Hi Ali,

I am not entirely sure that I understand your question correctly.

I believe that the decrease in RSA is contrary to what is expected to happen.

Typically RSA/HRV increases as a result of slow breathing.

This phenomenon is strongly associated with increased firing of the vagal nerve of the heart.

I hope this helps.

Regards,

Artur

Hi Artur,

Yes RSA/HRV increases during slow breathing compared to resting baseline (and also compared to paced breathing at 14 bpm) and it's obvious also in our data. Consider the left y axis, RSA is something between 290 and 410 msec which is much more than resting state.

However, over 3 minutes of slow breathing RSA decreases, it starts from around 400 msec to around 300 msec untill the end of slow breathing. And the question is why it decreases over time? Of course, 300 msce is still higher than resting state RSA.

This decrease in RSA cannot be due to less efficient slow breathing since the blood pressure variation in each breathing cycle stays same meaning that breathing is deep enough over 3 minutes.

Considering the baroreflex as a main factor for RSA during slow breating it seems that the reflex response decreases over time, and that may be due to habituation of the reflex.

Hi Ali,

We have observed the same phenomenon in the past.

The problem with FRSA (forced respiratory sinus arrhythmia) is that it is not only a baroreflex generated effect on heart rate, the respiratory centers themselves influence vagal outflow, moreover pulmonary stretch receptors (to name but some) are involved. You do not specify the body position, but this may have an effect as well via venous return and ventricular filling

Finally, and possibly most importantly, end-tidal pCO2 will drop with uncontrolled deep breathing; it does so even if you control pCO2, but then you may try to train the subjects to minimize this effect.

In short: this is not baroreflex habituation, to answer your question.

Hi John,

Thanks for your reply. Subjects were in sitting position. Tidal volume was almost stable over time, and drop in EtCO2 was only ~ 0.5% (at group level). Is there any data on phasic stimulation of baroreceptors showing that the baroreflex doesn't habituate over time? like for example using phasic neck suction or LBNP?

Ali, do you have a figure of the levels of MAP and mean HR (or IBI) over the same period as your RSA- & BPV-picture? I would like to see that there is no sign of increasing sympathetic activation during the 3 min test.

data was averaged in 5 windows of one min each with 50% overlap:

there is decrease in average IBI over time but small or no change in SBP, DBP, and MAP.

mean IBI in 3 min resting baseline is not diff with meanIBI in 3 min of slow breating. So, at the beginning of slow breathing meanIBI is higher but it decreases over time. This indicates that at the beginning of slow breathing there is increase in cardiac vagal tone but it then decreases over time.

what can be the reason for decrease in IBI? still the baroreflex and cardiac vagal outflow may be involved, not?

Dear Ali,

this drop in IBI, small though it is, still convinces me of a drop in vagal outflow (rather than sympathetic activation). Whatever the reason for it (the drop in PetCO2?), it still can be a good reason for a lower RSA. I attach a paper by Farmer et al from the J Physiol 2016 ( Open Access DOI: 10.1113/JP273164 ) which throws a new light on the complexity of RSA and average cardiac vagal traffic.

Dear Ali

I want to express my opinion on this phenomenon based on the results obtained in our studies.

1. Slow breathing in healthy individuals compared to spontaneous is likely to lead to an increase in heart rate (sitting up).

2. During the test with 6-fold breathing of heart rate within 2 minutes, one person increases, others - remains unchanged (average HR from breathing to breathing).

3. Indicator of baro-reflex in slow breathing may be informative, in my opinion, only with short records.

4. Why? Slow breathing is uncharacteristic for most people, so when it is performed, the mechanisms of the device are switched on. But not baroreceptors (although this is also possible), but systemic hemodynamics. First of all, reducing the return of venous blood to the right heart. The latter, in my opinion, leads to an increase in heart rate and a decrease in the sensitivity of the baroreflex.

With best regards.

Alexander Romanchuk

Ali,

I think it is time for a little self-promotion: In a recent publication (attached, Open Access DOI: http://dx.doi.org/10.18053/jctres.201503.005) I show in acute rabbit exps. by stimulating the vagus nerve burst-wise as it happens in vivo, that a small variation in timing or strength of such a burst can have very different effects on sinus node rhythm depending on the timing in the cycle. Heart rate of the subjects in your study was around 75/min or 800 ms. This is a critical value for baroreflex-vagus nerve feedback to occur in the same interval or in the next (with diminished effectiveness). The latter point has been elaborated (again) in a letter to the Editor of J Physiol, which Dr. DeBoer and I wrote (DOI: 10.1113/JP273766), also attached.

I hope this helps,

John

Nice to read everybody. May I remember you, that chemo (including CO2) receptors are colocated with pressures receptors in the carotid arteries. Even if these signals are separately process in some brain and cerebellum structures, the "baroreflex" (it should not be named like this, but no matter) is the result of the processing and exchanges of information. So, by changing pCO2 by slow breathing you get what you get....

Dear All,

I think, your data was collected from participants that breathed 6 times/min (6P breathing) first time.

We used 6P breathing (HRV biofeedback) for treatment asthma, depression, and fibromyalgia. Our patients (n > 100) received 10 sessions during 10 weeks. The session included four 5-minute tasks. We taught them to find individual breathing rate and trained to breathe not so deeply. Treatment effect was received after 4 procedure when patients caught the right skill of the breathing. Each patient found individual breathing frequency in range (0.076- 0.107 Hz) and individual tidal volume. After 4 sessions amplitude RRI oscillation was stable for 5 minute and usually HR decreased. Sometime HR increased if in base lane it was low (50-60 BPM).

Evgeny

Dear Evgeny,

You can agree. However, the main effect of training with breathing 6 times per minute, in my opinion, is to reduce the respiratory volume (even more volumetric speed). This, in turn, leads to a number of regulatory adjustments that have a therapeutic effect. First of all it concerns chemo-receptor mechanisms. Of course, under such conditions adapts and baroreflex. On the other hand, it does not make it possible to determine the functional reserve of the baro-reflex, which is most activated with slow deep breathing.

Regards,

Alexander Romanchuk

Dear Evgeny,

This data is very interesting. Have published it, so I can look into more details?

Ali,

Please see the papers:

I would suggest to test the null hypothesis of habituation of the cardiac baroreflex via causality analysis from systolic arterial pressure (SAP) to heart period (HP) conditioned on respiration (RESP) versus causality analysis from RESP to HP conditioned on SAP. If the strength of the causal relation from SAP to HP conditioned on RESP remained stable (or increased) and that from RESP to HP conditioned on SAP decreased with time, the null hypothesis of habituation of the cardiac baroreflex should be rejected and the alternative hypothesis of a decreased cardiorespiratory coupling via e.g. a reduced action of respiratory centers on vagal outflow might be accepted (see A. Porta et al, PLoS ONE, 10, e0132851, 2015 and A. Porta and L. Faes, Proc IEEE, 104, 282-309, 2016 for the tools).