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Low Muscle Glycogen Levels in Muscle Biopsy

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
@RYO I am including you in this thread because I found a thread some years ago where I think you said that low glycogen in muscles was common in ME but I haven't been able to find any research on it or ever mentioned in forums...

One of the results of my muscle biopsy along with severe type 11 atrophy and inflammation in a single fascicle was a 'moderate reduction in glycogen levels'...

Has anybody else who has had a biopsy ever had this result or does anyone have any ideas why this might occur in ME/CFS?

Thanks- Rossy
 

Runner5

Senior Member
Messages
323
Location
PNW
I think this (original post) is my issue but have not had my muscle tested. I'm a retired runner (at age 43) and I have trouble accessing my glycogen and fat stores and tend to burn amino acids for fuel in my cells or just break down my muscle for fuel. That's not supposed to happen so I've been rather perplexed about how / why. I've run dozens of personal experiments to see how I can overcome the issue. I guess I figured it was a rather aggressive form of insulin resistance and have worked on it from the angle of metabolic disorder and too much intramyocellular fat.

I'm about 50lbs overweight these days and I think I would benefit greatly if I could drop the weight permanently. I seem to be able to shift up and down 5-10lbs, over and over again, but not make real headway.
 

Runner5

Senior Member
Messages
323
Location
PNW
@robinhood12345 -- you mean complex carbs though right? I'm Vegan and really trying to do 80-10-10 (but I'm rubbish at diets, I'll admit it) but I do try very hard to stay away from refined white flour, refined white sugar and anything that has been taken away from it's original fiber packet. Fiber really helps to blunt that insulin surge. I guess I'm nervous about insulin because I'm prediabetic and my family is all diabetic / metabolic diseases.

I have a sweet tooth and that doesn't help :( I had so much stress this weekend I kinda fell apart on my eating.
 
Messages
151
Yeah complex carbs as another study said maltose, which is what complex carbs break down into, is the main trigger for feelings of satiety. But IMO simple carbs like sucrose really are not that bad anyway. Palmitic acid fat in animal dairy, and whatever the fat is in the oils used to fry chips in are the macros to avoid.
 

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
Perhaps not eating enough carbs can do it. Or b vitamin deficiency which would be cofactors for enzymes in carb metabolism/storage

Here is the good things insulin (raised by eating carbs) does

http://sci-hub.tw/https://doi.org/10.1016/S0168-8227(11)70014-6
Thanks for your reply @robinhood12345 the interesting thing is except for when I am in a crash my carb intake is good. I guess the low muscle glycogen matches some of the hypotheses that at least in a subset of patients there is impaired metabolism of carbs..
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
Sedentary? That would match with the atrophy in the Type II muscle fibers.

Or is there elevated CK (creatine kinase) pointing to muscle breakdown?
 

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
@Sherlock my CK is quite low and research has found that disuse causes type 1and II atrophy together but not selective type II atrophy

Selective type II atrophy often caused by inflammatory process or nutrition deficits
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Low muscle glycogen also raises the possibility of a glycogen storage disease. It might be good to investigate this. there are a whole bunch of different glycogen storage diseases.

On the other hand, insulin does not do much in ME. We have insulin resistance of a type different to diabetes, and there is so little research so far that nobody is sure what that means. However even without that our cells do not use much carbs, they burn fat and protein, and its mostly protein. There is carb metabolism but it is rate limited. It does not increase for anything, including insulin, from what the science is implying ... that might change but for now that is the implication.

For anyone with ME a much higher protein intake is suggested. I have not investigated if this be obtained from tofu etc. due to the amino balance issues. Our amino needs are not the same as most people, but again we don't have enough research. This will probably change in the next several years.

The main point I want to make is that all current dietary theory, when applied to ME, is problematic. Without sound research this means we often have to experiment to see what works for ourselves. I used to be vegetarian but I ate some meat one day (I was too sick to make food) and I immediately felt much better. I still do not like meat like I used to, but I am much worse without it, in many ways.

Given the close connection between ME and gut dysbiosis I expect to see lots more research on diet in a few years.
 

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
Low muscle glycogen also raises the possibility of a glycogen storage disease. It might be good to investigate this. there are a whole bunch of different glycogen storage diseases.

On the other hand, insulin does not do much in ME. We have insulin resistance of a type different to diabetes, and there is so little research so far that nobody is sure what that means. However even without that our cells do not use much carbs, they burn fat and protein, and its mostly protein. There is carb metabolism but it is rate limited. It does not increase for anything, including insulin, from what the science is implying ... that might change but for now that is the implication.

For anyone with ME a much higher protein intake is suggested. I have not investigated if this be obtained from tofu etc. due to the amino balance issues. Our amino needs are not the same as most people, but again we don't have enough research. This will probably change in the next several years.

