Heart Rate Variability and ME/CFS

mariovitali said:
EDIT : I believe that Dr Morten is being researching the response of ME/CFS patients to cold.
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Yes, I believe he is. Will be interesting to see the results.

My own anecdotal observations of cold water effect:

I have significant issues with OI and blood pooling in the feet and this is unsurprisingly particularly bad when taking a hot shower. A shower seat stops me from fainting altogether but that's about all.

My shower takes a little while to heat up and the cold water coming out initially is very, very cold. I've taken to directing that painfully cold water on to my lower legs (knees down) and feet. The idea was that it would constrict the blood vessels and thus reduce the blood pooling once the shower heats up. I don't know if my hypothesis of the mechanism is correct - maybe it has something to do with sympathetic/parasympathetic/vagal tone/HRV instead? - but it is quite effective. I get through my shower much better.

I only measure HRV once a day, about 4 hours after I have my shower. There is no difference between days when I do have a shower and days when I don't (only comparing 'good' days with or without showers, and excluding PEM days when I never have showers and when my HRV is down because of PEM). So if there is any HRV effect at all it looks to be a very short term one.
 
And my anecdotal observations of cold ambient temperature effect:

Late last winter I thought I'd noticed a correlation between feeling colder and feeling better, so this winter I'm monitoring the relationship more closely. So far it seems to fit. The observations:
  • Staying constantly at a slightly uncomfortable cold temperature reduces overall ME symptoms.
  • It increases HRV*.
  • It decreases resting HR.
  • It does not allow me to increase my activity level before triggering PEM.
  • It may speed up recovery from PEM.
  • It's a fine line. Getting too cold causes PEM.
  • It has side-effects: it increases my Raynauds and I've just made the highly unwelcome aquaintance of chilblains for the first time in my life. And of course I'm uncomfortably cold all the time.
  • It causes a marital struggle for control of the heatpump remote.
As with the cold water effect, my hypothesis here was that it's to to with constricting the blood vessels in the extremities and having more blood available in the core and brain. But who knows, maybe there's some sympathetic/parasympathetic effect as well or instead.

* I should note that I don't measure pure HRV but some sort of HRV-based algorhythm used by my Polar wrist monitor. I'm too lazy to fiddle with a chest band but am considering getting the Oura ring when the new model comes out for Android (the iPhone one is already out - if anyone has any experience with it I'd love to know).
 
I am tagging @Perrier @ScottTriGuy @feeb @Ravn @Andy @rvallee @diwa @wigglethemouse just to make sure you will see this. Within 3 days i see major differences both in HRV but my symptoms as well :

This is how it looks today :

IMG_3492.PNG


These are snapshots from the recording process. On the snapshot below observe the 2 valleys. These are extra heartbeats (arrhythmias) :

IMG_3490.PNG



and here things are more smooth (no valleys). This is from the same recording just today :

IMG_3489.PNG


Before continuing, arrhythmias (irregular heartbeat) was a problem i had when i had ME/CFS symptoms :

https://forums.phoenixrising.me/thr...onomic-dysfunction-in-mecfs.59420/post-978223


In the past 15 days i started dieting , i would eat my last meal at 20:00 the latest. I then began seeing some old symptoms one of which was irregular heartbeat. Then tinnitus came back and then some fatigue. Within 3 days the motility is restored in my gut, there is no bloating, no constipation and i feel more relaxed ( i was getting anxiety attacks for no reason)

I believe that this happened because of norepinephrine that kicks in to generate lipolysis (= to lose fat). i started reading on ways to lessen norepinephrine and found this :


Magnesium inhibits norepinephrine release by blocking N-type calcium channels at peripheral sympathetic nerve endings.
Shimosawa T1, Takano K, Ando K, Fujita T.
Author information

