Baroreflex physiology studied in healthy subjects with very infrequent muscle sympathetic bursts

Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arte...

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Published inJournal of applied physiology (1985) Vol. 114; no. 2; pp. 203 - 210
Main Authors Diedrich, André, Crossman, Alexandra A., Beightol, Larry A., Tahvanainen, Kari U. O., Kuusela, Tom A., Ertl, Andrew C., Eckberg, Dwain L.
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 15.01.2013
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Abstract Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7–43) vs. 24 (8–45) ms/mmHg], and highly significant, according to linear regression ( r 2 = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.
AbstractList Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7-43) vs. 24 (8-45) ms/mmHg], and highly significant, according to linear regression (r(2) = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7-43) vs. 24 (8-45) ms/mmHg], and highly significant, according to linear regression (r(2) = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.
Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7-43) vs. 24 (8-45) ms/mmHg], and highly significant, according to linear regression (r2 = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts. [PUBLICATION ABSTRACT]
Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7–43) vs. 24 (8–45) ms/mmHg], and highly significant, according to linear regression ( r 2 = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.
Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7-43) vs. 24 (8-45) ms/mmHg], and highly significant, according to linear regression (r(2) = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.
Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7–43) vs. 24 (8–45) ms/mmHg], and highly significant, according to linear regression ( r 2 = 0.91, P = 0.001). Our results indicate that 1 ) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2 ) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.
Author Crossman, Alexandra A.
Beightol, Larry A.
Ertl, Andrew C.
Diedrich, André
Tahvanainen, Kari U. O.
Kuusela, Tom A.
Eckberg, Dwain L.
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  givenname: Kari U. O.
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– sequence: 7
  givenname: Dwain L.
  surname: Eckberg
  fullname: Eckberg, Dwain L.
  organization: Departments of Medicine and Physiology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Medical College of Virginia at Virginia Commonwealth University, Richmond, Virginia
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Cites_doi 10.1113/jphysiol.1981.sp013604
10.1152/ajpheart.01024.2005
10.1016/0002-9149(73)91021-7
10.1152/ajpheart.1997.273.4.H1629
10.1152/ajpheart.00924.2009
10.1161/01.HYP.25.5.1058
10.1152/ajpheart.1982.242.4.H638
10.1152/ajpheart.2001.280.6.H2674
10.1152/jappl.1999.87.1.97
10.1152/ajpheart.1987.253.3.H680
10.1111/j.1748-1716.1952.tb00889.x
10.1152/ajpregu.1987.253.6.R929
10.1016/0022-510X(80)90098-2
10.1152/ajpheart.1989.256.6.H1573
10.1152/ajpregu.1991.260.3.R635
10.1016/0165-1838(79)90004-3
10.1161/01.RES.29.4.424
10.1152/jappl.1996.80.3.869
10.1056/NEJM197110142851602
10.1097/01.hjh.0000125439.28861.ed
10.1097/00004872-200018010-00003
10.1042/cs0640455
10.1113/jphysiol.1985.sp015766
10.1111/j.1475-097X.1991.tb00452.x
10.1016/S0140-6736(95)91748-9
10.1161/01.RES.47.2.208
10.1113/jphysiol.1994.sp020025
10.1016/0735-1097(91)90761-W
10.1093/oso/9780198576938.001.0001
10.1152/ajpheart.1996.271.3.H1240
10.1152/ajpheart.2001.280.6.H2804
10.1007/BF02441589
10.1113/jphysiol.1978.sp012170
10.1161/01.RES.24.1.109
10.1016/0165-1838(88)90113-0
10.1007/978-3-662-28813-9
10.1007/BF01826234
10.1113/jphysiol.2005.091090
10.1152/ajpheart.00645.2006
10.1111/j.1542-474X.1997.tb00331.x
10.1113/jphysiol.1976.sp011445
10.1016/S0140-6736(86)90837-8
10.1152/ajpregu.1986.251.6.R1086
10.1161/01.HYP.12.6.600
10.1161/01.HYP.10.5.538
10.1152/ajpheart.1982.242.2.H185
10.1161/01.HYP.0000091370.83602.E6
10.1016/0735-1097(89)90551-2
10.1161/01.CIR.59.4.632
10.1113/jphysiol.1977.sp011915
10.1152/ajpregu.00709.2002
10.1152/ajpheart.00602.2002
10.1109/TBME.1986.325789
10.1152/japplphysiol.91107.2008
10.1016/0165-1838(82)90002-9
