On 2017 Mar 19, Paul Grossman commented:

Unfortunately, the authors of this paper so far refuse to discuss key most likely severely flawed assumptions of their "recommendations" paper in any open forum available to scientists (here, ResearchGate or PubMed Commons: see their reply to my qnd others's comments in ResearchGate, https://www.researchgate.net/publication/313849201_Heart_Rate_Variability_and_Cardiac_Vagal_Tone_in_Psychophysiological_Research_Recommendations_for_Experiment_Planning_Data_Analysis_and_Data_Reporting )

I have been active in this field for over 30 years. Vagal tone is not "variability in heart rate between inhalation and exhalation"; the latter is termed respiratory sinus arrhythmia (RSA, or also high-frequency heart-rate variability, HRV ) and under very specific conditions may sometimes partially reflect, or be a marker of, cardiac vagal tone. Cardiac vagal tone--on the other hand--is defined as the magnitude of mean heart rate change from one condition to another (e.g. rest to different levels of physical exertion or to pharmacological blockade of parasympathetic control) that is a specific consequence of parasympathetic effects. Obviously the two phenomena are not equivalent: Resipratory sinus arrhythmia is an inherently phasic (not tonic) phenomenon (heart rate shifting rhythmically from inspiration to expiration). Cardiac vagal tone characterizes the average effect of vagal influences upon heart rate during a particular duration of time. Changes in breathing frequency can have dramatic effects upon magnitude of RSA without any effects upon cardiac vagal tone. There are also other conditions in which the two phenomena do not change proportionally to each other: e.g. sometimes when sympathetic activity substantially changes; or when efferent vagal traffic to the heart is blocked by chemicals before it can reach the sinus atrial node; or probably when vagal discharge is so great that the vagal traffic saturates the sinus atrial node leading to profound slowing of heart rate during both inspiration and expiration. These effects are rather clearly shown in the autonomic cardiovascular physiological literature but fail to be acknowledged in much of the psychological or psychophysiological publications. Thus it is plain wrong to believe that RSA is vagal tone. There is really so much evidence that is often systematically ignored, particularly by psychologists working in the field.

On 2017 Mar 13, Paul Grossman commented:

The issue of the influence of respiration (breathing rate and volume) confounding heart-rate variability (HRV) as an index of within-individual changes of cardiac vagal tone remains inadequately covered in this review. My colleagues' and my 1991 and 1993 papers (Grossman , Karemaker & Wieling, 1991; Grossman & Kollai, 1993) using pharmacological blockade controls, rather conclusively show that respiratory sinus arrhythmia (RSA, or high-frequency HRV) under spontaneously varying rates and/or depths of breathing does not provide an accurate reflection of quantitative within-individual variations in cardiac vagal tone. Our results are also clearly far from the only findings demonstrating this fact (see also literature of Saul and Berger, as well as others). Yet this rich resource of findings is neither cited nor addressed in the paper. I would be curious why? The research clearly and consistently shows that when a person's heart rate changes from one condition to another are completely vagally mediated (documenting changes in cardiac vagal tone), changes in RSA WILL NOT ACCURATELY REFLECT those variations in cardiac vagal tone whenever breathing parameters substantially change as well: The alterations in RSA amplitude will be much more closely correlated with respiratory pattern changes, but may not at all reflect vagal tone alterations! The proper method to correct for this issue is, however, another question. The crucial point is that this confound must no longer be swept under the carpet. I welcome any dialogue about this from the authors or others..

A bit simpler explanation: We and others (e.g. Grossman , Karemaker & Wieling, 1991; Grossman & Kollai, 1993; Eckberg, various publications; JP Saul, various publications; R Berger, various publications) have consistently shown that changes in breathing rate and volume can easily and dramatically alter heart-rate variability (HRV) indices of cardiac vagal tone, without actual corresponding changes in cardiac vagal tone occurring! This point is not at all considered in this or many other HRV papers. Any paper purporting to provide standards in this area must deal with this issue. If the reader of this comment is a typically young healthy person, this point can easily be documented by noting your pulse rate as you voluntarily or spontaneously alter your breathing frequency substantially: slow breathing will bring about an often perceptibly more irregular pulse over the respiratory cycle than fast breathing, but there will be little-to-no change in average heart rate over the time (which would almost certainly have to occur for such dramatic perceptible changes in HRV to reflect cardiac vagal tone: heart rate should slow as vagal tone increases, and should speed as vagal tone decreases, provided there are no sympathetic shifts in activity--extremely unlikely in this little experiment!).

