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This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 103/3/941    most recent 00412.2007v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Fisher, J. P. Articles by Fadel, P. J. Search for Related Content PubMed PubMed Citation Articles by Fisher, J. P. Articles by Fadel, P. J.

Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans

¹Department of Medical Pharmacology and Physiology, and ²Dalton Cardiovascular Research Center, University of Missouri, Columbia; ³Harry S. Truman Memorial Veterans Hospital, Department of Veterans Affairs Medical Center, Columbia, Missouri; ⁴Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth; and ⁵Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas

Submitted 16 April 2007 ; accepted in final form 16 June 2007

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 5 s at end expiration to stimulate the CBR at rest, at the onset of HG (<1 s), and after 40 s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (–12 ± 2 beats/min) and 30% (–10 ± 2 beats/min) MVC HG were similar to rest (–10 ± 1 beats/min). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (–6 ± 2 and –4 ± 1 beats/min, 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, whereas carotid baroreflex regulation of blood pressure is well-maintained.

arterial baroreflex; blood pressure; heart rate