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

1 Department of Medical Pharmacology and Physiology, and 2 Dalton Cardiovascular Research Center, University of Missouri, Columbia; 3 Harry S. Truman Memorial Veterans Hospital, Department of Veterans Affairs Medical Center, Columbia, Missouri; 4 Department of Integrative Physiology, University of N...

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Published inJournal of applied physiology (1985) Vol. 103; no. 3; pp. 941 - 947
Main Authors Fisher, James P, Ogoh, Shigehiko, Young, Colin N, Keller, David M, Fadel, Paul J
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Physiological Soc 01.09.2007
American Physiological Society
Subjects
Online AccessGet full text
ISSN8750-7587
1522-1601
DOI10.1152/japplphysiol.00412.2007

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Abstract 1 Department of Medical Pharmacology and Physiology, and 2 Dalton Cardiovascular Research Center, University of Missouri, Columbia; 3 Harry S. Truman Memorial Veterans Hospital, Department of Veterans Affairs Medical Center, Columbia, Missouri; 4 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth; and 5 Department 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 Address for reprint requests and other correspondence: P. J. Fadel, Dept. of Medical Pharmacology and Physiology, MA415 Medical Sciences Bldg., Univ. of Missouri, Columbia, MO 65212 (e-mail: fadelp{at}health.missouri.edu )
AbstractList 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 approximately 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 approximately 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.
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 similar to 40 s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (-12 plus or minus 2 beats/min) and 30% (-10 plus or minus 2 beats/min) MVC HG were similar to rest (-10 plus or minus 1 beats/min). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (-6 plus or minus 2 and -4 plus or minus 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 similar to 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.
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 (< 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. (ProQuest: ... denotes formulae/symbols omitted.)
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.
1 Department of Medical Pharmacology and Physiology, and 2 Dalton Cardiovascular Research Center, University of Missouri, Columbia; 3 Harry S. Truman Memorial Veterans Hospital, Department of Veterans Affairs Medical Center, Columbia, Missouri; 4 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth; and 5 Department 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 Address for reprint requests and other correspondence: P. J. Fadel, Dept. of Medical Pharmacology and Physiology, MA415 Medical Sciences Bldg., Univ. of Missouri, Columbia, MO 65212 (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 5 s at end expiration to stimulate the CBR at rest, at the onset of HG (<1 s), and after approximately 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 approximately 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.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 approximately 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 approximately 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.
Author Keller, David M
Fadel, Paul J
Fisher, James P
Young, Colin N
Ogoh, Shigehiko
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Issue 3
Keywords Physical exercise
Human
Heart rate
Vertebrata
Mammalia
Baroreflex
Intensity
arterial baroreflex
Blood pressure
Hemodynamics
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Snippet 1 Department of Medical Pharmacology and Physiology, and 2 Dalton Cardiovascular Research Center, University of Missouri, Columbia; 3 Harry S. Truman Memorial...
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...
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SubjectTerms Adult
Baroreflex - physiology
Biological and medical sciences
Blood pressure
Blood Pressure - physiology
Carotid Sinus - physiology
Exercise
Exercise - physiology
Female
Fundamental and applied biological sciences. Psychology
Heart - physiology
Heart rate
Heart Rate - physiology
Humans
Male
Neck - physiology
Veins & arteries
Title Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans
URI http://jap.physiology.org/cgi/content/abstract/103/3/941
https://www.ncbi.nlm.nih.gov/pubmed/17585044
https://www.proquest.com/docview/222224067
https://www.proquest.com/docview/20490262
https://www.proquest.com/docview/68209469
Volume 103
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