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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.