Muscle atrophy

Note from the moderators:
We've copied some posts from a thread where the discussion focussed on the BPS theory of deconditioning to this new thread.
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Hi Everyone

My recent muscle biopsy of my thigh has led to what seems like very relevant research findings that should be followed up urgently by researchers looking at muscle biopsies.

I am bed bound and had been for 5 months before the biopsy.

One of my results was: Severe Type II Muscle Atrophy

First I looked for other research and found this 1991 study: Mitochondrial abnormalities in the postviral fatigue syndrome* W. M. H. Behan1, I. A. R. More1, and P. O. Behan

In it they found that 39 of 50 patients that they classified as CFS has Type II muscle atrophy

But here's the thing...

In the most recent 2 papers that I could find that differentiated between the type of circumstances that result in specifically Type 1 or Type 2 muscle fibre atrophy...
Muscle type and fiber type specificity in muscle wasting☆
Author links open overlay panelStefanoCiciliota1Alberto C.Rossia12Kenneth A.DyaraBertBlaauwabStefanoSchiaffinoac

Muscle type and fiber type specificity in muscle wasting.
Ciciliot S1, Rossi AC, Dyar KA, Blaauw B, Schiaffino S.

They explain that disuse/inactivity results in such more Type 1 atrophy than Type II atrophy so one would expect to see a lot more Type 1 atrophy in Muscle Biopsies of ME patients. Yet on the limited evidence so far and certainly in my case where I hadn't used legs for 5 months that doesn't seem to be the case.

Interestingly, the 2nd paper generalises the group of conditions that cause Type II atrophy as Malnutrition and Inflammation which fits the Metabolic/Immune ME theories pretty well.

I am not a biomedical mind but they mention different pathways which may contribute to Type II atrophy including TGFb (for those of you who are scientific minds you might be interested in reading these papers as at least in my view they counter the deconditioning arguments nicely if research groups doing muscle biopsies find that we have Type II atrophy and might point towards factors that are contributing to this.

 

I know we all know that the deconditioning theory is ridiculous. But maybe I should have viewed this a different way.

The type II muscle atrophy study seems to me to be vital to follow up for those groups who are talking about doing muscle studies (I think Julia Newton, NIH)

If they can repeat these findings much more than debunking deconditioning again, its another piece to the puzzle which can lead towards finding the cause/causes of ME by looking at the pathways that can create this type II specific atrophy

 

I think there was a study recently done in Dr Sytrom's group that found muscle biopsy abnormalities in 10 of 11 patients.

From Cort:
Mitochondrial disease is usually associated with genetic abnormalities, but Systrom emphasized that most mitochondrial diseases are not genetic but are “acquired”; that is, at some point, an autoimmune or other process has taken an axe to the mitochondria. As there’s no evidence of mitochondrial disease at the genetic level in ME/CFS, if the mitochondria are involved – and we know they are in at least some people with ME/CFS – the mitochondrial problems were acquired later in life.

One way we know the mitochondria are involved is that a muscle biopsy done at Baylor found citrate synthase deficiency in 10/11 patients.

 

The most obvious part of me that 'goes' due to activity is the calves/lower leg. e.g. when working and I was certainly not 'moving less' than healthy people around me, if the amount of walking I did or had to do 'upped' this got worse. It was the area that just seems to 'wear away'. For using it more rather than less.

It was also the zone where I knew for sure something was weird after one illness because, without really having rested for long enough any wastage from that could have been behind it, suddenly just driving a short distance would give deep aches to the level that wouldn't have been achieved with running serious distances or sprints days in a row could have achieved. More like an inflammation reaction akin to what I'd get across the shoulders. I'd had that before but not been at a point where I hadn't also been having to exercise etc so they always had felt awful rather than the drive and wake up next day with deep ache.

I might be wrong but got the sense the bigger muscles particularly over the top of the upper leg involved with the sitting and standing weight-bearing less so. And I've had twitches in many other muscles but less easy to say the same definitive patterns for various reasons.

I don't think anyone who has been around me would ever acknowledge this because....that is what people are like - they can't see past certain cliches and you'd have no proof of that claimed history, just them saying you don't do much now etc. So who would ever try and mention it?