Review Suggests Muscles May be Aging in ME/CFS

Discussion in 'Chronic Fatigue Syndrome (ME/CFS) Research' started by Cort, Oct 31, 2018.

  1. Cort

    Cort Founder of Health Rising and Phoenix Rising Staff Member

    Fascinating review. We forget how much evidence there is for muscle dysfunction in ME/cFS. Most of the studies are, as I remember, small but the results are interesting.

    Several other studies involving telomere's suggest aging is happening more rapidly in ME/CFS. Plus it appears from metabolomic studies that men with ME/cFS are catabolizing their muscles to provide substrates for energy production. Plus some studies showing that the motor cortex in the brain may not be activating muscle properly.

    Now this on muscles showing
    1. high rates of oxidative stress
    2. issues with muscle contraction
    3. problems with glucose uptake
    4. problems with mitochondrial activity
    5. problems with energy production
    They do get into some dangerous group with "appropriate training program" and some CBT stuff but overall it appears highly physiological. They even get into potential NAD and NADPH issues, which if memory serves, is something the Metabolic Trap hypothesis suggests.

    It the first full blown review of muscle metabolism that I can remember.

    Eur J Transl Myol. 2018 Sep 7;28(3):7688. doi: 10.4081/ejtm.2018.7688. eCollection 2018 Jul 10.
    Old muscle in young body: an aphorism describing the Chronic Fatigue Syndrome.
    Pietrangelo T1,2, Fulle S1,2, Coscia F3,4, Gigliotti PV3,4, Fanò-Illic G1,2,5,6.
    Author information

    The chronic fatigue syndrome (CFS) otherwise known as myalgic encephalomyelitis (ME), is a debilitating syndrome whose identification is very complex due to lack of precise diagnostic criteria. This pathology begins with limitations in duration and intensity of exercise and rapid onset of pain during physical activity. Its etiology is unknown, and symptoms are not limited to the muscles. Epidemiology is rather difficult to delimit, even if it affects mainly young (20-40 years), female subjects. The results of muscular research show some peculiarities that can justify what has been observed in vivo. In particular,

    1. presence of oxidative damage of lipid component of biological membranes and DNA not compensated by the increase of the scavenger activity;
    2. Excitation-Contraction (E-C) alteration with modification of Ca2+ transport;
    3. passage from slow to fast fiber phenotype;
    4. inability to increase glucose uptake;
    5. presence of mitochondrial dysfunction; and
    6. genes expressed differentially (particularly those involved in energy production).

    The skeletal muscles of CFS / ME patients show a significant alteration of the oxidative balance due to mitochondrial alteration and of the fiber phenotype composition as shown in sarcopenic muscles of the elderly. Vice versa, the muscle catabolism does not appear to be involved in the onset of this syndrome.

    The data support the hypothesis that patients with CFS are subjected to some of the problems typical for muscle aging, which is probably related to disorders of muscle protein synthesis and biogenesis of mitochondria.

    Patients with CFS can benefit from an appropriate training program because no evidence suggests that physical exercise worsens symptoms. Type, intensity and duration of any physical activity that activates muscle contraction (including Electrical Stimulation) require further investigation even if it is known that non-exhaustive physical activity decreases painful symptomatology.
    Not dead yet! and Forebearance like this.
  2. Not dead yet!

    Not dead yet! Well-Known Member

    #6 is interesting because Vitamin A can turn on/off several genes involved in that. Most vitamins only provide beta carotene, so if someone has a problem with the conversion, they would be functionally deficient and feeling the effects, but we tend to think symbolically of Vitamin A and only count it as a problem when night blindness occurs.

    Here's a place to start about Vitamin A and the many studies on it looking for synthetic derivatives, to make into drugs. It's a bit of a dark horse.