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References B20
B21
B23
B24
B25
B26
Bertinieri G (B6) 1985; 3
B27
B28
B29
B30
B31
B32
B33
B34
B35
B36
B37
B38
B1
B2
B3
B4
B5
B7
B8
B9
B40
B41
B42
B43
B44
B45
B46
B47
B48
B49
Eckberg DL (B22) 1992
B50
B51
B52
B53
B10
B54
B11
B55
B12
B56
B13
B57
B14
B15
B16
B17
B18
B19
Peňáz J (B39) 1973
References_xml – ident: B4
  doi: 10.1113/jphysiol.1981.sp013604
– ident: B55
  doi: 10.1152/ajpheart.01024.2005
– ident: B57
  doi: 10.1016/0002-9149(73)91021-7
– ident: B9
  doi: 10.1152/ajpheart.1997.273.4.H1629
– ident: B29
  doi: 10.1152/ajpheart.00924.2009
– ident: B38
  doi: 10.1161/01.HYP.25.5.1058
– start-page: 104
  volume-title: Digest of the 10th International Conference on Medical and Biologic Engineering
  year: 1973
  ident: B39
– ident: B18
  doi: 10.1152/ajpheart.1982.242.4.H638
– ident: B2
  doi: 10.1152/ajpheart.2001.280.6.H2674
– ident: B30
  doi: 10.1152/jappl.1999.87.1.97
– ident: B12
  doi: 10.1152/ajpheart.1987.253.3.H680
– ident: B32
  doi: 10.1111/j.1748-1716.1952.tb00889.x
– ident: B41
  doi: 10.1152/ajpregu.1987.253.6.R929
– ident: B24
  doi: 10.1016/0022-510X(80)90098-2
– ident: B35
  doi: 10.1152/ajpheart.1989.256.6.H1573
– ident: B27
  doi: 10.1152/ajpregu.1991.260.3.R635
– ident: B31
  doi: 10.1016/0165-1838(79)90004-3
– ident: B28
  doi: 10.1161/01.RES.29.4.424
– ident: B48
  doi: 10.1152/jappl.1996.80.3.869
– ident: B17
  doi: 10.1056/NEJM197110142851602
– ident: B56
  doi: 10.1097/01.hjh.0000125439.28861.ed
– ident: B37
  doi: 10.1097/00004872-200018010-00003
– ident: B40
  doi: 10.1042/cs0640455
– ident: B21
  doi: 10.1113/jphysiol.1985.sp015766
– ident: B47
  doi: 10.1111/j.1475-097X.1991.tb00452.x
– ident: B8
  doi: 10.1016/S0140-6736(95)91748-9
– ident: B16
  doi: 10.1161/01.RES.47.2.208
– ident: B51
  doi: 10.1113/jphysiol.1994.sp020025
– ident: B45
  doi: 10.1016/0735-1097(91)90761-W
– volume-title: Human Baroreflexes in Health and Disease.
  year: 1992
  ident: B22
  doi: 10.1093/oso/9780198576938.001.0001
– ident: B44
  doi: 10.1152/ajpheart.1996.271.3.H1240
– ident: B50
  doi: 10.1152/ajpheart.2001.280.6.H2804
– ident: B11
  doi: 10.1007/BF02441589
– ident: B49
  doi: 10.1113/jphysiol.1978.sp012170
– ident: B46
  doi: 10.1161/01.RES.24.1.109
– ident: B23
  doi: 10.1016/0165-1838(88)90113-0
– ident: B42
  doi: 10.1007/978-3-662-28813-9
– volume: 3
  start-page: S79
  year: 1985
  ident: B6
  publication-title: J Hyperten
– ident: B25
  doi: 10.1007/BF01826234
– ident: B20
  doi: 10.1113/jphysiol.2005.091090
– ident: B10
  doi: 10.1152/ajpheart.00645.2006
– ident: B1
  doi: 10.1111/j.1542-474X.1997.tb00331.x
– ident: B13
  doi: 10.1113/jphysiol.1976.sp011445
– ident: B7
  doi: 10.1016/S0140-6736(86)90837-8
– ident: B26
  doi: 10.1152/ajpregu.1986.251.6.R1086
– ident: B36
  doi: 10.1161/01.HYP.12.6.600
– ident: B43
  doi: 10.1161/01.HYP.10.5.538
– ident: B52
  doi: 10.1152/ajpheart.1982.242.2.H185
– ident: B34
  doi: 10.1161/01.HYP.0000091370.83602.E6
– ident: B54
  doi: 10.1016/0735-1097(89)90551-2
– ident: B15
  doi: 10.1161/01.CIR.59.4.632
– ident: B14
  doi: 10.1113/jphysiol.1977.sp011915
– ident: B33
  doi: 10.1152/ajpregu.00709.2002
– ident: B3
  doi: 10.1152/ajpheart.00602.2002
– ident: B5
  doi: 10.1109/TBME.1986.325789
– ident: B19
  doi: 10.1152/japplphysiol.91107.2008
– ident: B53
  doi: 10.1016/0165-1838(82)90002-9
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Snippet Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the...
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StartPage 203
SubjectTerms Adolescent
Adult
Baroreflex - physiology
Blood pressure
Blood Pressure - physiology
Data collection
Female
Humans
Linear Models
Male
Muscle, Skeletal - innervation
Muscle, Skeletal - physiology
Muscular system
Physiology
Regression analysis
Retrospective Studies
Sympathetic Nervous System - physiology
Vagus Nerve - physiology
Veins & arteries
Young Adult
Title Baroreflex physiology studied in healthy subjects with very infrequent muscle sympathetic bursts
URI https://www.ncbi.nlm.nih.gov/pubmed/23195626
https://www.proquest.com/docview/1270583916
https://www.proquest.com/docview/1273584801
https://pubmed.ncbi.nlm.nih.gov/PMC3544503
Volume 114
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