The main point I want to make is that all current dietary theory, when applied to ME, is problematic. Without sound research this means we often have to experiment to see what works for ourselves. I used to be vegetarian but I ate some meat one day (I was too sick to make food) and I immediately felt much better. I still do not like meat like I used to, but I am much worse without it, in many ways.

Given the close connection between ME and gut dysbiosis I expect to see lots more research on diet in a few years.

Hi @alex3619 thanks for your contribution. I did research the glycogen storage diseases some time ago and my memory is that they actually result in high muscle glycogen rather than low such as in my case. I agree the advice in diet is just a guessing game. For the most part I am able to eat a really full diet yet even though I am bed bound I lost about a quarter of my body weight early in disease and can't put any back on. I have low blood proteins and some amino acids which John Whiting has suggested is result of body using proteins for energy and I think its possible I have the low muscle glycogen because of poor carb metabolism but the more I try to piece together the possible dietary and metabolism links the more confused I get...
 

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
There is good evidence for this, but you could find the likely aminos and see if they match. Specific amino mixes, like bodybuilders use, might help if they are a match for your specific issues.

So far I have tried protein powder each day and also bcaa's as well as trying to eat more protein but haven't noticed any difference.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
So far I have tried protein powder each day and also bcaa's as well as trying to eat more protein but haven't noticed any difference.
Its good to know how you respond. This is very much a search, and I wrote a lemon rule for it years ago, in one of my blogs here -

22. Most treatments for ME are lemons, they don't suit everyone - but you often wont know if it suits you until you suck it and see. If you see a soured look on my face you will know why.
 

Moof

Senior Member
Messages
778
Location
UK
...tend to burn amino acids for fuel in my cells or just break down my muscle for fuel.

I'm not sure of your sex, @Runner5, but wasn't there a metabolomics study that reported abnormally low levels of amino acids in women with ME, suggesting they may be using them as an energy substrate – but which also indicated that male patients appear to be using different routes around the energy blockade, including consuming their own muscle tissue?
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
@Sherlock my CK is quite low and research has found that disuse causes type 1and II atrophy together but not selective type II atrophy

Selective type II atrophy often caused by inflammatory process or nutrition deficits
Hi, this is from the NIH:
Atrophy can uniformly affect myofibers or selectively target specific muscle fiber types. Type II fibers are selectively affected when atrophy is associated with disuse, cachexia, or malnutrition. Chronic administration of corticosteroids in rats results in the selective atrophy of type II fast-twitch fibers. Conversely, type I fibers are selectively targeted during experimentally induced thyrotoxicosis.
(It doesn't say if the observation that I bolded is from rodents only, though.)
https://ntp.niehs.nih.gov/nnl/musculoskeletal/skel_musc/atrophy/skeletal-muscle-atrophy_508.pdf

Or another musing: is the disuse perhaps selectively of the Type IIB fibers only? IIB store the most glycogen, after all. They (glycolytic) are used for short bursts of the most power, say lifting a very heavy weight once or running full out for 10 meters. But IIA (oxidative) would be used in lifting a medium-heavy weight many times, or running 100 meters.

I would bet that researchers completely immobilize a leg, but don't partially limit activity as might be found in a CFS patient.

The nerve controlling that single bad fascicle is possibly damaged (which is a far better possibility than your single fascicle being the start of many).

It might help to post the entire biopsy report.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
For the most part I am able to eat a really full diet yet even though I am bed bound I lost about a quarter of my body weight early in disease and can't put any back on. I have low blood proteins and some amino acids which John Whiting has suggested is result of body using proteins for energy and I think its possible I have the low muscle glycogen because of poor carb metabolism but the more I try to piece together the possible dietary and metabolism links the more confused I get...
Oh, this info changes everything. Especially if you can't even put on fat?

Have you tracked calories and believe you are daily in calorie excess but still gain zero weight?

But if you are not in calorie excess, then the diet macro composition should hardly matter.

[edit: eating and absorbing calories]
 
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RYO

Senior Member
Messages
350
Location
USA
@Rossy191276
I am not aware of any researchers studying this phenomenon. I mentioned it to NIH while undergoing intramural study. I suspect many of us with ME/CFS have an acquired mitochondrial abnormality. As mentioned by Dr. David Systrom in an ME/CFS alert, I believe there is an abnormality in muscle tissue oxygen utilization. Fascinating hypothesis of small fiber neuropathy and vascular bed abnormality.

I got emotional watching Dr. David Systrom interview. He confirmed and gave voice to my experience/suspicions.

My experience is that altering your carbohydrate or protein intake may help someone with normal muscle physiology but not someone with ME/CFS.
 

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
Hi, this is from the NIH:

(It doesn't say if the observation that I bolded is from rodents only, though.)
https://ntp.niehs.nih.gov/nnl/musculoskeletal/skel_musc/atrophy/skeletal-muscle-atrophy_508.pdf

Or another musing: is the disuse perhaps selectively of the Type IIB fibers only? IIB store the most glycogen, after all. They (glycolytic) are used for short bursts of the most power, say lifting a very heavy weight once or running full out for 10 meters. But IIA (oxidative) would be used in lifting a medium-heavy weight many times, or running 100 meters.