Abstract
Although Mg2+ contributes to blood pressure regulation partly in terms of vasodilator action, its sympatholytic effect may also play an important role to control blood pressure. Thus, in the present study, we investigated the effect of Mg2+ on sympathetic tone and blood pressure. We studied its actions on the blood pressure response to hydralazine, a direct vasodilator, in conscious spontaneously hypertensive rats (SHRs), and to electrical stimulation in the pithed Sprague-Dawley rat; catecholamine release by peripheral sympathetic nerve endings; and the N-type Ca2+ channels of cultured neural cells. Intravenous Mg2+ infusion (MgSO4: 3x10(-6) mol/kg body weight/min) induced the greater hypotensive response to hydralazine with attenuated reflex tachycardia in SHRs. In pithed rats, Mg2+ infusion significantly attenuated the blood pressure elevation (2+/-2 mm Hg versus 27+/-6 mm Hg, P<0.01) in response to spinal electrical stimulation. In the perfused mesenteric arteries system, norepinephrine release was significantly attenuated (51+/-2%, P<0.01) by high Mg2+ concentration solution (4.8 mmol/L) compared with normal Mg2+ solution (1.2 mmol/L). When we applied the perforated whole-cell patch clamp method to nerve growth factor-treated PC12 cells, Mg2+ blocked voltage-gated Ca2+ currents in a concentration-dependent manner. The majority of the voltage-gated Ca2+ currents were carried through N-type channels, followed by L-type channels. Mg2+ blocked both of these channels. These findings suggest that Mg2+ blocks mainly N-type Ca2+ channels at nerve endings, and thus inhibits norepinephrine release, which decreases blood pressure independent of its direct vasodilating action.
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A yet more interesting quality of magnesium is that it is an NMDA inhibitor (that keeps the excitotoxicity which shows as "tinnitus" - cc @feeb - this is a hypothesis) :


https://www.sciencedirect.com/science/article/pii/S1044576584710128


Interestingly, melatonin (cc @wigglethemouse ) is also an NMDA inhibitor :

https://www.fasebj.org/doi/abs/10.1096/fasebj.21.6.A1277-c


So all i did is start on a very safe dose of magnesium, 250 mg per day. This was a game changer.


Everything is restored apart from sleep (i opened my eyes 2-3 times during the night but was able to go back to sleep immediately). My racing heart rate is now back to 60.


HRV is also a game changer -at least for me- and i will inform SolveCFS about its potential value.
 
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More coming up :


[Long-term HRV analysis shows stress reduction by magnesium intake].
[Article in German]
Wienecke E1, Nolden C2.
Author information

Abstract
BACKGROUND:
Mental pressure and stress represent an ever-increasing socio-political challenge. The heart rate variability (HRV) measurement, which has its origin in the cardiac function diagnosis, gives information on the neurovegetative activity. A low HRV shows an imbalance of the sympathetic and parasympathetic efferents and thus is an indicator of stress.

METHOD:
A randomized, controlled, two-armed parallel study with 100 participants and a period of 90 days was performed. Main object of investigation was to what extent the mineral magnesium, which is also a high-quality natural calcium antagonist in cardiology, can influence the sympathovagal balance, when given in combination with a strength-endurance training. The effect on intracellular magnesiumconcentration was investigated as an additional parameter.

RESULTS:
In the group with daily supplementation of 400 mg of magnesium, HRV parameters clearly increased: pNN50 - an indicator of parasympathetic activity - increased. LF-HF ratio as well as stress index - low values for each represent a good balance of the vegetative nervous system - decreased. In the control group no positive changes in HRV parameters could be shown. Vagus activity, and thus the adaptive and regenerative capacity of the body, veritably increased by magnesium supplementation. No effect on the intracellular magnesiumconcentration could be shown in the study.

CONCLUSIONS:
The results of this study point out that persons with mental and physical stress can benefit from a daily intake of magnesium. This might lead to an improved physiological regulation of the sympathetic and parasympathetic efferents and, furthermore, prevent magnesium deficiency and diseases such as, for example, restlessness, irritability, lack of concentration, sleep disorder or depression.
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Trish said:
@mariovitali I am confused by the sequence of events in your post #25 above. You seem to be indicating that you no longer have the symptoms of ME, but that they came back when you started dieting, then went away when you started magnesium. I suspect I've misunderstood. Could you clarify?
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Sure, around 15-20 days ago (cant remember exactly) i began dieting. The plan was to eat small portions and have the last bite by 20:00. In the first 4-5 days of the diet i began having old symptoms. A bit of tinnitus, my intestines were somewhat bloated. As time passed by within these 15 days my symptoms got much worse. On 5th June i had an Ultrasound at my Liver and Gallbladder area and the doctor said that there was a lot of gas and that i should try to relax because this is the sympathetic nervous system kicking in. This is when it all started coming together.

