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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/H467    most recent 00045.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kim, Y.-S. Articles by van Lieshout, J. J. Search for Related Content PubMed PubMed Citation Articles by Kim, Y.-S. Articles by van Lieshout, J. J.

Effects of hyperglycemia on the cerebrovascular response to rhythmic handgrip exercise

¹Department of Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; ²Departments of Anesthesiology and Infectious Diseases, ³The Center of Inflammation and Metabolism, and ⁴The Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Denmark; and ⁵Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas

Submitted 12 January 2007 ; accepted in final form 14 March 2007

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_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_mean 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 V_mean 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 V_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