I would bet that researchers completely immobilize a leg, but don't partially limit activity as might be found in a CFS patient.

The nerve controlling that single bad fascicle is possibly damaged (which is a far better possibility than your single fascicle being the start of many).

It might help to post the entire biopsy report.
Oh, this info changes everything. Especially if you can't even put on fat? Have you tracked calories and believe you are daily in calorie excess but still gain zero weight? But if you are not in calorie excess, then the diet macro composition should hardly matter.
Thank you for your details response @Sherlock. Its amazing to think that we can get more helpful contributions from the members of our group than doctors supposed to be helping.

I have included the biopsy report and welcome anyone's thoughts. In answer to your questions I did do quite an extensive research review on causes of selective type II atrophy in humans and while the research was limited I did find a couple of really in depth review papers done in about 2014. The basic findings have been that with disuse Type I atrophy occurs first followed by type II atrophy. It's interesting that the NIH document states selective type II atrophy can occur from disuse but as you say that may have only included the rodent research. But given that I had been bed bound for nearly 3 months before the biopsy what is almost more surprising to me is that my Type I fibres were 'relatively well preserved'.

My biopsy report didn't differentiate Type II A and B fibres. Also given that I didn't have the biopsy until nearly 2 years into illness the finding of the single fascicle myositis is much more likely to be a one off rather than the start of many...

Re weight i haven't tracked calories but I know that I should be in calorie excess but still don't put on any fat at all. Each day I have a protein shake with half a banana (30 grams I think) with extra bcaa's. An egg with some avocado on a piece of toast. A lunch which I would say is of average size and generally includes some sort of meat and salad + maybe a soup and usually a small serving of fruit. A light snack of some biscuits with a spread. And for dinner typically again some sort of meat and salad or veg. And I am 100% bed bound using bedside commode for toileting. I would say that the amount of food I eat is not that much less than when I was highly active running 3-4 times a week.

Given that I first got sick when I went on a paleo diet when I was exercising a lot the idea of some sort of metabolic failure or switch makes a lot of sense for me. That is why I am so intrigued by the low glycogen in atrophied muscles...
 

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Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
@Rossy191276
I am not aware of any researchers studying this phenomenon. I mentioned it to NIH while undergoing intramural study. I suspect many of us with ME/CFS have an acquired mitochondrial abnormality. As mentioned by Dr. David Systrom in an ME/CFS alert, I believe there is an abnormality in muscle tissue oxygen utilization. Fascinating hypothesis of small fiber neuropathy and vascular bed abnormality.I got emotional watching Dr. David Systrom interview. He confirmed and gave voice to my experience/suspicions. My experience is that altering your carbohydrate or protein intake may help someone with normal muscle physiology but not someone with ME/CFS.

I watched Dr Systrom's video and also found it fascinating. Yes it seems his theory of ANS dysfunction, vascular abnormalities, and muscle problems could also contribute to muscle physiology. I had what I believe are similar findings to what he talked about in a lack of pre-load power reported on my tilt-table test with echocardiography.

Interesting about one month after I first crashed I had a period of about 2 weeks where I got an incredible appetite where I needed to eat basically double of what I had previously. This was followed by what I thought was a complete recovery. I built up to pre-illness activity levels over about 3 months before crashing again. Since then my experience has been similar to you in that food alterations doesn't seem to help.
 

Runner5

Senior Member
Messages
323
Location
PNW
I'm not sure of your sex, @Runner5, but wasn't there a metabolomics study that reported abnormally low levels of amino acids in women with ME, suggesting they may be using them as an energy substrate – but which also indicated that male patients appear to be using different routes around the energy blockade, including consuming their own muscle tissue?

I'm a 43 year old female and I used to crash really hard (PEM for days, muscle breakdown, unable to get out of bed, flu symptoms etc.) after exercise.

I've been tracking progress on my blog here on PR.

Dietary changes completely cleared up my CFS, along with a few lifestyle tweaks, but it took me 5 years to get here. 5 years of daily note taking, watching videos, and being utterly confused by conflicting but really convincing sounding evidence. (And I still take notes and track stuff!)

Freak remission? Maybe but I am building muscle and building health. Even my hair is growing back in thick. I now look kinda like a troll doll with my short hair just going all over the darn place as it grows out. My nails are healthy, my skin looks pretty good.

Still working on my GI health but this is the best I've felt in the last ten years although still a little weak from years of being inactive and so weak I wasn't sure how to get off the toilet by myself. Not a good spot to be in during your early 40's.

I'm looking for a job now and life is pretty good.

I didn't do just one thing, but once I tackled it as a metabolic issue that involved too much fat where fat shouldn't be then it all started to click, but it has been a multi-pronged approach.