I began looking at the sympathetic / parasympathetic aspect and found the document of the MEAssociation discussing HRV. I purchased the belt 4 days ago and immediately started getting my HRV. The first reading was a mere 39 (=sympathetic system in overdrive). I began researching more and found magnesium and the role of epinephrine. 3 days ago i started taking magnesium and the supplements that i already take. I began having immediate improvements both in symptoms and HRV. Today was the first day that i woke up without any issues.
 
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Thanks, @mariovitali.

I think Mg is pretty well known by people with ME as helping with relaxation and some find it helps with sleep, and I have heard of doctors prescribing Mg but I've not heard of it completely clearing ME symptoms.

If I understand you correctly, you are saying that you once had ME and now are in remission or recovery, but that when you started dieting a couple of weeks ago you started having some of the digestive issues you associated with your ME, and the magnesium seems to have cleared these. Surely a few days in one person is not enough to draw any generalisations about Mg and ME and/or HRV.

Edit: Sorry, that sounds more distrusting than I meant it to. It is interesting reading how individuals are getting on with testing their HRV and experimenting with what affects it. I'm just unclear how this relates to ME. When I've tried taking Mg it made no difference.
 
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Trish said:
Thanks, @mariovitali.

I think Mg is pretty well known by people with ME as helping with relaxation and some find it helps with sleep, and I have heard of doctors prescribing Mg but I've not heard of it completely clearing ME symptoms.

If I understand you correctly, you are saying that you once had ME and now are in remission or recovery, but that when you started dieting a couple of weeks ago you started having some of the digestive issues you associated with your ME, and the magnesium seems to have cleared these. Surely a few days in one person is not enough to draw any generalisations about Mg and ME and/or HRV.
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I am just reporting on what happened to me and will be reporting whether this amelioration of symptoms continues. Obviously I do not want to suggest with my post that magnesium stops ME/CFS!
 
I've actually been taking a 125mg magnesium citrate supplement daily for about 2 months. It seems to have neutralised the suicidal depression I was plagued with every month around ovulation (the reason I started the supplementation in the first place), but it's not made the slightest bit of difference to any M.E. symptoms, including the tinnitus. Will be interesting to see if your observations hold for you longer term.

I've been recording HRV for about 20 days or so and to be honest I've not really noticed any patterns as yet with regards to symptoms. But my HRV will change throughout my menstrual cycle, so I don't expect to be able to draw any useful conclusions from it for another 4-5 months or so. This kind of data tracking is certainly a long game!
 
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Trish said:
Thanks, sorry, I just added a comment to my last reply. I realised I was sounding rather hostile when I was just trying to understand.
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@Trish,

I was out and couldn't write a proper reply. I wanted to say looking back at all of my posts since Phoenix Rising that i do appear to be over-confident and over-excited. I guess the reason for this was that i wanted to keep going, to have strength to find a solution and to go to the root of the problem.

I do appreciate anyone giving reality checks and i want to Thank you and others who do these reality checks. We definitely need them so as not to be biased.

Unfortunately i cannot say much about Petter Brodin's -from Karolinska- email on what they found. I can say that the vagus nerve may deserve a very close look. I hypothesise that HRV and Vagus stimulation may be applicable for a subset of ME patients. We shall see.

@obeat

Thank you for your post which mentions Mestinon which is an acetylcholinesterase inhibitor.

During my 15 day crash period i made the mistake to try two of these (Mestinon was not tried). I do not know if it is prudent from my side to say which of these 2 were but i feel that i must discuss at least one of them because it added to my problems and i will explain why i think is so.

