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Dynamic cerebral autoregulation (CA) is challenged by exercise and may become less effective when exercise is exhaustive. Exercise may increase arterial glucose concentration, and we evaluated whether the cerebrovascular response to exercise is affected by hyperglycemia. The effects of a hyperinsulinemic euglycemic clamp (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRI) and systemic vascular resistance index (SVRI) responses were evaluated in seven healthy subjects at rest and during rhythmic handgrip exercise. Transfer function analysis of the dynamic relationship between beat-to-beat changes in mean arterial pressure and middle cerebral artery (MCA) mean blood flow velocity ([V.sub.mean]) was used to assess dynamic CA. At rest, SVRI decreased with HY and EU (P < 0.01). CVRI was maintained with EU but became reduced with HY [11% (SD 3); P < 0.01], and MCA [V.sub.mean] increased (P < 0.05), whereas brain catecholamine uptake and arterial [PCO.sub.2] did not change significantly. HY did not affect the normalized low-frequency gain between mean arterial pressure and MCA [V.sub.mean] or the phase shift, indicating maintained dynamic CA. With HY, the increase in CVRI associated with exercise was enhanced (19 [+ or -] 7% vs. 9 [+ or -] 7%; P < 0.05), concomitant with a larger increase in heart rate and cardiac output and a larger reduction in SVRI (22 [+ or -] 4% vs. 14 [+ or -] 2%; P < 0.05). Thus hyperglycemia lowered cerebral vascular tone independently of CA capacity at rest, whereas dynamic CA remained able to modulate cerebral blood flow around the exercise-induced increase in MCA [V.sub.mean]. These findings suggest that elevated blood glucose does not explain that dynamic CA is affected during intense exercise. cerebral autoregulation; cardiac output; human; vascular tone doi:10.1152/ajpheart.00045.2007

Postural stress requires immediate autonomic nervous action to maintain blood pressure. We determined time-domain cardiac baroreflex sensitivity (BRS) and time delay ([tau]) between systolic blood pressure and interbeat interval variations during stepwise changes in the angle of vertical body axis ([alpha]). The assumption was that with increasing postural stress, BRS becomes attenuated, accompanied by a shift in -r toward higher values. In 10 healthy young volunteers, [alpha] included 20 degrees head-down tilt (-20[degrees]), supine (0[degrees]), 30 and 70 degrees head-up tilt (30[degrees], 70[degrees]), and free standing (90[degrees]). Noninvasive blood pressures were analyzed over 6-min periods before and after each change in [alpha]. The BRS was determined by frequency-domain analysis and with xBRS, a cross-correlation time-domain method. On average, between 28 (-20[degrees]) to 45 (90[degrees]) xBRS estimates per minute became available. Following a change in [alpha], xBRS reached a different mean level in the first minute in 78% of the cases and in 93% after 6 min. With increasing [alpha], BRS decreased: BRS = -10.1-sin([alpha]) + 18.7 ([r.sup.2] = 0.99) with tight correlation between xBRS and cross-spectral gain ([r.sup.2] ~ 0.97). Delay [tau] shifted toward higher values. In conclusion, in healthy subjects the sensitivity of the cardiac baroreflex obtained from time domain decreases linearly with sin([tau]), and the start of baroreflex adaptation to a physiological perturbation like postural stress occurs rapidly. The decreases of BRS and reduction of short [tau] may be the result of reduced vagal activity with increasing [alpha]. blood pressure regulation; tilt; sequential and spectral analysis; vagal and sympathetic tone

Vasovagal syncope is the most common cause of transient loss of consciousness, and recurrent vasovagal fainting has a profound impact on quality of life. Physical countermaneuvers are applied as a means of tertiary prevention but have so far only proven useful at the onset of a faint. This placebo-controlled crossover study tested the hypothesis that leg crossing increases orthostatic tolerance. Nine naive healthy subjects [6 females, median age 25 yr (range 20-41 yr), mean body mass index 23 (SD 2)] were subjected to passive head-up tilt combined with a graded lower body negative pressure challenge (20, 40, and 60 mmHg) determining orthostatic tolerance thrice, in randomized order: 1) control, 2) with leg crossing, and 3) with oral placebo. Blood pressure (Finometer), heart rate, and changes in thoracic blood volume (impedance), stroke volume, and cardiac output (Modelflow) were followed during orthostatic stress. Primary outcome was time to presyncope (systolic blood pressure [less than or equal to] 85 mmHg, heart rate [greater than or equal to] 140 beats/min). With leg crossing, orthostatic tolerance increased from 26 [+ or -] 2 to 34 [+ ro -] 2 min (placebo 23 [+ or -] 3 min, P < 0.001). During leg crossing, mean arterial pressure (81 vs. 81 mmHg) and cardiac output (95 vs. 94% supine) remained unchanged; heart rate increase was lower (13 vs. 18 beats/min, P < 0.05); stroke volume was higher (79 vs. 74% supine, P < 0.05); and there was a trend toward lower thoracic impedance. Leg crossing increases orthostatic tolerance in healthy human subjects. As a measure of prevention, it is a worthwhile addition to the management of vasovagal syncope. blood pressure; lower body negative pressure; prevention; syncope

