Frontiers review - Chronotropic incompetence an overlooked determinant of symptoms and activity limitation in ME/CFS (prov. 2019) Davenport et al

Provisionally accepted 26 Feb 2019, full text soon

Chronotropic incompetence: an overlooked determinant of symptoms and activity limitation in myalgic encephalomyelitis/chronic fatigue syndrome?
Davenport et al

https://www.frontiersin.org/articles/10.3389/fped.2019.00082/abstract

 

Drinking too much hard liquor? Singing too loudly at church?

As you can probably tell I have no clue.

 

It's something that was noted in most of the regular (single day) exercise studies. I wondered what's it's about and why nobody was writing about it. One of the largest 1 day CPET studies for examples wrote:

 

There is a section about this on the MEpedia PEM page. It provides references and reads:

 

Cook et al. (2003), the research team of Benjamin Natelson, even suggested that this indicates that HR may not be the most adequate physiological measure to prevent PEM.

This was all a long time ago. Don't know why these findings weren't followed up on. Will be interesting to read what the Workwell Foundation team has to say about this...

 

I'll comment again in more depth when I've read the full paper, but I think this paper is barking up the wrong tree for most patients (there are other reasons for the lower HR peak). But it is equally disappointing that researchers have been mentioned chronotropic incompetence for years, but no one has actually bothered to measured EMG signalling and whether there is increased latency of HR rise or reduced rate of increase.
Simply finding patients HR didn't reach predicted norms is insufficient since there are a wide variety of reasons for this, beyond being limited by insufficient sympathetic drive.

There is a paper that will hopefully be published soon which examined rate of change of heart rate rises/reductions/recovery associated with the 2 day CPET and the results were normal.

That said, in a small minority of patients, there may be specific disease (particularly genetic issues) causing chronotropic incompetence and this needs to be diagnosed...

Oh and some additional reading while you wait:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065291/

 

I'm confused about the interplay between chronotropic incompetence - assuming for a moment that we do have it - and POTS?
The first, if I understand correctly, would lead to HR not increasing enough upon exertion.
The second leads to HR increasing too much upon (orthostatic) exertion.
There seems to be a contradiction here?

 

When I started wearing a heart rate monitor I was amazed to see that my heart rate was higher at those times I felt I had to lie down since there had never been any physical test that matched what I felt.

On a usual day my HR is about 85 to 90 at rest down to about 75 when lying down motionless and up to 105 when I am doing something. However I have found from experience that if I am experiencing a crash my HR goes down to the 60's or even 50's if it is bad. I assume it is because I do not have the energy available to speed up my heart.

My blood pressure also does strange things.

Over the past few years my symptoms vary but I have episodes of severe POTS, particularly in hot weather where my heart rate goes up to 150 when I am upright, with all the vertigo, nausea and so on associated with it.

I think that we may have a secondary POTS which could be different from normal, more associated with a malfunctioning hypothalamus. With ME I believe the availability of ATP at any given moment determines how well every system works. It would explain why everything is normal when tested but then doesn't work when it is needed.

 

Didn't Baraniuk suggest this? Not sure he linked it to the hypothalamus.

I think this is what I'm thinking of https://www.s4me.info/threads/verif...illness-2018-garner-rayhan-and-baraniuk.6756/

 

Before CFS the basal ganglia and the hypothalamus were implicated in ME. The lack of homeostasis was seen as being an important symptom with temperature regulation and so on being very bad for most people. I always thought that POTS is a form of this but I am not very knowledgeable about the science.

 

Full paper now out;
Review ARTICLE
Front. Pediatr., 22 March 2019
https://www.frontiersin.org/articles/10.3389/fped.2019.00082/full

"
Empirical Data Suggest Chronotropic Impairment is Present in People With ME/CFS"

 

ME Action has published a press release from the Workwell Foundation:

https://www.meaction.net/2019/03/23...es-to-activity-intolerance-in-people-with-me/

 

Check my conversation with Todd Davenport:

https://twitter.com/user/status/1109472694028943366

 

It's possible that POTS and the heart rate problems in ME are not actually caused by the same disease process.

 

I'm very curious- what could be determined if EMG signalling is measured? On which nerve(s) would the EMG be conducted?

What would an increased latency or reduced rate of HR rise indicate?

If you’ve addressed this elsewhere, just point me in the right direction...

ETA:
Ok, I have gone back and read some of your previous posts, @Snow Leopard .

Do you think the lowered HR increase is secondary to impaired muscle tissue metabolism, perhaps by dysautonomic failure to recruit sufficient muscle fibers or perhaps by dysautonomic failure to dilate the arterioles supplying the muscle fibers with oxygen?

 

I'm confused by that graph:



Why aren't PWME's heart rates going about 60 bpm? I thought our problem was struggling to keep our HRs below our aerobic (or something) thresholds?