An assessment of hypercapnia-induced elevations in regional cerebral perfusion during combined orthostatic and heat stresses.

We investigated that the effects of hypercapnia-induced elevations in cerebral perfusion during a heat stress on global cerebrovascular responses to an orthostatic challenge. Seven volunteers completed a progressive lower-body negative pressure (LBNP) challenge to presyncope during heat stress, with or without breathing a hypercapnic gas mixture. Administration of the hypercapnic gas mixture increased the partial pressure of end-tidal CO2 greater than pre-heat stress alone, and increased both internal carotid artery (ICA) and vertebral artery (VA) blood flows (P < 0.05). During LBNP, both ICA and VA blood flows with the hypercapnic gas mixture remained elevated relative to the control trial (P < 0.05). However, at the end of LBNP due to pre-syncopal symptoms, both ICA and VA blood flows decreased to similar levels between trials. These findings suggest that hypercapnia-induced cerebral vasodilation is insufficient to maintain cerebral perfusion at the end of LBNP due to pre-syncope in either the anterior or posterior vascular beds.

The effect of muscle metaboreflex on the distribution of blood flow in cerebral arteries during isometric exercise.

The present study examined the effect of muscle metaboreflex on blood flow in different cerebral arteries. Eleven healthy participants performed isometric, one-leg knee extension at 30% maximal voluntary contraction for 2 min. Activated muscle metaboreflex was isolated for 2 min by post-exercise muscle ischemia (PEMI). The contralateral internal carotid (ICA), vertebral (VA), and ipsilateral external carotid arteries (ECA) blood flows were evaluated using Doppler ultrasound. The ICA blood flow increased at the beginning of exercise (P  = 0.004) but returned to the baseline level at the end of exercise (P  = 0.055). In contrast, the VA blood flow increased and it was maintained until the end of the exercise (P = 0.011), while the ECA blood flow gradually increased throughout the exercise (P  = 0.001). These findings indicate that isometric exercise causes a heterogeneous cerebral blood flow response in different cerebral arteries. During PEMI, the conductance of the VA as well as that of the ICA was significantly lower compared with the baseline value (P  = 0.020 and P  = 0.032, at PEMI90), while the conductance of the ECA was not different from the baseline (P  = 0.587), suggesting that the posterior and anterior cerebral vasculature were similarly affected during exercise by activation of muscle metaboreceptors, but not in the non-cerebral artery. Since ECA branches from ICA, the balance in the different influence of muscle metaboreflex on ECA (vasodilation via exercise-induced hypertension) and ICA (vasoconstriction) may contribute to the decrease in ICA blood flow at the end of isometric exercise.

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.

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.

Heterogeneous Regulation of Brain Blood Flow during Low-Intensity Resistance Exercise.

PURPOSE: The present study was designed to explore to what extent low-intensity resistance exercise-induced acute hypertension influences intracranial cerebral perfusion. METHODS: Twelve healthy participants performed one-legged static knee extension exercise at 30% maximal voluntary contraction for 2 min. Blood flow to the internal and external carotid arteries (ICA/ECA) were evaluated by duplex ultrasonography. RESULTS: ICA blood flow increased and reached a plateau before stabilizing 60 s into exercise despite continued increases in cardiac output and arterial blood pressure. ICA conductance significantly decreased by -14.4% ±13.8% at the end of exercise (P < 0.01), whereas in contrast, ECA blood flow (P < 0.01) and conductance were shown to increase (P < 0.05). CONCLUSIONS: The present findings demonstrate that low-intensity resistance exercise was associated with vasodilation of the ECA that was accompanied by vasoconstriction of the ICA. We propose that the heterogeneity and reciprocal regulation of intracranial cerebral blood flow reflect an adaptive neuroprotective mechanism that serves to protect the brain and associated vasculature against the structural damage associated with resistance exercise-induced hypertension.

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.

