The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
Discuss the article on the Forums.

Functional characterization of muscle fibres from patients with CFS

Discussion in 'Latest ME/CFS Research' started by Dolphin, Aug 18, 2011.

  1. Dolphin

    Dolphin Senior Member

    Messages:
    10,671
    Likes:
    28,172
    Again, because of my lack of knowledge of muscles, I probably won't be able to contribute much to this thread. But like with their other research, it seems very interesting.

     
    MeSci and Mark like this.
  2. mellster

    mellster Marco

    Messages:
    804
    Likes:
    189
    San Francisco
    Wowsa! I think I hypothesized about a possible shift from slow to fast-twitching fibres in one of my early posts cause that matches my experience after exercise and might explain increased muscle-twitching (via increased number of fast-twitching fibres). This might also explain why there is no decrease in strength, but a much faster exhaustion/depletion.
     
    Mark and PennyIA like this.
  3. Marco

    Marco Grrrrrrr!

    Messages:
    2,379
    Likes:
    3,174
    Near Cognac, France
    This is a good run of papers Dolphin. Good find.

    This chimes very much with my own experience also as I still appear to cope with heavy loading but not with any aerobic activity. Slow twitch fibres are also the type that we use when standing still - something many of us can't tolerate for long.

    As is often the case - bodybuilding types have a good handle on muscle physiology :

    http://www.musclemagfitness.com/bod...twitch-muscle-fibers...what-it-all-means.html


    I would hope of course that they have controlled for the possiblity that the change to type II muscle fibres isn't just as a consequence of an enforced sedentary lifestyle (again my own experience would suggest this is not the case).


    More interesting, to me, is that factors such as a high fat diet leading to obesity, or ageing result in reduced mitochondrial efficiency and a switch to type II (glycolytic myofibres) muscle fibres :

    MAP kinase phosphatase-1 - a new player at the nexus between sarcopenia and metabolic disease


    http://www.impactaging.com/papers/v2/n3/full/100135.html

    This suggests to me that a major part of our problem is either a primary or secondary mitochondrial dysfunction.
     
  4. In Vitro Infidelium

    In Vitro Infidelium Guest

    Messages:
    646
    Likes:
    280
    This is a real problem and not easily addressed because 'sedentary' can mean different things (for exmple it may exlude non aerobic exercise such as yoga which can maintain muscle tone ), while different bodies can respond differently over differing periods of time, and as noted diet may impact upon the type of response (likely mediated by genetic variability) to sedentary behaviour. I think to have effective controls for M.E/CFS physiology research, there needs to be not only age and gender matching but a much more detailed set of controls including BMI, duration of lifestyle habit and lifetime diet, plus age based comparison. Finding muscle changes in long term ill 40 year olds is one thing - finding it in teenagers with less than a years ill health, may be something vey different.

    IVI
     
  5. Valentijn

    Valentijn Senior Member

    Messages:
    14,281
    Likes:
    45,811
    It seems unlikely sedentary behavior is causing these muscle abnormalities, since those abnormalities can cause the initial symptoms of M.E. In this case of chicken versus egg, it's pretty obvious to most PWME that the symptoms came first, followed by a forced reduction in activity levels.

    On a more personal level, I think the deconditioning theories regarding M.E. are pretty worthless. I started having a (thus far) significant recovery 10 days ago, immediately after starting neurotransmitter-regulating supplements. My ability to do physical stuff, like climb a flight of stairs, immediately increased dramatically. I've had sore muscles the past few days from being more active, but I think it would be impossible for a PWME to confuse M.E. muscle pain with this normal soreness, after months or years of enduring the M.E. pain. Undoubtedly there is muscle deconditioning, but it is a very minor concern: it is not even close to being the limiting factor when it comes to physical activity.
     
    NK17 likes this.
  6. Dolphin

    Dolphin Senior Member

    Messages:
    10,671
    Likes:
    28,172
    As somebody who became ill as a sporty/athletic teenager, I'm not convinced muscle symptoms are due to deconditioning - as I never went to bed. Nobody in our house used to go to bed (my father has always been self-employed so that may have influenced him) - the most I did was potter around at home for a couple of days (I wasn't diagnosed till five years into it). I had over 100 physiotherapy (=physical therapy) appointments in the early years when I was constantly on my feet in full time education and had all sorts of weird muscle symptoms. It certainly felt like there was something odd in my muscles. I could accept there might be some central factors but I'm not at all convinced deconditioning could explain the symptoms as I never was that deconditioned.
     
    NK17 likes this.
  7. Sean

    Sean Senior Member

    Messages:
    3,257
    Likes:
    17,984
    Similar story here, Dolphin.

    Conventional deconditioning just does not fit my particular circumstances preceding, during, and for at least 4 years after onset. You do not have to be very active to avoid serious deconditioning, and I easily met that mark. Yet I continued seriously deteriorating, no matter what I did.

    Far as I can see, the overall evidence fairly strongly points to towards any deconditioning being a secondary consequence of the limited activity imposed by ME/CFS, not a cause of it.
     
  8. Dolphin

    Dolphin Senior Member

    Messages:
    10,671
    Likes:
    28,172
    Authors deal with whether finding could be down to disuse

    I actually hadn't read this one.

    The discussion section is very interesting.

    Here, they briefly explain why they don't think the changes are down to disuse:

     
  9. Marco

    Marco Grrrrrrr!