One of them was the active ingredient Galantamine (aka Reminyl) which is an acetylcholinesterase inhibitor. What i failed to identify before taking it however is that Galantamine increases Glutamate :

Increased glutamate in the hippocampus after galantamine treatment for Alzheimer disease.
Penner J1, Rupsingh R, Smith M, Wells JL, Borrie MJ, Bartha R.
Author information

Abstract
Galantamine is a cholinesterase inhibitor and allosteric potentiating ligand modulating presynaptic nicotinic acetylcholine receptors that is used in the treatment of Alzheimer disease (AD). The purpose of this study was to determine if galantamine treatment would result in detectable hippocampal metabolite changes that correlated with changes in cognition, as measured by the Mini-Mental State Examination (MMSE) and the Alzheimer Disease Assessment Scale-cognitive subscale (ADAS-cog). Short echo-time proton magnetic resonance (MR) spectra were acquired from within the right hippocampus of ten patients using a 4 Tesla magnetic resonance imaging (MRI) scanner. Spectra were used to quantify absolute metabolite levels for N-acetylaspartate (NAA), glutamate (Glu), choline (Cho), creatine (Cr), and myo-inositol (mI). Patient scans and cognitive tests were performed before and 4 months after beginning galantamine treatment, which consisted of an 8 mg daily dose for the first month and a 16 mg daily dose for the remaining three months. The levels of Glu, Glu/Cr, and Glu/NAA increased after four months of treatment, while there were no changes in MMSE or ADAS-cog scores. Additionally, changes (Delta) in Glu over the four months (DeltaGlu) correlated with DeltaNAA, and Delta(Glu/Cr) correlated with DeltaMMSE scores. Increased Glu and the ratio of Glu to Cr measured by MR spectroscopy after galantamine treatment were associated with increased cognitive performance. The increase in Glu may be related to the action of galantamine as an allosteric potentiating ligand for presynaptic nicotinic acetylcholine receptors, which increases glutamatergic neurotransmission.
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I hypothesise that Glutamate along with Liver disease may be the missing pieces of the puzzle *if* a subset of ME patients does not respond to an acetylcholinesterase inhibitor assuming that such a medication is found to be ameliorating ME symptoms to some patients.

EDIT for clarification : I hypothesise that the action of Glutamate is not beneficial to ME patients
 
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Reading up on HRV on wikipedia I thought this section was interesting:
Biofeedback[edit]
The technique called resonant breathing biofeedback teaches how to recognize and control involuntary heart rate variability. A randomized study by Sutarto et al. assessed the effect of resonant breathing biofeedback among manufacturing operators; depression, anxiety and stress significantly decreased.[51] A first overall meta-analysis by Goessl VC et al. (24 studies, 484 individuals, 2017) indicates ''HRV biofeedback training is associated with a large reduction in self-reported stress and anxiety'', while mentioning that more well-controlled studies are needed.[52]
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https://en.wikipedia.org/wiki/Heart_rate_variability#Biofeedback
 
A couple of studies I found by Googling that may be of interest to the discussion.

Heart rate variability in women exposed to very cold air (−110 °C) during whole-body cryotherapy

Heart rate monitoring was used to measure heart rate variability (HRV) at thermoneutral conditions (Ta 24 °C) in healthy women resting in supine position before and after acute and after repeated (3 times a week during a 3-month period) whole-body cryotherapies (WBC), at −110 °C. The observed acute cooling-related increase in high frequency power (HFP) of RR-intervals indicates an increase in cardiac parasympathetic modulation. After 3 months of repeated WBC the increase in parasympathetic tone was attenuated, which may be interpreted as an adaptation of autonomic function. The repeated WBC exposures-related increase in resting low frequency power (LFP) of RR-intervals during the 3 months resembles the response observed related to exercise training.
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https://www.sciencedirect.com/science/article/pii/S0306456506000313
https://sci-hub.se/10.1016/j.jtherbio.2006.01.004

Head Exposure to Cold during Whole-Body Cryostimulation: Influence on Thermal Response and Autonomic Modulation

Recent research on whole-body cryotherapy has hypothesized a major responsibility of head cooling in the physiological changes classically reported after a cryostimulation session. The aim of this experiment was to verify this hypothesis by studying the influence of exposing the head to cold during whole-body cryostimulation sessions, on the thermal response and the autonomic nervous system (ANS). Over five consecutive days, two groups of 10 participants performed one whole-body cryostimulation session daily, in one of two different systems; one exposing the whole-body to cold (whole-body cryostimulation, WBC), and the other exposing the whole-body except the head (partial-body cryostimulation, PBC).10 participants constituted a control group (CON) not receiving any cryostimulation. In order to isolate the head-cooling effect on recorded variables, it was ensured that the WBC and PBC systems induced the same decrease in skin temperature for all body regions (mean decrease over the 5 exposures: -8.6°C±1.3°C and -8.3±0.7°C for WBC and PBC, respectively), which persisted up to 20-min after the sessions (P20).