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

NEW FINDINGS: 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. Recently, the heterogeneity of the cerebral arterial circulation has been argued, but the characteristics of vertebral artery (VA) and internal carotid artery (ICA) blood flow during graded orthostatic stress remain unknown. We hypothesized that the change in blood flow in VA is not similar to that in ICA blood flow during graded orthostatic stress. We measured blood flows in both ICA and VA during graded lower body negative pressure (LBNP; -20, -35 and -50 mmHg) by using two colour-coded ultrasound systems. The effect of graded orthostatic stress on the VA blood flow was different from that on the ICA blood flow (LBNP × artery, P = 0.006). The change in ICA blood flow was associated with the level of LBNP (r = 0.287, P = 0.029), and a reduction in ICA blood flow from pre-LBNP was observed during -50 mmHg LBNP (from 411 ± 35 to 311 ± 40 ml min(-1) , P = 0.044) without symptoms of presyncope. In contrast, VA blood flow was unchanged during graded LBNP compared with the baseline (P = 0.597) relative to the reduction in ICA blood flow and thus there was no relationship between VA blood flow and the level of LBNP (r = 0.167, P = 0.219). These findings suggest that the change in ICA blood flow is due to the level of LBNP during graded orthostatic stress, but the change in VA blood flow is different from that in ICA blood flow across the different levels of LBNP. These findings provide the possibility that posterior cerebral blood flow decreases only during severe orthostatic stress and is therefore more likely to be linked with orthostatic tolerance.

Anatomical vertebral artery hypoplasia and insufficiency impairs dynamic blood flow regulation.

Recent studies have suggested that vertebral artery (VA) hypoplasia is a predisposing factor for posterior cerebral stroke. We examined whether anatomical vertebrobasilar ischemia, i.e., unilateral VA hypoplasia and insufficiency, impairs dynamic blood flow regulation. Twenty-eight female subjects were divided into three groups by defined criteria: (i) unilateral VA hypoplasia (n = 8), (ii) VA insufficiency (n = 6), and (iii) control (n = 14). Hypoplastic VA criterion was VA blood flow of 40 ml min(-1) , whereas VA insufficiency criterion was net (left + right) VA blood flow of 100 ml min(-1) or less. We evaluated left, right, and net VA blood flows by ultrasonography during hypercapnia, normocapnia, and hypocapnia to evaluate VA CO2 reactivity. The unilateral VA hypoplasia group showed lower CO2 reactivity at hypoplastic VA than at non-hypoplastic VA (2.65 ± 0.58 versus 3.00 ± 0.48% per mmHg, P = 0.027) and net VA CO2 reactivity was preserved (Unilateral VA hypoplasia, 2.95 ± 0.48 versus Control, 2.93 ± 0.42% per mmHg, P = 0.992). However, the VA insufficiency group showed a lower net VA CO2 reactivity compared to the control (2.29 ± 0.55 versus 2.93 ± 0.42% per mmHg, P = 0.032) and the unilateral VA hypoplasia (P = 0.046). VA hypoplasia reduced CO2 reactivity, although non-hypoplastic VA may compensate this regulatory limitation. In subjects with VA insufficiency, lowered CO2 reactivity at the both VA could not preserve normal net VA CO2 reactivity. These findings provide a possible physiological mechanism for the increased risk of posterior cerebral stroke in subjects with VA hypoplasia and insufficiency.

Superficial venous vascular response of the resting limb during static exercise and postexercise muscle ischemia.

Superficial venous vascular response to exercise is mediated sympathetically, although the mechanism is not fully understood. We examined whether sympathetic activation via muscle metaboreflex plays a role in the control of a superficial vein in the contralateral resting limb during exercise. The experimental condition involved selective stimulation of muscle metaboreceptors: 12 subjects performed static handgrip exercises at 45% maximal voluntary contraction for 1.5 min followed by a recovery period with arterial occlusion of the exercise arm (OCCL). For the control condition (CONT), the same exercise protocol was performed except that the recovery period occurred without arterial occlusion. Heart rate (HR) and mean arterial blood pressure (MAP) were measured. The cross-sectional area of the basilic superficial vein (CSAvein) and blood velocity (Vvein) in the resting upper arm were measured by ultrasound while the cuff on resting upper arm was inflated constantly to a subdiastolic pressure of 50 mm Hg. Basilic vein blood flow (BFvein) was calculated as CSAvein × Vvein. During exercise under both OCCL and CONT, HR and MAP increased (p < 0.05), while CSAvein decreased (p < 0.05). During recovery under OCCL, HR returned to baseline, but the exercise-induced increase in MAP and decrease in CSAvein were maintained (p < 0.05). During recovery under CONT, HR, MAP, and CSAvein returned to baseline. BFvein did not change during exercise or recovery under either condition. These results suggest that sympathoexcitation via muscle metaboreflex may be one of the factors responsible for exercise-induced constriction of the superficial veins per se in the resting limb.

