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Arterial Baroreflex Control of the Peripheral Vasculature in Humans: Rest and Exercise


Medicine & Science in Sports & Exercise: December 2008 - Volume 40 - Issue 12 - p 2055-2062
doi: 10.1249/MSS.0b013e318180bc80
BASIC SCIENCES: Symposium: Recent Advances in Baroreflex Control of Blood Pressure during Exercise in Humans

Arterial baroreceptors originating in the carotid arteries and aorta play a pivotal role in the rapid reflex adjustments that accompany acute cardiovascular stressors. There is now ample evidence to indicate that the arterial baroreflex remains functional during exercise by resetting in direct relation to the intensity of exercise from rest to maximum. Moreover, there is convincing evidence that a properly functioning arterial baroreflex is requisite for an appropriate neural cardiovascular response to exercise. Importantly, an understanding of the underlying means by which the baroreflex responds to changes in blood pressure has been elucidated. In this regard, both at rest and during exercise, alterations in stroke volume do not appear to contribute to the maintenance of arterial blood pressure (ABP) by the carotid baroreceptors (CBR), and therefore, any reflex-induced changes in cardiac output are the result of CBR-mediated changes in heart rate (HR). More importantly, it appears that CBR-induced changes in ABP are primarily mediated by alterations in vascular conductance with only minimal contributions from cardiac output. Therefore, the capacity of the CBR to regulate ABP depends critically on its ability to alter vascular tone both at rest and during exercise. Indeed, studies have clearly indicated that active and inactive skeletal muscle vascular beds contribute to mediating CBR-induced changes in ABP. The purpose of this review is to describe the mechanisms by which the CBR responds to alterations in ABP both at rest and during exercise in humans with a particular emphasis on the importance of baroreflex-mediated vascular responses.

Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri, and Harry S. Truman Memorial Veterans Hospital, Department of Veterans Affairs Medical Center, Columbia, MO

Address for correspondence: Paul J. Fadel, Ph.D., Department of Medical Pharmacology and Physiology, MA415 Medical Sciences Building, University of Missouri, Columbia, MO 65212; E-mail:

Submitted for publication December 2007.

Accepted for publication January 2008.

©2008The American College of Sports Medicine