Muscle abnormalities worsen after post-exertional malaise in long COVID, 2023/4, Wüst, van Vugt, Appelman et al

Amw66 said:
https://twitter.com/user/status/1889336899107696644



Minor addendum: part of picking VO2max is using respiratory exchange ratio or blood lactate concentration. Meeting these criteria has nothing to do with your perception of your body’s internal environment. You either have too much lactate or breathe off more CO2 than O2 or not.


Psychiatrists have never been able to figure out what to do with VO2max as an objective marker. It’s like their kryptonite and it can end the discussion rather instantly. The rest of it just becomes silly bullshit masquerading as a serious scholarly discussion after that.

Of course, this group also has added the wrinkle of seeming to fundamentally misunderstand deconditioning, but aside from that and not getting exercise testing, they seem to have the requisite grasp of the material necessary to participate in an exchange in a prestige journal.
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I don't understand what Todd is saying.

VO2 max as an objective marker? A marker of what? Percentual decline in VO2 max looks to a substantial degree similar between ME/CFS patients and healthy controls when retesting on a 2-day exercise test.

Garner et al aren't claiming that patients are unable to expend maximal effort, but rather that their condition is due to them wanting to avoid this. What objective marker is he talking about?
 
Saw these on X. Not sure which Wüst study it was.
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Missconception that pacing means bed rest. In the study by Wüst et al the PASC cohort had around 5000 steps per day, average person walks 4900. Only difference healthy people can walk eg 10.000 steps without feeling „sick“ next day, in PEM PASC it’s not the case

https://twitter.com/user/status/1744804973999759716
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—-.
Source for average person figure:

Large-scale physical activity data reveal worldwide activity inequality
https://www.nature.com/articles/nature23018
 
EndME said:
VO2 max as an objective marker? A marker of what? Percentual decline in VO2 max looks to a substantial degree similar between ME/CFS patients and healthy controls when retesting on a 2-day exercise test.
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Yes, I think the decline in VO2max on the second CPET is not nearly as cut and dried an objective marker as Todd is suggesting and as we would all like it to be. I can understand the psychosomatic people being skeptical of that.

Unless I have missed a study somewhere, we need a better study to be confident about it.
 
Hutan said:
we need a better study to be confident about it
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I wish they'd all just stop having pissing contests on Xitter.

All we really know is that people who get PEM say they feel more ill, and have less capacity for activity, a day or two after exercise. And the ill feeling and reduced capacity can persist for a long time.

There's no proof they're not all lying through their teeth, but when reports are as consistent as that, they're usually given credence.

People firing competing bits of "truth" at one another in public gets us absolutely no further than listening to what people say.
 
J. Coeburgh et. al. said:
The implications of erroneous interpretation of these data could result in patients fearing that PEM causes physical damage and consequently avoiding approaches to rehabilitation that could help them.
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There it goes again, the fear of PEM as the cause of the fatigue without ever addressing PEM itself. It's as if they are saying PEM is not real.

R. C. I. Wüst et. al. said:
PEM encompasses a variety of symptoms and not only muscle soreness.
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So, they acknowledge PEM is worsening of variety of symptoms, not just worsening of fatigue. I wonder when they will get around to explaining the worsening of other symptoms like light sensitivity or brain fog with their muscle anomaly model. It seems unlikely that multiple mechanisms are responsible for different PEM symptoms.
 
poetinsf said:
There it goes again, the fear of PEM as the cause of the fatigue without ever addressing PEM itself. It's as if they are saying PEM is not real.
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Yes, they just elide straight over that critical bit, making sure to never examine the possibility that patients' reluctance to push through PEM is completely justified. IOW, that patients are actually interpreting the somatic signals from their bodies correctly.

As they have been doing for decades.
 
