The purpose of the present study was to assess the effect of heat stress-induced changes in systemic circulation on intra-and extracranial blood flows and its distribution. Twelve healthy subjects with a mean age of 22 ± 2 (s.d.) years dressed in a tube-lined suit and rested in a supine position. Cardiac output (Q), internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) blood flows were measured by ultrasonography before and during whole body heating. Esophageal temperature increased from 37.0 ± 0.21C to 38.4 ± 0.21C during whole body heating. Despite an increase in Q (59 ± 31%, Po0.001), ICA and VA decreased to 83 ± 15% (P ¼ 0.001) and 87 ± 8% (P ¼ 0.002), respectively, whereas ECA blood flow gradually increased from 188 ± 72 to 422±189 mL/minute ( þ 135%, Po0.001). These findings indicate that heat stress modified the effect of Q on blood flows at each artery; the increased Q due to heat stress was redistributed to extracranial vascular beds.

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.

Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (P a,CO 2 ) via limiting changes in brain [H + ] modulates ventilatory control. It remains unclear, however, how exercise-induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), in particular the cerebrovascular reactivity to CO 2 . The respiratory chemoreflex system controlling ventilation consists of two subsystems: the central controller (controlling element), and peripheral plant (controlled element). In order to examine the effect of exercise-induced alterations in ventilatory chemoreflex on cerebrovascular CO 2 reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO 2 reactivity were evaluated (n = 7) by the administration of CO 2 as well as by voluntary hypo-and hyperventilation at rest and during steady-state exercise. During exercise, in the central controller, the regression line for the P a,CO 2 -minute ventilation (V E ) relation shifted to higherV E and P a,CO 2 with no change in gain (P = 0.84). The functional curve of the peripheral plant also reset rightward and upward during exercise. However, from rest to exercise, gain of the peripheral plant decreased, especially during the hypercapnic condition (−4.1 ± 0.8 to −2.0 ± 0.2 mmHg l −1 min −1 , P = 0.01). Therefore, under hypercapnia, total respiratory loop gain was markedly reduced during exercise (−8.0 ± 2.3 to −3.5 ± 1.0 U, P = 0.02). In contrast, cerebrovascular CO 2 reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 ± 0.2 to 2.8 ± 0.2% mmHg −1 , P = 0.03). These findings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations in cerebrovascular reactivity might help maintain CO 2 homeostasis in the brain during exercise.

. Low-frequency oscillation of sympathetic nerve activity decreases during development of tiltinduced syncope preceding sympathetic withdrawal and bradycardia. Am J Physiol Heart Circ Physiol 289: H1758 -H1769, 2005. First published June 2, 2005; doi:10.1152/ajpheart.01027.2004.-Sympathetic activation during orthostatic stress is accompanied by a marked increase in low-frequency (LF, ϳ0.1-Hz) oscillation of sympathetic nerve activity (SNA) when arterial pressure (AP) is well maintained. However, LF oscillation of SNA during development of orthostatic neurally mediated syncope remains unknown. Ten healthy subjects who developed head-up tilt (HUT)-induced syncope and 10 agematched nonsyncopal controls were studied. Nonstationary timedependent changes in calf muscle SNA (MSNA, microneurography), R-R interval, and AP (finger photoplethysmography) variability during a 15-min 60°HUT test were assessed using complex demodulation. In both groups, HUT during the first 5 min increased heart rate, magnitude of MSNA, LF and respiratory high-frequency (HF) amplitudes of MSNA variability, and LF and HF amplitudes of AP variability but decreased HF amplitude of R-R interval variability (index of cardiac vagal nerve activity). In the nonsyncopal group, these changes were sustained throughout HUT. In the syncopal group, systolic AP decreased from 100 to 60 s before onset of syncope; LF amplitude of MSNA variability decreased, whereas magnitude of MSNA and LF amplitude of AP variability remained elevated. From 60 s before onset of syncope, MSNA and heart rate decreased, index of cardiac vagal nerve activity increased, and AP further decreased to the level at syncope. LF oscillation of MSNA variability decreased during development of orthostatic neurally mediated syncope, preceding sympathetic withdrawal, bradycardia, and severe hypotension, to the level at syncope. autonomic nervous system; baroreflex; blood pressure; heart rate variability; hemodynamics HUMANS HAVE BEEN SUBJECTED to ceaseless orthostatic stresses since they first evolved and assume an orthostatic posture for most of their lives. During standing, gravitational fluid shift toward the lower part of body (i.e., abdominal vascular bed and lower limbs) would cause severe orthostatic hypotension if it were not countered by compensatory mechanisms (23). Orthostatic sympathetic activation has a crucial role in preventing orthostatic hypotension and maintaining arterial blood pressure (AP) (23). Recent studies have reported that orthostatic sympathetic activation is accompanied by an increase in lowfrequency (LF, ϳ0.1-Hz) oscillation of sympathetic nerve activity (SNA) (1, 5). Tilt maneuvers of 75°and 80°greatly increase the LF oscillatory patterns of muscle SNA (MSNA), which mirrored similar changes in LF oscillation of AP (1, 5). However, LF oscillation of SNA has been investigated only in the steady-state orthostatic condition, when AP remains well maintained. It remains unclear whether LF oscillation of SNA changes during development of orthostatic neurally mediated s...