The WBC sessions caused an almost certain decrease in tympanic temperature from Pre to P20 (-0.28 ±0.11°C), while it only decreased at P20 (-0.14±0.05°C) after PBC sessions. Heart rate almost certainly decreased after PBC (-8.6%) and WBC (-12.3%) sessions. Resting vagal-related heart rate variability indices (the root-mean square difference of successive normal R-R intervals, RMSSD, and high frequency band, HF) were very likely to almost certainly increased after PBC (RMSSD:+49.1%, HF: +123.3%) and WBC (RMSSD: +38.8%, HF:+70.3%). Plasma norepinephrine concentration was likely increased in similar proportions after PBC and WBC, but only after the first session. Both cryostimulation techniques stimulated the ANS with a predominance of parasympathetic tone activation from the first to the fifth session and in slightly greater proportion with WBC than PBC. The main result of this study indicates that the head exposure to cold during whole-body cryostimulation may not be the main factor responsible for the effects of cryostimulation on the ANS.
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Open access, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4411165/

Parasympathetic Activity and Blood Catecholamine Responses Following a Single Partial-Body Cryostimulation and a Whole-Body Cryostimulation

The aim of this study was to compare the effects of a single whole-body cryostimulation (WBC) and a partial-body cryostimulation (PBC) (i.e., not exposing the head to cold) on indices of parasympathetic activity and blood catecholamines. Two groups of 15 participants were assigned either to a 3-min WBC or PBC session, while 10 participants constituted a control group (CON) not receiving any cryostimulation. Changes in thermal, physiological and subjective variables were recorded before and during the 20-min after each cryostimulation.

According to a qualitative statistical analysis, an almost certain decrease in skin temperature was reported for all body regions immediately after the WBC (mean decrease±90% CL, -13.7±0.7°C) and PBC (-8.3±0.3°C), which persisted up to 20-min after the session. The tympanic temperature almost certainly decreased only after the WBC session (-0.32±0.04°C). Systolic and diastolic blood pressures were very likely increased after the WBC session, whereas these changes were trivial in the other groups. In addition, heart rate almost certainlydecreased after PBC (-10.9%) and WBC (-15.2%) sessions, in a likely greater proportion for WBC compared to PBC. Resting vagal-related heart rate variability indices (the root-mean square difference of successive normal R-R intervals, RMSSD, and high frequency band, HF) were very likely increased after PBC (RMSSD: +54.4%, HF: +138%) and WBC (RMSSD: +85.2%, HF: +632%) sessions without any marked difference between groups. Plasma norepinephrine concentrations were likely to very likely increased after PBC (+57.4%) and WBC (+76.2%), respectively. Finally, cold and comfort sensations were almost certainly altered after WBC and PBC, sensation of discomfort being likely more pronounced after WBC than PBC.

Both acute cryostimulation techniques effectively stimulated the autonomic nervous system (ANS), with a predominance of parasympathetic tone activation. The results of this study also suggest that a whole-body cold exposure induced a larger stimulation of the ANS compared to partial-body cold exposure.
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Open access, https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0072658
 
mariovitali said:
@Trish,

I was out and couldn't write a proper reply. I wanted to say looking back at all of my posts since Phoenix Rising that i do appear to be over-confident and over-excited. I guess the reason for this was that i wanted to keep going, to have strength to find a solution and to go to the root of the problem.

I do appreciate anyone giving reality checks and i want to Thank you and others who do these reality checks. We definitely need them so as not to be biased.

Unfortunately i cannot say much about Petter Brodin's -from Karolinska- email on what they found. I can say that the vagus nerve may deserve a very close look. I hypothesise that HRV and Vagus stimulation may be applicable for a subset of ME patients. We shall see.

@obeat

Thank you for your post which mentions Mestinon which is an acetylcholinesterase inhibitor.

During my 15 day crash period i made the mistake to try two of these (Mestinon was not tried). I do not know if it is prudent from my side to say which of these 2 were but i feel that i must discuss at least one of them because it added to my problems and i will explain why i think is so.

