto

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.

Different blood flow responses to dynamic exercise between internal carotid and vertebral arteries in women

The blood flow regulation in vertebral system during dynamic exercise in humans remains unclear. We examined the blood flow responses in both the internal carotid artery (QICA) and vertebral artery (QVA) simultaneously during graded dynamic exercise by Doppler ultrasound to evaluate whether cerebrovascular responses to exercise were similar. In the semisupine position, 10 young women performed a graded cycling exercise at three loads of 30, 50, and 70% of peak oxygen uptake (VO2peak) for 5 min for each workload. Mean arterial pressure, heart rate, and cardiac output increased progressively with three workloads (P<0.01). The end-tidal partial pressure of CO2 (PetCO2) in the expired gas increased from the resting level (P<0.01) at 30 and 50% VO2peak. The PetCO2 at 70% VO2peak (43.2±1.6 Torr) was significantly lower than that at 50% VO2peak (45.3±1.4 Torr). In parallel with the changes in PetCO2, QICA increased from resting level by 11.6±1.5 and 18.4±2.7% at 30 and 50% VO2peak (P<0.01), respectively, and leveled off at 70% VO2peak. In contrast, QVA did not show a leveling off and increased proportionally with workload: 16.8±3.1, 32.8±3.6, and 39.5±3.4% elevations at the three exercise loads, respectively (P<0.01). With increasing exercise load, the cerebrovascular resistance in internal carotid artery increased (P<0.01), while cerebrovascular resistance in vertebral artery remained stable during exercise. The different responses between QICA and QVA in the present study indicate a heterogenous blood flow and cerebrovascular control in the internal carotid and vertebral systems during dynamic exercise in humans.

Quantification of delayed oxygenation in ipsilateral primary motor cortex compared with contralateral side during a unimanual dominant-hand motor task using near-infrared spectroscopy

Using near-infrared spectroscopy (NIRS) techniques, it is possible to examine bilateral motor cortex oxygenation during a static motor task. Cortical activation was assumed to be reflected by increased oxygenation. The purpose of the present study was to examine the time course of oxygenation in the bilateral motor cortex during a low-intensity handgrip task. Six healthy, right-handed subjects participated in the study. The near-infrared spectroscopy probes positioned over the bilateral motor cortex were used to measure the cortical activation throughout a handgrip task carried out. The subjects performed a 3-min handgrip task with increasing intensity in a ramp-like manner [10-30% of the maximal voluntary contraction (MVC) at 6.67% MVC.min(-1)]. Contralateral motor cortex oxygenation increased significantly from 100 to 180 s after the start of the motor task compared with the baseline value (p<0.05). Ipsilateral motor cortex oxygenation also increased significantly from 130 to 180 s after the start of the motor task (p<0.05). The onset of increase in oxyhemoglobin ([HbO2]) and decrease in deoxyhemoglobin ([Hb]) in contralateral motor cortex area (M1) were significantly earlier than in ipsilateral M1 (respectively, p<0.05). These results show that there is a delayed oxygenation in ipsilateral primary motor cortex area compared with contralateral side during a unimanual dominant-hand motor task.

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 and the increase in middle cerebral artery blood flow velocity during static arm exercise in women

We examined the role of central command in static exercise‐induced increase in middle cerebral artery mean blood flow velocity (VMCA). Eleven young female subjects performed static elbow flexion for 2 min at 30% maximal voluntary contraction without (control exercise; CONT) and with vibrations to the biceps brachii tendon (EX+VIB) in order to reduce the effort needed to maintain the set contraction intensity. The rating of perceived exertion in exercising muscle (Arm RPE) at the end of EX+VIB was lower than that of CONT (mean ±s.d.; 4.8 ± 1.1 for CONT versus 3.5 ± 1.0 for EX+VIB; P < 0.05). The increases in mean arterial pressure (36 ± 8 versus 22 ± 7%; P < 0.05), heart rate (36 ± 16 versus 21 ± 7%; P < 0.05) and cardiac output (56 ± 26 versus 39 ± 14%; P < 0.05) during EX+VIB were also lower than those during CONT. Similarly, the increase in the VMCA during EX+VIB was lower than that during CONT (29 ± 5 versus 17 ± 14%; P < 0.05). These results suggest that the influence of central command contributes to cerebral blood flow regulation during static exercise and the decrease in VMCA is likely to be caused by attenuated brain activation in the central command network and/or by the reduction in cardiac output.