    Messages:
    2,379
    Likes:
    3,174
    Near Cognac, France
    I think we can safely rule out deconditioning as a cause for ME. There never was any evidence for the proposition and quite a lot of evidence to counter it. As for deconditioning as a perpetuating factor, again there is no evidence of any affect specific to ME. This doesn't exclude the possibility that if deconditioning has occurred in a subset of patients that this could skew the results of physiological studies such as this.

    The new International criteria (if eventually widely adopted or at least used in tandem) do not require 6 month duration for a diagnosis and therefore raise the possibility of studying patients before there is any realistic chance of deconditioning (post onset).

    Unfortunately I can't find the full Pietrangelo et al paper but the reference to Lane et al is interesting.

    From the abstract :

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2169994/

    Edited to add :

    From reading the Lane et al abstract and the slightly contradictory results I suspected we were dealing with an 'Oxford' cohort. This is indeed the case. The full Lane et al paper is very well worth reading though as general background and in particular the comments about type II dominance in those suffering heatstroke (a tendency in mitochondrial diseases).
     
  10. mellster

    mellster Marco

    Messages:
    804
    Likes:
    189
    San Francisco
    Agreed - I do not experience any atrophy/weakness related symptoms though I have muscle-twitching and suffer from PENE occasionally. I even don't experience a high degree of soreness, I def think this is not related to deconditioning. Also there are theories that muscle-twitching is a result of immune-system activity rather than something wrong at the location of the nerves/muscles themselves, more like a sort of hyper-excitability.
     
  11. Valentijn

    Valentijn Senior Member

    Messages:
    14,281
    Likes:
    45,811
    I just did a tiny bit of reading on slow vs fast twitch muscles, and it's pretty interesting. I'm wondering if it's type IIx found more in the study, which doesn't have as much mitochondria and myglobin (and capillaries?), versus IIa which has similar amounts to slow twitch muscles. If so, maybe a process in our bodies (faulty mitochondria, insufficient oxygen) causes the body to switch to type IIx.

    Also an interesting note in wikipedia regarding type IIx fast twitch muscles:
    I know that not-quite-lactic-acid burning sensation very well :p
     
  12. Dolphin

    Dolphin Senior Member

    Messages:
    10,671
    Likes:
    28,172
    Yes, it is 2x that are different and 2a that are the same.

    I can't imagine it is a pre-existing condition (I played a lot of sports competitively) so the body must switch.
     
  13. mellster

    mellster Marco

    Messages:
    804
    Likes:
    189
    San Francisco
    Yes, I even continued kickboxing when I weakened but had not significant PENE at that time at I noticed the increased twitching, first only following strenuous exercise, then it became permanent slowly over time (but 90% of the twitches occur at night and/or at rest). Def a body switch.
     
  14. mellster

    mellster Marco

    Messages:
    804
    Likes:
    189
    San Francisco
    One thing that's odd though is that the twitches are everywhere, like although mostly in extremities and butt, some are in tongue or scalp, so it seems weird that those areas are affected too as you would not think that those areas suffer a lot of oxidative stress or endure hard workouts - which points again to a widespread body switch which might be "mis"-induced by ME/CFS type conditions (or their causing pathogens).
     
  15. anciendaze

    anciendaze Senior Member

    Messages:
    1,806
    Likes:
    4,650
    I have regularly had people surprised at my short-term muscle strength, despite being seriously debilitated in terms of aerobic capacity and orthostatic tolerance. In one case I was able to lift a chest single-handedly and carry it downstairs, while another person my size was looking for help. This is very different from having stamina. An explanation in terms of fast vs slow muscle fibers makes sense, but does not reach the original cause.

    I think it is obvious this is not the result of some peculiar strength training, but I will state this here to avoid confusion: I have not been doing resistance training. The only form of exercise which has helped, beyond very low-level things like walking to the mailbox regularly, has been slow stretching, as described here. The primary aim in that book is to avoid injuries during subsequent exercise. My experience is that ME/CFS patients are especially vulnerable to these, even in ordinary activity -- for reasons that have never been explained. I even do some stretches before I try to get out of bed. Waiting until a patient shows up at an exercise class, when they may have already pushed close to their limits, indicates a complete misunderstanding of the problem.

    This is very different from general deconditioning.

    For our Latin interlocutor, "Sed nescio quo modo nihil tam absurde dici potest quod non dicatur ab aliquo philosophorum."
     
    Last edited: Aug 25, 2014
    NK17, MeSci and Valentijn like this.
  16. Marco

    Marco Grrrrrrr!

    Messages:
    2,379
    Likes:
    3,174
    Near Cognac, France
    I did of course mean 'effect' but the original would also be true "again there is no evidence of any affect specific to ME"
     
    MeSci likes this.
  17. Marco

    Marco Grrrrrrr!

    Messages:
    2,379
    Likes:
    3,174
    Near Cognac, France
    Strangely enough, I was lining up to do a comparison between the autonomic symptoms of diabetic/cardiac autonomic neuropathy and autonomic symptoms in ME/CFS (as you do and there's a large overlap) when this thread popped up.

    One paper on diabetic autonomic neuropathy contains this :

    http://www.ccjm.org/content/68/11/928.full.pdf

    That being the case you would expect impaired blood flow to peripheral muscles to also result in impaired oxygen delivery (relative to demand) which would be expected to impact more on the aerobic slow twitch fibres. I can't say how reduced blood flow would impact on the fast twitch glycolytic fibres. Its plausible that over time this impairment might result in a compensatory relative switch from slow to fast twitch fibres.

    Turns out there does appear to be a switch to fast twitch muscle fibres in Type II diabetes which

    http://www.ncbi.nlm.nih.gov/pubmed/16567834
     

See more popular forum discussions.

Share This Page