One of them was the active ingredient Galantamine (aka Reminyl) which is an acetylcholinesterase inhibitor. What i failed to identify before taking it however is that Galantamine increases Glutamate :




I hypothesise that Glutamate along with Liver disease may be the missing pieces of the puzzle *if* a subset of ME patients does not respond to an acetylcholinesterase inhibitor assuming that such a medication is found to be ameliorating ME symptoms to some patients.
Click to expand...
Do you mean that patients should supplement with glutamate if taking acetylcholinesterase inhibitors?
I think galantamine was trialled about 25 years ago?
 
obeat said:
Do you mean that patients should supplement with glutamate if taking acetylcholinesterase inhibitors?
I think galantamine was trialled about 25 years ago?
Click to expand...

No I hypothesise that glutamate induces excitotoxicity and therefore will not be beneficial to ME patients and may induce further symptoms. Again, please note that this is a hypothesis
 
mariovitali said:
So all i did is start on a very safe dose of magnesium, 250 mg per day. This was a game changer.
Click to expand...
There are soooooo many variables it is often hard to see what has been the cause of a downturn and what has a an effect on an upturn. I hope you have found something for you.

May I suggest that if you think Mg is having the positive effect that you stop it for a few days and see if HRV gets lower. If it does go lower restart Mg and see if HRV increases. I know this is hard if you think something is working, but remember if it's not the Mg causing the improvement you may be adding something your body doesn't need.

Many of us think we have found the next great thing, only to discover it no longer works, or it wasn't the thing that caused the improvement after all.

Do you also wear a HR watch that tracks daily resting HR? I was intrigued by @diwa post that shows resting HR inversely correlates with HRV with HRV lagging resting HR slightly (did I get that right?).
 
mariovitali said:
I am tagging @Perrier @ScottTriGuy @feeb @Ravn @Andy @rvallee @diwa @wigglethemouse just to make sure you will see this. Within 3 days i see major differences both in HRV but my symptoms as well :

This is how it looks today :

View attachment 7565


These are snapshots from the recording process. On the snapshot below observe the 2 valleys. These are extra heartbeats (arrhythmias) :

View attachment 7566



and here things are more smooth (no valleys). This is from the same recording just today :

View attachment 7567


Before continuing, arrhythmias (irregular heartbeat) was a problem i had when i had ME/CFS symptoms :

https://forums.phoenixrising.me/thr...onomic-dysfunction-in-mecfs.59420/post-978223


In the past 15 days i started dieting , i would eat my last meal at 20:00 the latest. I then began seeing some old symptoms one of which was irregular heartbeat. Then tinnitus came back and then some fatigue. Within 3 days the motility is restored in my gut, there is no bloating, no constipation and i feel more relaxed ( i was getting anxiety attacks for no reason)

I believe that this happened because of norepinephrine that kicks in to generate lipolysis (= to lose fat). i started reading on ways to lessen norepinephrine and found this :





A yet more interesting quality of magnesium is that it is an NMDA inhibitor (that keeps the excitotoxicity which shows as "tinnitus" - cc @feeb - this is a hypothesis) :


https://www.sciencedirect.com/science/article/pii/S1044576584710128


Interestingly, melatonin (cc @wigglethemouse ) is also an NMDA inhibitor :

https://www.fasebj.org/doi/abs/10.1096/fasebj.21.6.A1277-c


So all i did is start on a very safe dose of magnesium, 250 mg per day. This was a game changer.


Everything is restored apart from sleep (i opened my eyes 2-3 times during the night but was able to go back to sleep immediately). My racing heart rate is now back to 60.


HRV is also a game changer -at least for me- and i will inform SolveCFS about its potential value.
Click to expand...
I also have a irregular heartbeat. Or anyway I'm not sure if it's the right term but I regularly skip beats. Beat-beat-skiiip-beatbeat-beat-beat etc.

I have no idea how to check for that. My heart has been checked several times and it's apparently fine but I've had those skips for a long time and either it's normal or it wasn't noticeable with the tests I did.

I used a Fitbit for a while and it doesn't seem to be part of the data. I guess you need a specific device for that?
 
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