Physiology and pathophysiology of heart rate and blood pressure variability in humans: Is power spectral analysis largely an index of baroreflex gain?

P. Sleight, T. La Rovere, A. Mortara, G. Pinna, R. Maestri, S. Leuzzi, B. Bianchini, L. Tavazzi, L. Bernardi

Research output: Contribution to journalArticle

Abstract

1. It is often assumed that the power in the low-around 0,10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects vagal and sympathetic tone respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Beer model). 2. We have applied the De Beer model of circulatory variability to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2Hz), which were both distinct from the controlled respiration rate (0.25Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Beer model. The low-frequency (0.1Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact. With a large stimulus to the carotid baroreceptor it was possible to influence the low-frequency R-R but not low-frequency blood pressure variability. This implies that it is too simplistic to use power spectral analysis as a simple measure of autonomic balance; its underlying modulation is more complex than generally believed. 4. It may be that power spectral analysis is more a sensitive indicator of baroreflex control, particularly of vagal control, than direct evidence of autonomic balance. Of course, there is often a correlation between the gain of the reflex and the autonomic balance of vagus and sympathetic. These considerations may help our understanding of some conditions, such as exercise or heart failure, when the power spectral analysis method fails to identify increased sympathetic discharge; this failure may partly be explained by the decrease in baroreflex sensitivity which occurs in these two conditions.

Original languageEnglish
Pages (from-to)103-109
Number of pages7
JournalClinical Science
Volume88
Issue number1
Publication statusPublished - 1995

Fingerprint

Baroreflex
Heart Rate
Blood Pressure
Pressoreceptors
Reflex
Heart Failure
Suction
Respiratory Rate
Power (Psychology)
Hypotension
Arm
Neck
Stroke
Exercise

Keywords

  • Autonomic nervous system
  • Baroreflex sensitivity
  • Heart failure
  • Heart rate variability

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Physiology and pathophysiology of heart rate and blood pressure variability in humans : Is power spectral analysis largely an index of baroreflex gain? / Sleight, P.; La Rovere, T.; Mortara, A.; Pinna, G.; Maestri, R.; Leuzzi, S.; Bianchini, B.; Tavazzi, L.; Bernardi, L.

In: Clinical Science, Vol. 88, No. 1, 1995, p. 103-109.

Research output: Contribution to journalArticle

@article{7313aff89848474893af31399e4811a0,
title = "Physiology and pathophysiology of heart rate and blood pressure variability in humans: Is power spectral analysis largely an index of baroreflex gain?",
abstract = "1. It is often assumed that the power in the low-around 0,10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects vagal and sympathetic tone respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Beer model). 2. We have applied the De Beer model of circulatory variability to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2Hz), which were both distinct from the controlled respiration rate (0.25Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Beer model. The low-frequency (0.1Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact. With a large stimulus to the carotid baroreceptor it was possible to influence the low-frequency R-R but not low-frequency blood pressure variability. This implies that it is too simplistic to use power spectral analysis as a simple measure of autonomic balance; its underlying modulation is more complex than generally believed. 4. It may be that power spectral analysis is more a sensitive indicator of baroreflex control, particularly of vagal control, than direct evidence of autonomic balance. Of course, there is often a correlation between the gain of the reflex and the autonomic balance of vagus and sympathetic. These considerations may help our understanding of some conditions, such as exercise or heart failure, when the power spectral analysis method fails to identify increased sympathetic discharge; this failure may partly be explained by the decrease in baroreflex sensitivity which occurs in these two conditions.",
keywords = "Autonomic nervous system, Baroreflex sensitivity, Heart failure, Heart rate variability",
author = "P. Sleight and {La Rovere}, T. and A. Mortara and G. Pinna and R. Maestri and S. Leuzzi and B. Bianchini and L. Tavazzi and L. Bernardi",
year = "1995",
language = "English",
volume = "88",
pages = "103--109",
journal = "Clinical Science",
issn = "0143-5221",
publisher = "Portland Press Ltd.",
number = "1",

}

TY - JOUR

T1 - Physiology and pathophysiology of heart rate and blood pressure variability in humans

T2 - Is power spectral analysis largely an index of baroreflex gain?

AU - Sleight, P.

AU - La Rovere, T.

AU - Mortara, A.

AU - Pinna, G.

AU - Maestri, R.

AU - Leuzzi, S.

AU - Bianchini, B.

AU - Tavazzi, L.

AU - Bernardi, L.

PY - 1995

Y1 - 1995

N2 - 1. It is often assumed that the power in the low-around 0,10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects vagal and sympathetic tone respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Beer model). 2. We have applied the De Beer model of circulatory variability to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2Hz), which were both distinct from the controlled respiration rate (0.25Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Beer model. The low-frequency (0.1Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact. With a large stimulus to the carotid baroreceptor it was possible to influence the low-frequency R-R but not low-frequency blood pressure variability. This implies that it is too simplistic to use power spectral analysis as a simple measure of autonomic balance; its underlying modulation is more complex than generally believed. 4. It may be that power spectral analysis is more a sensitive indicator of baroreflex control, particularly of vagal control, than direct evidence of autonomic balance. Of course, there is often a correlation between the gain of the reflex and the autonomic balance of vagus and sympathetic. These considerations may help our understanding of some conditions, such as exercise or heart failure, when the power spectral analysis method fails to identify increased sympathetic discharge; this failure may partly be explained by the decrease in baroreflex sensitivity which occurs in these two conditions.

AB - 1. It is often assumed that the power in the low-around 0,10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects vagal and sympathetic tone respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Beer model). 2. We have applied the De Beer model of circulatory variability to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2Hz), which were both distinct from the controlled respiration rate (0.25Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Beer model. The low-frequency (0.1Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact. With a large stimulus to the carotid baroreceptor it was possible to influence the low-frequency R-R but not low-frequency blood pressure variability. This implies that it is too simplistic to use power spectral analysis as a simple measure of autonomic balance; its underlying modulation is more complex than generally believed. 4. It may be that power spectral analysis is more a sensitive indicator of baroreflex control, particularly of vagal control, than direct evidence of autonomic balance. Of course, there is often a correlation between the gain of the reflex and the autonomic balance of vagus and sympathetic. These considerations may help our understanding of some conditions, such as exercise or heart failure, when the power spectral analysis method fails to identify increased sympathetic discharge; this failure may partly be explained by the decrease in baroreflex sensitivity which occurs in these two conditions.

KW - Autonomic nervous system

KW - Baroreflex sensitivity

KW - Heart failure

KW - Heart rate variability

UR - http://www.scopus.com/inward/record.url?scp=0028812076&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028812076&partnerID=8YFLogxK

M3 - Article

C2 - 7677832

AN - SCOPUS:0028812076

VL - 88

SP - 103

EP - 109

JO - Clinical Science

JF - Clinical Science

SN - 0143-5221

IS - 1

ER -