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. AbstractThe 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 (V O 2 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%V O 2 peak . However, at 80% V O 2 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 CO 2 (r = 0.72). The change in ICA blood flow from 60%V O 2 peak to 80%V O 2 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.
In five healthy males sustained isometric torques during elbow flexion, knee extension, and plantar flexion correlated positively with intramuscular tissue pressure (MTP) in the range 0-80% of the maximal voluntary contraction (MVC). During passive compression of the muscle at rest 133-Xenon muscle clearance stopped when MTP reached diastolic arterial pressure (DAP) indicating that the muscle vascular bed was occluded. However, during sustained contraction this relation between DAP, flow and MTP was not seen. In two cases 133-Xenon clearance from M. soleus did not stop in spite of an 80% maximal contraction and MTP stayed below DAP. In other cases MTP would reach as high as 240 mm Hg before clearance was zero. In the deeper parts of the muscles MTP during contraction was increased in relation to the more superficial parts. The means values for the % MVC that would stop MBF varied between 50 and 64% MVC for the investigated muscles. Mean rectified EMG (MEMG) showed a high correlation to MTP during sustained exhaustive contractions: When MEMG was kept constant MTP also remained constant while the exerted force decreased; when force was kept constant both MEMG and MTP increased in parallel. This demonstrated that muscle tissue compliance is decreasing during fatigue. Muscle ischemia occurring during sustained isometric contractions is partly due to the developed MTP, where especially the MTP around the veins in the deeper parts of the muscle can be considered of importance. However, ischemia is also affected by muscle fiber texture and anatomical distorsion of tissues.
Key points• Arterial CO 2 serves as a mediator of cerebral blood flow, and its relative influence on the regulation of cerebral blood flow is defined as cerebral CO 2 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 CO 2 as a measure of CO 2 reactivity across the whole brain.• We found that the vertebral artery has lower CO 2 reactivity than the internal carotid artery.Moreover, CO 2 reactivity in the external carotid artery was markedly lower than in the cerebral circulation.• These results demonstrate regional differences in CO 2 regulation of blood flow between the internal carotid, external carotid, and vertebro-basilar circulation.Abstract Arterial CO 2 serves as a mediator of cerebral blood flow (CBF), and its relative influence on the regulation of CBF is defined as cerebral CO 2 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 CO 2 reactivity may be different in the anterior and posterior cerebral circulation. The aim of this study was to identify cerebral CO 2 reactivity by measuring blood flow and examine potential differences in CO 2 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% CO 2 ), normocapnia and hypocapnia to estimate CO 2 reactivity. To characterize cerebrovascular reactivity to CO 2 , we used both exponential and linear regression analysis between CBF and estimated partial pressure of arterial CO 2 , calculated by end-tidal partial pressure of CO 2 . CO 2 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 CO 2 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, CO 2 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 CO 2 reactivity than internal carotid circulation, and that CO 2 reactivity of the external carotid circulation is
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.
New Findings r 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. r 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.
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