Talk:Muscle

Papers to add:

Relationship between musculoskeletal symptoms and blood markers of oxidative stress in patients with chronic fatigue syndrome

https://www.sciencedirect.com/science/article/abs/pii/S0304394002010583

Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome

https://jnnp.bmj.com/content/64/3/362.short

Muscle performance, voluntary activation, twitch properties and perceived effort in normal subjects and patients with the chronic fatigue syndrome https://academic-oup-com/brain/article/114A/1/85/330956

Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome https://www.ncbi.nlm.nih.gov/pubmed/9527150

Central basis of muscle fatigue in chronic fatigue syndrome https://www.ncbi.nlm.nih.gov/pubmed/8423875

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise https://www.ncbi.nlm.nih.gov/pubmed/15715687

1991. Mitochondrial abnormalities in the postviral fatigue syndrome. http://www.ncbi.nlm.nih.gov/pubmed/1792865

Abstract: We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.

1996. Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome. http://www.ncbi.nlm.nih.gov/pubmed/8859904

Abstract: Patients with chronic fatigue syndrome (CFS) mainly complain of symptoms in the musculoskeletal domain (myalgias, fatigue). In 21 CFS patients the deep (muscle) versus superficial (skin, subcutis) sensitivity to pain was explored by measuring pain thresholds to electrical stimulation unilaterally in the deltoid, trapezius and quadriceps and overlying skin and subcutis in comparison with normal subjects. Thresholds in patients were normal in skin and subcutis but significantly lower than normal (hyperalgesia) in muscles (P < 0.001) in all sites. The selective muscle hypersensitivity corresponded also to fiber abnormalities at muscle biopsy (quadriceps) performed in nine patients which were absent in normal subjects (four cases): morphostructural alterations of the sarchomere, fatty degeneration and fibrous regeneration, inversion of the cytochrome oxidase/succinate dehydrogenase ratio, pleio/polymorphism and monstruosity of mitochondria, reduction of some mitochondrial enzymatic activities and increments of common deletion of 4977 bp of mitochondrial DNA 150-3000 times the normal values. By showing both sensory (diffuse hyperalgesia) and anatomical (degenerative picture) changes at muscle level, the results suggest a role played by peripberal mechanisms in the genesis of CFS symptoms. They would exclude the heightened perception of physiological signals from all districts hypothesized by some authors, especially as the hyperalgesia is absent in skin/subcutis.

Ongoing. The NIH Post-Infectious ME/CFS Study is currently running a sub-study on the muscle biopsies of up to 40 patients who meet the Canadian Consensus Criteria for ME/CFS, 20 controls, and 20 post-lyme patients.