Reduced heart rate variability predicts fatigue severity in individuals with CFS/ME. Escorihuela et al. 2019

[Snow Leopard]

At the risk of sounding like a BPS proponent here, "it's deconditioning!" seems to be the appropriate response. More symptoms = increase probability of sedentary lifestyle = lower HRV. I don't see anything here that indicates ME/CFS patients have any difference in HRV from somebody who walks an equally few number of steps per day.

I agree, HRV is too non-specific to be a useful predictor.

 

[Ravn]

Recently developed time- and frequency-domain analyses further enhance the ability of HRV analysis to track active changes in cardiovascular autonomic function. These analyses are likely to become part of future diagnostic criteria for CFS/ME and may serve as a surrogate end-point marker in clinical trials

Given that HRV is affected by just about any stressor on the body, whether physical, psychological or environmental, I can see it has biomarker potential for showing the body struggling with something or other - but they don't seem to have found any ME-specific HRV signature (or have they? details were a bit over my head) so I can't see how HRV would be a useful part of any diagnostic criteria.

The bit about using HRV as an end-point marker in treatment trials could be worth looking at further though. I have a dim memory reading about just that being done in heart failure. If your HRV improves it means you're objectively getting better, and vice versa. And they do show here that HRV and the severity of certain symptoms correlate, which is also what many patients have found with their own monitoring. If reliable readings can be taken that would be better than a lot of the questionnaires we usually get.

 

[mariovitali]

I agree with @Michiel Tack and @Snow Leopard and @Ravn

It is very likely that HRV is a non-specific ME marker but nevertheless it can help us to identify potentially interesting mechanisms behind ME.

 

[Snow Leopard]

Escorihuela et al 2020 found reduced HF and LF in patients (and LF/HF ratio), compared to the case-controls, and inappropriately concluded this is due to "increased sympathetic hyperactivity". It is notable that they simply stated that participants had "natural breathing", without providing any measurements or evidence of respiratory rates, which can have a substantial impact on HRV...

If both LF and HF are reduced then the more likely cause for the findings is different respiration rates and reduced vagal/parasympathetic drive (and deconditioning is a big factor). If it was primarily due to "increased sympathetic hyperactivity" then the increase in LF/HF ratio would be due to an increase in LF power, not a decrease in both LF and HF.

Heart rate variability is considered an index of cardiac autonomic modulation. In the frequency domain, vagal (parasympathetic) activity is the major contributor to HF variability, whereas both vagal and sympathetic activity contributes to LF variability. The LF/HF ratio is considered an index of sympathovagal balance.

Of course it is not that simple!


Counter with:
"An Overview of Heart Rate Variability Metrics and Norms"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5624990/

LF/HF Ratio
The ratio of LF to HF power (LF/HF ratio) was originally based on 24 h recordings, during which both PNS and SNS activity contribute to LF power, and PNS activity primarily contributes to HF power. The intent was to estimate the ratio between SNS and PNS activity (12).

The assumptions underlying the LF/HF ratio is that LF power may be generated by the SNS while HF power is produced by the PNS. In this model, a low LF/HF ratio reflects parasympathetic dominance. This is seen when we conserve energy and engage in tend-and-befriend behaviors. In contrast, a high LF/HF ratio indicates sympathetic dominance, which occurs when we engage in fight-or-flight behaviors or parasympathetic withdrawal.

Billman (21) challenged the belief that the LF/HF ratio measures “sympatho-vagal balance” (78, 79). First, LF power is not a pure index of SNS drive. Half of the variability in this frequency band is due to the PNS and a smaller proportion is produced by unspecified factors. Second, PNS and SNS interactions are complex, non-linear, and frequently non-reciprocal. Third, confounding by respiration mechanics and resting HR creates uncertainty regarding PNS and SNS contributions to the LF/HF ratio during the measurement period.

