Submitted on January 12, 2007
Accepted on March 14, 2007
Effects of hyperglycemia on the cerebrovascular response to rhythmic handgrip exercise
Yu-Sok Kim1, Rikke Krogh-Madsen2, Peter Rasmussen3, Peter Plomgaard2, Shigehiko Ogoh4, Niels H. Secher5, and Johannes J. Van Lieshout6*
1 Department of Internal Medicine, Academic Medical Center, Amsterdam, Noord Holland, Netherlands
2 Department of Infectious Diseases, Centre of Inflammation and Metabolism, Copenhagen, Denmark; Copenhagen Muscle Research Centre, Copenhagen, Denmark; 7641, Rigshospitalet, Copenhagen, Denmark; Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
3 Department of Anesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; Copenhagen Muscle Research Centre, Copenhagen, Denmark; Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
4 Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas, United States
5 Dept. of Anaesthesia, Rigshospitalet 2102, Copenhagen, Denmark; Copenhagen Muscle Research Centre, Copenhagen, Denmark
6 Medium Care Unit, Department of Internal Medicine, Academic Medical Center, Amsterdam, Netherlands
* To whom correspondence should be addressed. E-mail: j.j.vanlieshout{at}amc.uva.nl.
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 (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRi) and systemic vascular (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 (MAP) 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±3%; P < 0.01) and MCA Vmean increased (P < 0.05), whereas brain catecholamine uptake and PaCO2 did not significantly change. HY did not affect the normalized low-frequency gain between MAP 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 to 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 an elevated blood glucose does not explain that dynamic CA is affected during intense exercise.
