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

That's another great response from the team.

Deconditioning has been proposed as causative of skeletal muscle changes in Long COVID patients. Our previous work on bed rest demonstrates that adaptations in skeletal muscle structure and function differ markedly between Long COVID patients and healthy persons exposed to severe deconditioning. Bed rest induces rapid muscle atrophy and loss of capillarization, which was not observed in our Long COVID patients. We did not observe alterations in fiber type composition after 60 days of strict bed rest, whereas our Long COVID patients exhibited a more glycolytic phenotype. Our Long COVID participants showed lower mitochondrial respiration, due to mitochondrial dysfunction rather than mitochondrial loss, the latter of which is more typically seen after long-term bed rest. The absence of a correlation between and succinate dehydrogenase activity also suggests that factors other than deconditioning contribute.
Click to expand...

We do not know the underlying factors contributing to these changes, and as good scientific practice, we refrained from drawing causal relationships in our publication. We were therefore surprised to read that Saris et al. drew such conclusions based on work which was not set up to be causal in nature.
Click to expand...

Saris et al. suggest that atrophied fibers cannot occur one-day following exercise, but the reference they provide proves the opposite.
Click to expand...
 
Has there been follow up on these people? It would also be interesting to test L-C's before and after the H1 and H" blocker protocols, which have helped some people.
Problem of use of the term PEM vs exercise intolerance vs exertion intolerance.
Sorry if others have already pointed this out.
 
Last edited:
EndME said:
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?
Click to expand...

Does he say why only on day 2? Why not on day 1?
 
Simon M said:
Interesting comment from Alan Carson, President of the FND Society, asking for a bedrest comparison.

He should read the analysis here. someone here (@ME/CFS Skeptic ?) has already pointed out the long Covid patients averaged 4000 steps a day: bedrest is not a relevant comparison. Plus, as Rob Wust, Jonathan Edwards and others here have pointed out, PEM is not the same as delayed onset muscle soreness.

Maybe I’m overgeneralising, but psychosocial enthusiasts always seem to respond with generic, knee-jerk criticisms. I don’t understand why they don’t just read the biomedical research that makes them uncomfortable: they might find real reasons to criticise the methodology (or might not). It’s almost as if they’re not able to operate outside their own bunker, or just don’t feel the need to engage properly with other scientists – never mind patients.

I’m a big fan of scientific debate and criticism, but it's only useful if it's thorough and thoughtful, not regurgitating vague criticisms in the hope that one will stick.

Anyway, I suspect tthat the RW bedrest study will settle Alan Carson's concerns on the bedrest point.
Click to expand...

Their criticism is primitive because they want an easy message to replace the false consciousness or false illness belief which they claim afflicts ME/LC sufferers. If they could get a result out of telling sufferers that they were going to send George Bush into their ears in a yellow submarine to smoke out evil , they would. They are not really interested in objective analysis but in whatever they can get to work in some and the rest "will have to go somewhere else".
 
Last edited:
Dakota15 said:
From Rob Wust's X account

https://twitter.com/user/status/1901736174299041845


Text: "I am super proud that our publication on muscle abnormalities in Long COVID is now the most read article in Nature Comms of 2024! Super proud of the team at Department of Human Movement Sciences at VU and @amsterdamumc"

Link: https://www.nature.com/collections/fabaifceda
Click to expand...

Quite a few other long COVID adjacent papers in the top 25. Almost as if, you know, long COVID is common and people have to read papers for themselves since doctors don’t usually bother to learn.
 
Jonathan Edwards said:
Rob Wüst replied to my email. He is going to look at some further comparative staining. He was aware of the cross-binding to nerve.

I think this is worth sorting out in detail. It may not have anything to do with cholinesterase but if not I think we need some sort of explanation for the strange distribution of staining if it is amyloid.
Click to expand...
Sorry to pull up an old post, it just might be relevant for something else I'm chasing down. @Jonathan Edwards did you ever get more details as to whether it is likely the signal came from nerves? I'd be very interested if it wasn't in fact nerves
 
jnmaciuch said:
Sorry to pull up an old post, it just might be relevant for something else I'm chasing down. @Jonathan Edwards did you ever get more details as to whether it is likely the signal came from nerves? I'd be very interested if it wasn't in fact nerves
Click to expand...

My understanding is that, that data will all be in the soon to published ME/CFS paper, where the ME/CFS data from this paper is coming from.
 
You must log in or register to reply here.
Back
Top Bottom