Influence of central command on cerebral blood flow at the onset of exercise in women

This study evaluated the role of central command in the regulation of common carotid artery blood flow and middle cerebral artery mean flow velocity (VMCA) at the onset of arm exercise. Eleven young women performed 2 min voluntary elbow flexion and extension exercise with no load (VOL) that was considered to activate both central command and the muscle mechanoreflex, and 2 min passive elbow flexion and extension exercise (PAS) that was considered to activate only the muscle mechanoreflex. Immediately before the onset of VOL, and VMCA began to increase from the baseline and peaked 5 s thereafter (mean ±s.d.; 20 ± 5 and 14 ± 5%, respectively; P < 0.05). Also, VOL increased heart rate (9 ± 2%; P < 0.05) and cardiac output (16 ± 3%; P < 0.05). Indexes of the cerebrovascular resistance (MAP/ and MAP/VMCA) were reduced at the onset of VOL (−13 ± 4 and −12 ± 4%, respectively; P < 0.05). However, there were no significant changes in these parameters during PAS. These results suggest that central command plays an important role in the increase of cerebral blood flow at the onset of voluntary exercise.

Blood flow in internal carotid and vertebral arteries during graded lower body negative pressure in humans

What is the central question of this study? Recently, the heterogeneity of the cerebral arterial circulation has been argued. Orthostatic tolerance may be associated with an orthostatic stress‐induced change in blood flow in vertebral arteries rather than in internal carotid arteries, because vertebral arteries supply blood to the medulla oblongata, which is the location of important cardiac, vasomotor and respiratory control centres. What is the main finding and its importance? The effect of graded orthostatic stress on vertebral artery blood flow is different from that on internal carotid artery blood flow. This response allows for the possibility that orthostatic tolerance may be associated with haemodynamic changes in posterior rather than anterior cerebral blood flow.

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.

Tendon vibration attenuates superficial venous vessel response of the resting limb during static arm exercise.

BackgroundThe superficial vein of the resting limb constricts sympathetically during exercise. Central command is the one of the neural mechanisms that controls the cardiovascular response to exercise. However, it is not clear whether central command contributes to venous vessel response during exercise. Tendon vibration during static elbow flexion causes primary muscle spindle afferents, such that a lower central command is required to achieve a given force without altering muscle force. The purpose of this study was therefore to investigate whether a reduction in central command during static exercise with tendon vibration influences the superficial venous vessel response in the resting limb.MethodsEleven subjects performed static elbow flexion at 35% of maximal voluntary contraction with (EX + VIB) and without (EX) vibration of the biceps brachii tendon. The heart rate, mean arterial pressure, and rating of perceived exertion (RPE) in overall and exercising muscle were measured. The cross-sectional area (CSAvein) and blood velocity of the basilic vein in the resting upper arm were assessed by ultrasound, and blood flow (BFvein) was calculated using both variables.ResultsMuscle tension during exercise was similar between EX and EX + VIB. However, RPEs at EX + VIB were lower than those at EX (P <0.05). Increases in heart rate and mean arterial pressure during exercise at EX + VIB were also lower than those at EX (P <0.05). CSAvein in the resting limb at EX decreased during exercise from baseline (P <0.05), but CSAvein at EX + VIB did not change during exercise. CSAvein during exercise at EX was smaller than that at EX + VIB (P <0.05). However, BFvein did not change during the protocol under either condition. The decreases in circulatory response and RPEs during EX + VIB, despite identical muscle tension, showed that activation of central command was less during EX + VIB than during EX. Abolishment of the decrease in CSAvein during exercise at EX + VIB may thus have been caused by a lower level of central command at EX + VIB rather than EX.ConclusionDiminished central command induced by tendon vibration may attenuate the superficial venous vessel response of the resting limb during sustained static arm exercise.