Hutan said:
Yes, I think the decline in VO2max on the second CPET is not nearly as cut and dried an objective marker as Todd is suggesting and as we would all like it to be. I can understand the psychosomatic people being skeptical of that.
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I have never been able to work out exactly what changes in VO2 max are supposed to be telling us. That is partly because I have never quite got clear in my mind what it is measuring but I think it is also due to something else. That is that in 10-20 years of people talking about this finding nobody seems to have come up with a theory of how it could be coming about. What are we supposed to think the mechanism might be?

It might be easy enough to suggest that following exertion there was some temporary structural shift in muscle, like macrophage activation or fluid ingress, or fibre apoptosis. And that is rather what Wust seems to be suggesting. But the problem with that is that we have evidence for any long term process of this sort. We do not see muscle atrophy and scarring of the sort seen in dermatomyositis.

The real problem I see for implicating the Workwell findings in a theory of PEM and 'damage' in ME/CFS is that there is no obvious way to link them to long term events. Muscle has huge regenerative powers - it is used to regenerating every day from usage. We would need a theory of why that changed. I am hearing nothing.
 
poetinsf said:
There it goes again, the fear of PEM as the cause of the fatigue without ever addressing PEM itself. It's as if they are saying PEM is not real.


So, they acknowledge PEM is worsening of variety of symptoms, not just worsening of fatigue. I wonder when they will get around to explaining the worsening of other symptoms like light sensitivity or brain fog with their muscle anomaly model. It seems unlikely that multiple mechanisms are responsible for different PEM symptoms.
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Sean said:
Yes, they just elide straight over that critical bit, making sure to never examine the possibility that patients' reluctance to push through PEM is completely justified. IOW, that patients are actually interpreting the somatic signals from their bodies correctly.

As they have been doing for decades.
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Is it just me? (I'm crashed, so it probably is). I'm struggling to follow which 'they' people are referring to.
 
Trial by Error by David Tuller GET Ideologues Try to Rebut Muscle Abnormality Study - and Fail

quote:

It is a pleasure to read a pointed and effective smack-down of an ill-informed argument, especially when the argument is pushing the graded exercise therapy/cognitive behavior therapy (GET/CBT) paradigm for ME/CFS, Long Covid and related illnesses. That’s how I felt about the excellent rebuttal this week to a letter from some of the usual GET/CBT ideologues criticizing a study published last year in Nature Communications. That study reported a link between post-exertional malaise (PEM) and muscle abnormalities in people with Long Covid.
 
dave30th said:
I decided I should probably have the disclaimer on each post.
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Probably a good idea! Better safe than sorry.
dave30th said:
I could have used xxxxx or **** like I do within a post.
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Not that you asked for it, but in my opinion, xxxxx could be interpreted as placeholder data - something is missing. 88888 could be interpreted as something gone wrong or something you forgot to delete. Unless you want to go really fancy, *****, ———, or ……. are probably the most pragmatic and universally recognized options. If you’re already using *****, I’d just stick with that.
 
Merged - response from the authors to a comment by Saris et al

We thank Saris et al. for their interest in our recent paper, which focused on the skeletal muscle components of post-exertional malaise (PEM) in Long COVID patients. We did not address the efficacy of exercise as a treatment, but our findings do not support that deconditioning or bed rest explains the skeletal muscle abnormalities in Long COVID. PEM is a distinct symptom that is poorly understood and not analogous to other conditions. We caution against generalizing our results to all Long COVID patients or drawing causal conclusions beyond the study’s design, and we advocate adherence to established guidelines that recommend avoiding activities triggering PEM.
LINK
 
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Utsikt said:
I don’t understand how it’s possible to get so many basic things wrong when you’re talking about the subject of your specialized education and years of professional experience.
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One of the things I’ve learnt with ME, is being an “expert” can sometimes make you worse off to explain it. When you are an expert and have been for a long time you often end up with vested interests in particular theories or angles.

In the case of ME it has led to some bubbles completely detached from reality, or in a completely alternate reality.
 
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