Shaffer et al. (12) warned that the LF/HF ratio is controversial because different processes appear to generate 24 h and 5 min values, and these values correlate poorly. Furthermore, the SNS contribution to LF power varies profoundly with testing conditions. For example, when LF is calculated while sitting upright during resting conditions, the primary contributors are PNS activity and baroreflex activity—not SNS activity (63, 80). Therefore, interpretation of 5 min resting baseline LF/HF ratios depends on specific measurement conditions.

LF Band
The LF band (0.04–0.15 Hz) is typically recorded over a minimum 2 min period (12). This region was previously called the baroreceptor range because it mainly reflects baroreceptor activity during resting conditions (1). LF power may be produced by both the PNS and SNS, and BP regulation via baroreceptors (11, 57, 64, 65), primarily by the PNS (66), or by baroreflex activity alone (67). The SNS does not appear to produce rhythms much above 0.1 Hz, while the parasympathetic system can be observed to affect heart rhythms down to 0.05 Hz (20 s rhythm). In resting conditions, the LF band reflects baroreflex activity and not cardiac sympathetic innervation (12).

During periods of slow respiration rates, vagal activity can easily generate oscillations in the heart rhythms that cross over into the LF band (68–70). Therefore, respiratory-related efferent vagally mediated influences are particularly present in the LF band when respiration rates are below 8.5 bpm or 7 s periods (70, 71) or when one sighs or takes a deep breath.

Go to:
HF Band
The HF or respiratory band (0.15–0.40 Hz) is conventionally recorded over a minimum 1 min period. For infants and children, who breathe faster than adults, the resting range can be adjusted to 0.24–1.04 Hz (72). The HF band reflects parasympathetic activity and is called the respiratory band because it corresponds to the HR variations related to the respiratory cycle. These phasic HR changes are known as RSA and may not be a pure index of cardiac vagal control (73).

Heart rate accelerates during inspiration and slows during expiration. During inhalation, the cardiovascular center inhibits vagal outflow resulting in speeding the HR. Conversely, during exhalation, it restores vagal outflow resulting in slowing the HR via the release of acetylcholine (74). Total vagal blockage virtually eliminates HF oscillations and reduces power in the LF range (12).

High-frequency power is highly correlated with the pNN50 and RMSSD time-domain measures (10). HF band power may increase at night and decrease during the day (1). Lower HF power is correlated with stress, panic, anxiety, or worry. The modulation of vagal tone helps maintain the dynamic autonomic regulation important for cardiovascular health. Deficient vagal inhibition is implicated in increased morbidity (75).

HF Power and RSA do not Represent Vagal Tone
In healthy individuals, RSA can be increased by slow, deep breathing. Respiration rate changes can produce large-scale shifts in RSA magnitude without affecting vagal tone, which is mean HR change across conditions (e.g., rest to exercise) (76). Grossman (76) proposed an experiment. If you slow your breathing to 6 bpm, you should observe increased HR fluctuations compared with 15 bpm. During this time, mean HR should not appreciably change because vagal tone did not change.

While HF power indexes vagal modulation of HR, it does not represent vagal tone. If shifts in HF power mirrored shifts in vagal tone, they should produce corresponding changes in average HR. But, breathing at different rates within the 9–24 bpm range, which changes HF power, does not change mean HR. RSA and vagal tone are dissociated during large-scale changes in SNS activity, chemical blockade of the SA node, and when intense vagal efferent traffic dramatically slows HR during inhalation and exhalation (73). Shifts in respiration rate and volume can markedly change HRV indices (HF power, RSA, pNN50, RMSSD) without actually affecting vagal tone.

It is always important not to confuse the directionality between cause and effect when measuring correlations. Many biological changes hypothesised as being the cause of an illness, may in fact be adaptations, either positive or negative. In this case, different activity patterns and lower fitness could result from more severe illness, which on its own (less intense activity patterns and lower fitness) has been shown to cause the aforementioned HRV findings in healthy participants.