This investigation was supported by a grant from the Netherlands Research Foundation Z.W.O. to Paul Grossman, who would also like to express appreciation to the German Research Society for their support while analyzing some of the data and writing the manuscript. Additionally, we would like to thank Annemieke Brinkman, Johan de Vries, and Wolfgang Mueller for their technical assistance, and Jochen Fahrenberg and Gerhard Stemmler for their comments upon an earlier version of this paper.
Prediction of Tonic Parasympathetic Cardiac Control Using Respiratory Sinus Arrhythmia: The Need for Respiratory Control
Version of Record online: 30 JAN 2007
Volume 28, Issue 2, pages 201–216, March 1991
How to Cite
Grossman, P., Karemaker, J. and Wieling, W. (1991), Prediction of Tonic Parasympathetic Cardiac Control Using Respiratory Sinus Arrhythmia: The Need for Respiratory Control. Psychophysiology, 28: 201–216. doi: 10.1111/j.1469-8986.1991.tb00412.x
- Issue online: 30 JAN 2007
- Version of Record online: 30 JAN 2007
- (Manuscript received April 2, 1989; accepted for publication April 29, 1990)
- Respiratory sinus arrhythmia;
- Parasympathetic cardiac control;
- Vagal tone;
- Heart period;
- Respiratory influences;
- Respiration rate;
- Tidal volume;
- Beta-adrenergic blockade;
Respiratory sinus arrhythmia (RSA) has received much attention in recent years due to the large body of evidence indicating that variations in this phenomenon represent alterations in parasympathetic cardiac control. Although it appears that respiratory sinus arrhythmia is mediated by vagal mechanisms, the extent to which the well-known respiratory influences (i.e., rate and tidal volume) on respiratory sinus arrhythmia (in altering its magnitude) may moderate the relationship between RSA and cardiac vagal tone has never been systematically studied.
We addressed this issue by examining intraindividual relationships among RSA magnitude, respiration (rate and tidal volume), and heart period among six healthy male adults after intravenous administration of 10 mg propranolol, a beta-adrenergic blocker. Subjects were exposed to various behavioral tasks which altered all physiological variables measured. Variations in heart period after beta blockade were assumed to be predominantly vagally mediated. Within-subject regression analyses consistently showed that respiratory parameters influenced RSA magnitude, but not tonic variations in beta-blocked heart period, suggesting that respiratory-mediated RSA alterations are not associated with changes in cardiac vagal tone. Only when respiratory variables were statistically controlled was there evidence of a reasonable correspondence between beta-blocked heart period and RSA amplitude, providing support for the idea that respiratory parameters need to be controlled when using RSA amplitude as an index of cardiac vagal tone. Repeated-measures analyses of variance of mean levels of heart period and respiratory sinus arrhythmia across subjects supplemented and supported the intraindividual results. These findings point to the importance of controlling for respiratory parameters when using respiratory sinus arrhythmia as a cardiac vagal index.