On 2017 Mar 13, Paul Grossman commented:

The issue of the influence of respiration (breathing rate and volume) confounding heart-rate variability (HRV) as an index of within-individual changes of cardiac vagal tone remains inadequately covered in this review. My colleagues' and my 1991 and 1993 papers (Grossman , Karemaker & Wieling, 1991; Grossman & Kollai, 1993) using pharmacological blockade controls, rather conclusively show that respiratory sinus arrhythmia (RSA, or high-frequency HRV) under spontaneously varying rates and/or depths of breathing does not provide an accurate reflection of quantitative within-individual variations in cardiac vagal tone. Our results are also clearly far from the only findings demonstrating this fact (see also literature of Saul and Berger, as well as others). Yet this rich resource of findings is neither cited nor addressed in the paper. I would be curious why? The research clearly and consistently shows that when a person's heart rate changes from one condition to another are completely vagally mediated (documenting changes in cardiac vagal tone), changes in RSA WILL NOT ACCURATELY REFLECT those variations in cardiac vagal tone whenever breathing parameters substantially change as well: The alterations in RSA amplitude will be much more closely correlated with respiratory pattern changes, but may not at all reflect vagal tone alterations! The proper method to correct for this issue is, however, another question. The crucial point is that this confound must no longer be swept under the carpet. I welcome any dialogue about this from the authors or others..

A bit simpler explanation: We and others (e.g. Grossman , Karemaker & Wieling, 1991; Grossman & Kollai, 1993; Eckberg, various publications; JP Saul, various publications; R Berger, various publications) have consistently shown that changes in breathing rate and volume can easily and dramatically alter heart-rate variability (HRV) indices of cardiac vagal tone, without actual corresponding changes in cardiac vagal tone occurring! This point is not at all considered in this or many other HRV papers. Any paper purporting to provide standards in this area must deal with this issue. If the reader of this comment is a typically young healthy person, this point can easily be documented by noting your pulse rate as you voluntarily or spontaneously alter your breathing frequency substantially: slow breathing will bring about an often perceptibly more irregular pulse over the respiratory cycle than fast breathing, but there will be little-to-no change in average heart rate over the time (which would almost certainly have to occur for such dramatic perceptible changes in HRV to reflect cardiac vagal tone: heart rate should slow as vagal tone increases, and should speed as vagal tone decreases, provided there are no sympathetic shifts in activity--extremely unlikely in this little experiment!).

On 2017 Mar 19, Paul Grossman commented:

Unfortunately, the authors of this paper so far refuse to discuss key most likely severely flawed assumptions of their "recommendations" paper in any open forum available to scientists (here, ResearchGate or PubMed Commons: see their reply to my qnd others's comments in ResearchGate, https://www.researchgate.net/publication/313849201_Heart_Rate_Variability_and_Cardiac_Vagal_Tone_in_Psychophysiological_Research_Recommendations_for_Experiment_Planning_Data_Analysis_and_Data_Reporting )

I have been active in this field for over 30 years. Vagal tone is not "variability in heart rate between inhalation and exhalation"; the latter is termed respiratory sinus arrhythmia (RSA, or also high-frequency heart-rate variability, HRV ) and under very specific conditions may sometimes partially reflect, or be a marker of, cardiac vagal tone. Cardiac vagal tone--on the other hand--is defined as the magnitude of mean heart rate change from one condition to another (e.g. rest to different levels of physical exertion or to pharmacological blockade of parasympathetic control) that is a specific consequence of parasympathetic effects. Obviously the two phenomena are not equivalent: Resipratory sinus arrhythmia is an inherently phasic (not tonic) phenomenon (heart rate shifting rhythmically from inspiration to expiration). Cardiac vagal tone characterizes the average effect of vagal influences upon heart rate during a particular duration of time. Changes in breathing frequency can have dramatic effects upon magnitude of RSA without any effects upon cardiac vagal tone. There are also other conditions in which the two phenomena do not change proportionally to each other: e.g. sometimes when sympathetic activity substantially changes; or when efferent vagal traffic to the heart is blocked by chemicals before it can reach the sinus atrial node; or probably when vagal discharge is so great that the vagal traffic saturates the sinus atrial node leading to profound slowing of heart rate during both inspiration and expiration. These effects are rather clearly shown in the autonomic cardiovascular physiological literature but fail to be acknowledged in much of the psychological or psychophysiological publications. Thus it is plain wrong to believe that RSA is vagal tone. There is really so much evidence that is often systematically ignored, particularly by psychologists working in the field.