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

BACKGROUND: The 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. METHODS: Eleven 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. RESULTS: Muscle 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. CONCLUSION: Diminished central command induced by tendon vibration may attenuate the superficial venous vessel response of the resting limb during sustained static arm exercise.

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(CBF), and its relative influence on the regulation of CBF is defined as cerebral CO2 reactivity. Our previous studies have demonstrated that there are differences in CBF responses to physiological stimuli (i.e. dynamic exercise and orthostatic stress) between arteries in humans. These findings suggest that dynamic CBF regulation and cerebral CO2 reactivity may be different in the anterior and posterior cerebral circulation. The aim of this study was to identify cerebral CO2 reactivity by measuring blood flow and examine potential differences in CO2 reactivity between the internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA). In 10 healthy young subjects, we evaluated the ICA, ECA, and VA blood flow responses by duplex ultrasonography (Vivid-e, GE Healthcare), and mean blood flow velocity in middle cerebral artery (MCA) and basilar artery (BA) by transcranial Doppler (Vivid-7, GE healthcare) during two levels of hypercapnia (3% and 6% CO2), normocapnia and hypocapnia to estimate CO2 reactivity. To characterize cerebrovascular reactivity to CO2,we used both exponential and linear regression analysis between CBF and estimated partial pressure of arterial CO2, calculated by end-tidal partial pressure of CO2. CO2 reactivity in VA was significantly lower than in ICA (coefficient of exponential regression 0.021 ± 0.008 vs. 0.030 ± 0.008; slope of linear regression 2.11 ± 0.84 vs. 3.18 ± 1.09% mmHg−1: VA vs. ICA, P <0.01). Lower CO2 reactivity in the posterior cerebral circulation was persistent in distal intracranial arteries (exponent 0.023 ± 0.006 vs. 0.037 ± 0.009; linear 2.29 ± 0.56 vs. 3.31 ± 0.87% mmHg−1: BA vs. MCA). In contrast, CO2 reactivity in ECA was markedly lower than in the intra-cerebral circulation (exponent 0.006 ± 0.007; linear 0.63 ± 0.64% mmHg−1, P <0.01). These findings indicate that vertebro-basilar circulation has lower CO2 reactivity than internal carotid circulation, and that CO2 reactivity of the external carotid circulation is markedly diminished compared to that of the cerebral circulation, which may explain different CBF responses to physiological stress.

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.

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

The mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (VO2 peak) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60% (VO2 peak). However, at 80% (VO2 peak), ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO2 (r = 0.72). The change in ICA blood flow from 60% (VO2 peak) to 80% (VO2 peak) was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.

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.

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.

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 (V(MCA)) 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 V(MCA) 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/V(MCA)) 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.

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 (V(MCA)). 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 V(MCA) 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 V(MCA) is likely to be caused by attenuated brain activation in the central command network and/or by the reduction in cardiac output.

Perceived exertion is not necessarily associated with altered brain activity during exercise.

Previous studies have investigated the relationship between prefrontal cortex activation and perceived exertion during prolonged exercise. However, the effect of perceived exertion on prefrontal cortex activity is confounded by exercise intensity. Therefore, the changes in prefrontal cortex activity in response to perceived exertion remain unclear. The purpose of the present study was to investigate the relationship between the activation (oxygenation) of the prefrontal cortex and perceived exertion during constant work-rate elbow-flexion exercise with or without muscle-spindle stimulation. Ten healthy, right-handed subjects participated in the study. Near-infrared spectroscopy with probes positioned over the prefrontal cortex measured its activation throughout elbow-flexion exercise. Subjects performed sustained elbow-flexion exercise at 25-35% of the maximal voluntary contraction (MVC) with or without muscle-spindle stimulation (vibration), which can decrease perceived exertion. The ratings of perceived exertion were significantly lower during exercise with vibration (Ex-Vib) than during exercise without vibration (Ex) (p<0.05). The oxygenation of the prefrontal cortex during Ex-Vib did not significantly differ from that during Ex (p>0.05). These results indicated that perceived exertion was not necessarily associated with prefrontal cortex activation during exercise.

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.