Transcription Profile Analysis of Vastus Lateralis Muscle from Patients with Chronic Fatigue Syndrome, 2009, Pietrangelo et al.

Transcription Profile Analysis of Vastus Lateralis Muscle from Patients with Chronic Fatigue Syndrome
T. Pietrangelo; R. Mancinelli; L. Toniolo; G. Montanari; J. Vecchiet; G. Fanò; S. Fulle

Chronic fatigue syndrome (CFS) is a disabling condition characterized by unexplained chronic fatigue that impairs normal activities. Many body systems are affected and etiology has not yet been identified. In addition to immunological and psychological aspects, skeletal muscle symptoms are prominent in CFS patients.

In an effort to establish which pathways might be involved in the onset and development of muscle symptoms, we used global transcriptome analysis to identify genes that were differentially expressed in vastus lateralis muscle of female and male CFS patients. We found that the expression of genes that play key roles in mitochondrial function and oxidative balance, including superoxide dismutase 2, were altered, as were genes involved in energy production, muscular trophism and fiber phenotype determination. Importantly, the expression of a gene encoding a component of the nicotinic cholinergic receptor binding site was reduced, suggesting impaired neuromuscular transmission.

We argue that these major biological processes could be involved in and/or responsible for the muscle symptoms of CFS.

Link | PDF (International Journal of Immunopathology and Pharmacology) [Open Access]

 

This is one of the Italian ME/CFS muscle biopsy and follow-on papers. Given findings in Muscle abnormalities worsen after post-exertional malaise in long COVID (2024, Nature Communications) and their planned follow-on in ME/CFS, I thought it was good to have this paper in view.

 

They used Fukuda/CDC 94 criteria with small, equal numbers of male and female patients, with HCs.

Some quotes from introduction and methods —

 

DEGs in both female and both male patients —

Upregulated

• POLB
• VLDLR

Downregulated

• SOD2
• FDXl
• NQOl
• PFKFB3
• PDK4
• ABCA5
• AMPD3
• CHRNAl
• MYF6
• CALMl
• TIEG

 

Some quotes from results section —

In Muscle abnormalities worsen after post-exertional malaise in long COVID (2024, Nature Communications) —

 

Good thinking!
Thanks a lot for all of your posts. Your highlights and comments are really helpful and highly appreciated. Sometimes, being a poor alpha, you can make even me understand a bit of the science behind ME/CFS.
I found a connection with muscle changes in space. Maybe of interest to you. If not feel free to delete.
Schenkman 2016 'From slow to fast: hypogravity-induced remodeling of muscle fiber myosin phenotype'.

 

Thank you @Turtle - I've downloaded and will read.

 

In Muscle abnormalities worsen after post-exertional malaise in long COVID (2024, Nature Communications) —[/QUOTE]

Appelmans.. Wüst mention that fibre-type shifts occur at a very slow pace. Discussion 2nd paragraph.

When rodents, having been in space, change muscles from slow to fast in just 7 days (even 4 is mentioned) could the pace of fibre-type shifts occur in a much faster pace in ME/CFS and LC?

From having lived with an avid time-trial cyclist, I remember that training a slow muscle into a fast muscle is incredibly difficult.

My first attempt at cycling after I got ME/CFS, a one meter high bridge halted me completely, after just having done 400 meters.
I was only bedridden for 3 days due to high fever. Not decondioned otherwise. The bike ride was just 2 months later.
I'm the pyknic type so I already must have had more fast muscles anyway.

Could hypoxia fast-track the muscle fibre shift?

 

Low AT, no Krebscycle on exertion, lipids problematic, greater use of amino-acids lead to an environment better suited for fast muscles?

 

@SNT Gatchaman. Perish or adapt?