Submitted on April 16, 2007
Accepted on June 16, 2007
Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans
James P Fisher1, Shigehiko Ogoh2, Colin N Young1, David Melvin Keller3, and Paul J Fadel4*
1 Department of Medical Pharmacology and Physiology, University of Missouri, One Hospital Drive, MA 415, Columbia, Missouri, 65212, United States; Department of Veterans Affairs Medical Center, Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri, United States
2 Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas, United States
3 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States
4 Department of Medical Pharmacology and Physiology, University of Missouri, One Hospital Drive, MA 415, Columbia, Missouri, 65212, United States; Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States; Department of Veterans Affairs Medical Center, Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri, United States
* To whom correspondence should be addressed. E-mail: fadelp{at}health.missouri.edu.
We sought to examine the influence of exercise intensity on carotid baroreflex (CBR) control of heart rate (HR) and mean arterial pressure (MAP) at the onset of exercise in humans. To accomplish this, eight subjects performed multiple 1-min bouts of isometric handgrip (HG) exercise at 15, 30, 45 and 60% maximal voluntary contraction (MVC), while breathing to a metronome set at eupneic frequency. Neck suction (NS) of -60 Torr was applied for 5s at end-expiration to stimulate the CBR at rest, at the onset of (<1s) and after ~40s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (-12±2 bpm) and 30% (-10±2 bpm) MVC HG were similar to rest (-10±1 bpm). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (-6±2 and -4±1 bpm, respectively; P<0.001). In contrast to HR, MAP responses to NS were not different from rest at exercise onset. Furthermore, both HR and MAP responses to NS applied at ~40s of HG were similar to rest. In summary, CBR control of HR was transiently blunted at the immediate onset of high intensity HG, whereas MAP responses were preserved demonstrating differential baroreflex control of HR and blood pressure at exercise onset. Collectively, these results suggest that carotid-cardiac baroreflex control is dynamically modulated throughout isometric exercise in humans, while carotid baroreflex regulation of blood pressure is well-maintained.
