Myopathy as a cause of fatigue in long-term post-COVID-19 symptoms: Evidence of skeletal muscle histopathology, 2022, Hejbøl et al

This is interesting. I find the periodic muscle weakness I get one of the most intriguing symptoms. Until we can get some idea of the content of the paper itself, here's some background on the non-paywalled stuff.

Researchers:
Danish researchers, most from Aarhus University Hospital
("Per Fink is head Professor of The Research Clinic for Functional Disorders and Psychosomatics at Aarhus Universitetshospital in Denmark" - potentially making for interesting tea room chats)
The authors seem to have a background in relevant things like myopathy in myasthenia gravis and polyneuropathy.

Sampling and study design:
The sample isn't random - there was probably selection of post-Covid patients reporting muscle weakness. 16 patients isn't a big sample, so there is the risk that at least some of the participants have some pathology going on unrelated to the Covid infection. There were no healthy controls, including controls who have had Covid-19 but don't have ongoing symptoms.

About quantitative electromyography:
Electromyography (EMG) measures muscle response or electrical activity in response to a nerve's stimulation of the muscle.
Quantitative methods have been developed to characterize MUP waveforms using statistical and probabilistic techniques that allow for greater objectivity and reproducibility in supporting the diagnostic process.

Muscle weakness and muscle fibre atrophy:
Could the findings just be a result of deconditioning?

@Snow Leopard

 

Mitochondrial changes

• Loss of COX activity

that's Cytochrome oxidase - otherwise known as Complex IV in the mitochondrial respiratory chain (RC). From memory, we haven't seen much about that molecule in ME/CFS. Rather, it was Complex V that was found to not be working properly by the Fisher, Missailidis team.

• Subsarcolemmal accumulation and/or abnormal cristae

(note: 'subsarcolemmal' seems to be the correct spelling, just one 'l' in the middle.)
Subsarcolemmal accumulation: that's an abnormal increase in the number of mitochondria in the cytoplasm adjacent to the muscle cell membrane.
Cristae are the folded bits inside the mitochondria.

A 2020 NCNED review: A systematic review of mitochondrial abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome/systemic exertion intolerance disease
mentioned that one study had looked at structural abnormalities relating to mitochondria in ME/CFS/SEID patients including sub-sarcolemmal mitochondrial aggregates, among many other things, but did not find any significant structural changes in ME/CFS/SEID patient mitochondria compared with HC participants.
There's nothing solid on abnormal cristae in ME/CFS in that 2020 review:

 

Basal lamina

Yes, 'affected' isn't very specific. It would be good to know how the injuries manifested.

"The basal lamina is a very thin layer of the extracellular matrix that lies between cells and underlying connective tissue and can be observed under an electron microscope only."



"The complex network of the extracellular matrix of basal lamina acts as the scaffold on which cells are anchored. Most cells that have aggregated into tissues have a basal lamina. The basal lamina performs two major functions. It stabilizes the layer of cells attached to it and acts as a barrier to cells that migrate."

"The components that make up basal lamina are glycoproteins such as laminin, perlecan, entactin, and proteins such as collagen IV. Proteases, enzymes that degrade proteins, such as transforming growth factor-beta, insulin-like growth factor, and fibroblast growth factor may also be present in the basal lamina. ... [the laminin sheet] is connected to the cells by the protein integrin, which anchors the cells to the laminin sheet"


There's this 2021 study by Germain and Hanson that mentions the extracellular matrix in relation to ME/CFS:
In-Depth Analysis of the Plasma Proteome in ME/CFS Exposes Disrupted Ephrin-Eph and Immune System Signaling

The basal lamina is part of the extracellular matrix.

That's two proteins out of the 9 proteins highlighted as most significantly different between controls and ME/CFS, both were upregulated. And that's 9 proteins out of 4979 tested.


Pathway descriptions fitting the altered levels of proteins related to immunity and

 

My question about whether the finding is due to deconditioning relates to the study that is in the first post of this thread i.e. problems found in muscles.

The chart with the blue and the red relates to the concentrations of two proteins that were reported by Maureen Hansen's team- I posted that because the proteins relate to the issues with the basal lamina that the first study reported.