Dynamic cerebral autoregulation (CA) is challenged by exercise and may become less effective when exercise is exhaustive. Exercise may increase arterial glucose concentration, and we evaluated whether the cerebrovascular response to exercise is affected by hyperglycemia. The effects of a hyperinsulinemic euglycemic clamp (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRI) and systemic vascular resistance index (SVRI) responses were evaluated in seven healthy subjects at rest and during rhythmic handgrip exercise. Transfer function analysis of the dynamic relationship between beat-to-beat changes in mean arterial pressure and middle cerebral artery (MCA) mean blood flow velocity (Vmean) was used to assess dynamic CA. At rest, SVRI decreased with HY and EU (P < 0.01). CVRI was maintained with EU but became reduced with HY [11% (SD 3); P < 0.01], and MCA Vmean increased (P < 0.05), whereas brain catecholamine uptake and arterial Pco2 did not change significantly. HY did not affect the normalized low- frequency gain between mean arterial pressure and MCA Vmean or the phase shift, indicating maintained dynamic CA. With HY, the increase in CVRI associated with exercise was enhanced (19 ± 7% vs. 9 ± 7%; p < 0.05), concomitant with a larger increase in heart rate and cardiac output and a larger reduction in SVRI (22 ± 4% vs. 14 ± 2%; P < 0.05). Thus hyperglycemia lowered cerebral vascular tone independently of CA capacity at rest, whereas dynamic CA remained able to modulate cerebral blood flow around the exercise-induced increase in MCA Vmean. These findings suggest that elevated blood glucose does not explain that dynamic CA is affected during intense exercise. [ABSTRACT FROM AUTHOR]

Regulation of cerebral blood flow during physiological activation including exercise remains unknown but may be related to the arterial lactate-to-pyruvate (L/P) ratio. We evaluated whether an exercise-induced increase in middle cerebral artery mean velocity (MCA Vmean) relates to the arterial L/P ratio at two plasma lactate levels. MCA Vmean was determined by ultrasound Doppler sonography at rest, during 10 min of rhythmic handgrip exercise at ∼65% of maximal voluntary contraction force, and during 20 min of recovery in seven healthy male volunteers during control and a ∼15 mmol/l hyperglycemic clamp. Cerebral arteriovenous differences for metabolites were obtained by brachial artery and retrograde jugular venous catheterization. Control resting arterial lactate was 0.78 ± 0.09 mmol/l (mean ± SE) and pyruvate 55.7 ± 12.0 p.mol/l (LIP ratio 16.4 ± 1.0) with a corresponding MCA Vmean of 46.7 ± 4.5 cm/s. During rhythmic handgrip the increase in MCA Vmean to 51.2 ± 4.6 cm/s was related to the increased L/P ratio (23.8 ± 2.5; r² = 0.79; P < 0.01). Hyperglycemia increased arterial lactate and pyruvate to 1.9 ± 0.2 mmol/l and 115 ± 4 μmol/1, respectively, but it did not significantly influence the L/P ratio or MCA Vmean at rest or during exercise. Conversely, MCA Vmean did not correlate significantly, neither to the arterial lactate nor to the pyruvate concentrations. These results support that the arterial plasma LIP ratio modulates cerebral blood flow during cerebral activation independently from the plasma glucose concentration. [ABSTRACT FROM AUTHOR]

Tensing of lower body muscles without or with leg crossing (LBMT, LCMT), whole body tensing (WBT), squatting, and sitting with the head bent between the knees ("crash position," HBK) are believed to abort vasovagal reactions. The underlying mechanisms are unknown. To study these interventions in patients with a clinical history of vasovagal syncope and a vasovagal reaction during routine tilt table testing, we measured blood pressure (BP) continuously with Finapres and derived heart rate, stroke volume, cardiac output (CO), and total peripheral resistance using Modelflow. In series A (n = 12) we compared LBMT to LCMT. In series B (n = 9), WBT was compared with LCMT. In series C (n = 14) and D (n = 9), we tested squatting and HBK. All maneuvers caused an increase in BP, varying from a systolic rise from 77 ± 8 to 104 ± 18 mmHg (P < 0.05) in series A during LBMT to a rise from 70 ± 10 to 123 ± 9 mmHg (P < 0.05) in series B during LCMT. In each maneuver, the BP increase started within 3-5 s from start of the maneuver. In all maneuvers, there was an increase in CO varying from 54 ± 12% of baseline to 94 ± 21% in WBT to a rise from 65 ± 17% to 110 ± 22% in LCMT in series A. No maneuver caused significant change in total peripheral resistance. We conclude that the mechanism underlying the effects of these maneuvers is exclusively an increase in CO. [ABSTRACT FROM AUTHOR]

The article discusses the sympathetic influence of cerebral blood flow (CBF) in managing patients with low blood pressure. It states that studies performed in patients with heart failure provide direct and indirect support for modulation of cerebral perfusion by vasoconstriction to reduce cardiac output (CO). Information on the effect of stroke volume on the arterial baroreceptors which is important in regulating sympathetic activity in human and on the cerebral oxygenation is also offered.

A letter to the editor is presented in response to the article "Arterial oxygenation, central motor output and exercise performance in humans," by T.D. Noakes and F.E. Marino.

A response by C. T. Paul Krediet, Johannes J. van Lieshout and Wouter Wieling to the letter to the editor about his article "Improved orthostatic tolerance by leg crossing and muscle tensing: indisputable evidence for the arteriovenous pump existence" in the previous issue is presented.