HRV spectral analysis

With my suitcase in my hand, on my way to Richmond, to speak at what is going to be a great seminar, the CVASPS 2014 organized by my friend Jay de Mayo and after that travelling to Minneapolis to Cal Dietz for another presentation.  I am honored to get invited to speak there and happy to meet many of my good colleagues again and to learn something.

Maybe in my last post I sounded a little bit outspoken about the use of frequency-domain parameters or spectral analysis, a method used by many HRV-testing systems for health, fitness and performance.  But at least I am in good company. I will give you a short overview of the ideas of some experts about this way of analyzing HRV. (Italics are mine)

1.    Karemaker, J,M: Heart rate variability: why do spectral analysis?; Heart, Vol.77, 1997, pg.99-101:

“The origin and meaning of HRV are much debated in various circles of researchers. Some have tried to fit the experimental observations to simple physiological models. The task force report adopts a more global view, emphasizing the distinction between low frequency (LF) and high frequency (HF) HRV and viewing LF as sympathetic and HF as parasympathetic cardiovascular control. This is an oversimplification and detracts from the unsolved fundamental problems in HRV analysis.”     

2.    Mamiy, V.I: Spectral Analysis and Interpretation of Spectral Components of Heart Rate Variability; Human Physiology, Vol.32, No.2, 2006, pg.169-176:

“1.The generally accepted method of spectral analysis has a pitfall. It is only tested
whether the process in question is stationary, whereas its components are not analyzed. This approach yields correct results for simple processes. A complex process may be stationary while its components are not. In this case, the results of
spectral analysis will be ambiguous.
2.  The procedure of spectral analysis should be supplemented with analyzing the spectral components of the process studied, e.g., by digital filtration, to test if they are also stationary.
3. In my opinion, there is no generally accepted notion on the nature of HRV spectral components precisely because the results of spectral analysis are ambiguous.
4. The spectrum of cardiac-rhythm fluctuations obtained by analyzing 3- to 5-min fragments of rhythmograms is neurogenic. The periods of LF and HF waves in the cardiac rhythm are determined by the periods of pulse burst transmission through sympathetic and parasympathetic nerve fibers, respectively, the number of pulses per burst determining the amplitudes of these waves. The VLF fluctuations of the cardiac rhythm are related to antiphase fluctuations of the sympathetic and parasympathetic effects on the cardiac rhythm. The position of the VLF spectral peak on the frequency axis of the HRV spectrum and the peak amplitude are determined, respectively, by the frequency and the depth of the modulation of the number of pulses per burst traveling along parasympathetic and sympathetic nerve fibers to the sinoatrial node.”

3.    Bernardi, L: Effects of controlled breathing, mental activity and mental stress with and without verbalization on heart rate variability; J.Am.Coll.Cardiol.Vol.35, No.6, 2000, pg.1462-1469:

“One should, therefore, be cautious in the interpretation of short sequences
of data (in the range of 4 to 10 min) and not uncritically attribute an increase in LF to sympathetic activation, as this increase might simply be the effect of
speech-induced slower breathing. Alternatively, the normal sympathetic activation seen during mental tasks might be masked or accentuated by addition of frequencies generated by unequal or slow respiratory patterns. Thus, in the absence of simultaneous analysis of respiration, the changes in LF/HF ratio should not be taken as clear evidence of changes in autonomic tone”

4.    Houle, M.S; Billmann, G.E: Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity; Am. J.Physiol. Vol.276, (1 pt.2), H215-223:

“In summary, the present study demonstrates that low-frequency (0.06–0.10 Hz) fluctuations in the R-R interval variability may not accurately reflect changes in sympathetic activity.
Changes in sympathetic activity may contribute to the low-frequency peak, but a large influence of the parasympathetic activity is also present. As such, the interpretation of the low frequency component of the HRV spectrum becomes problematic and, under most circumstances, cannot be taken as an accurate measurement of cardiac sympathetic input.
The present study supports a review by Eckberg (10) in which the author outlines the complexity of the HRV spectrum. Eckberg argues that often the language and the mathematical manipulations used to describe the parameters associated with the HRV spectrum may be in danger of obscuring the physiology behind the spectrum.
The author states that there is little doubt that sympathetic neural mechanisms contribute to the low-frequency component, yet this does not necessarily mean that the low-frequency component is a ‘‘quantitative probe for sympathetic traffic.’’

Sloan, R.P: Relationships between circulating catecholamines and low frequency heart period variability as indices of cardiac sympathetic activity during mental stress; Psychosomatic Med. Vol.58, No.1, 1996, pg.25-31:

We conclude that under conditions of psychological stress, LF power provides no useful information about cardiac sympathetic activity, both because power in this frequency band falls whereas HR rises and because there is no relationship between LF power and plasma NE.

5.    Billman, G.E: The LF/HF ratio does not accurately measure cardiac sympatho-vagal balance; Frontiers in Physiology, Feb.20.2013;

As we have seen, the hypothesis that LF/HF quantifies “sympatho-vagal balance” depends upon four interrelated assumptions, all of which can be proven to be false. The facts are in direct opposition to the assumptions. In particular, the complex nature of LF power, its exceedingly poor relationship to sympathetic nerve activation, and the non-linear (and often non-reciprocal) interactions between sympathetic and parasympathetic nerve activity that are confounded by the mechanical effects of respiration and prevailing heart rate, make it impossible to delineate the physiological basis for LF/HF with any degree of certainty. Thus, the LF/HF sympatho-vagal balance hypothesis has been disproven—the preponderance of evidence confirms that LF/HF data cannot accurately quantify cardiac “sympatho-vagal balance” either in health or disease.”

Rather convincing evidence that spectral analysis might not  be the adequate way to analyse HRV, to put it mildly, or draw conclusions from that.

I hope that my next blog will be about the new developments in learned in the US.




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