Exhaustion in ME/CFS, what is it and what causes it - discussion thread

We agree on all of this, at least up to "But there is an inability to use them etc" I think this is inaccurate. As sick as we can get, we ALWAYS have volition, we usually can put forth an effort (although admittedly some times we are so debilitated virtually no effort is possible); however, those ingrained capabilities don't translate into much substance because we are too sick. For me, effort and volition are inherent, part of our fabric just as our height or reach or shoe size are. None of those characteristics have any bearing on what I am unable to do because of my ME/CFS or Lyme or Babesia or POTS. Those diseases limit me because they destroy my balance, weaken me to invalid status, corrode my brain, confine me to bed.

Volition and effort are with me always, just like my height, but just like my height, they bring no import to what has disabled me. They have no relevance other than if they are called into question by people challenging my contested disease - and by extension, my integrity.

That is why they do not belong in any serious conversation about us and our disease.

ETA: I cannot think of any disease where volition and effort are assigned a diagnostic role or assume any part in disease characterization. If there are others, I suspect those illness have some contested history.

 

Hey, I got beat over the head for resorting to an analogy. Maybe we should all get the equal treatment!

So, you chop wood all day, and you can't do anything else. Is that a fatigue? exhaustion? Whatever you call it, it's the same thing: it's a sensation that your body/brain creates to stop you from doing more. It doesn't matter whether it is caused by micro-damage, energy depletion, infection or depression. In fact, the way you describe MECFS fatigue as depletion is how depressed people describe their fatigue. Does that mean MECFS is a form of depression? Hyper-focusing on the subjective sensation without any testable difference is more likely to lead you to a false belief rather than any real insights.

How?

And subjective sensation is more medical somehow? Show me a measurement showing they are different, and I'll accept it as medical/scientific. If anything, the evidence is against the energy/depletion theory: MECFS patients can produce enough power to pedal 10-100w for 10 minutes with no discernible difference to similarly deconditioned controls.

"The boxer had a flu, felt so fatigued/exhausted that he couldn't throw a punch". How does that make the word change so significant?

 

That's what fatigue is in exercise to failure: your muscles can no longer generate power to move the weight another inch.

 

These are discussions that would benefit from someone with a channelopathy chiming in. There's a reason that Australian school of thought believe ME/CFS may be a channelopathy. Fatigue and exhaustion and effort and volition take on a different hue in that context.

 

I agree that we’ve an issue where many don’t understand that the iller you get the more gargantuan effort is required for things less ill don’t even think about doing - brushing their teeth is nothing and almost automatic whilst they get ready and think about the day. The determination when you are severe to find a moment where you are well enough to sit leaning against something and trying and hold your arm up for long enough to have done a half decent job is huge.

which was why ‘effort’ was a real misleading problem term for Walutt to pick on

I’d forgotten this thread for a while and the volition idea needs me more on form to think through on precise terms. There is of course the issue most reading volition don’t really bother with precise so take what they want from it - and that can’t be ignored even if theoretically if people were being precise then …. It doesn’t help us to have a moral superior position of saying ‘well they just are interpreting volition wrongly and don’t know their terms’ because they go off and create whole initiatives and wrong treatment on it which can last for years.

 

Thats an excellent infographic! You dont have a link to the source do you, i cant read at the bottom where it's coming from its a bit blurred on my screen & I'ld like to print & use it?

 

Fourth page of the PDF of "Diagnosis and Management of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome" (Mayo Clinic Proceedings Journal):

Link | PDF

 

Thanks @Nightsong

 

Central fatigue is stimulated by peripheral afferents and the purpose of which is to lower peripheral fatigue! The two are 100% linked together in a relatively simple way.

Studies in humans show that the afferent feedback reduces motor cortex excitability, which in turn requires greater effort to maintain the same force output, which in turn also means a greater ventilatory effort for a given force output. If that afferent feedback is blocked, ventilatory responses don't keep up and severe peripheral fatigue is the result.

https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/JP276460

Jonathan, it is very important to understand that the supramaximal twitch interpolation methdology used in the Lloyd (and other similar studies at the time) is not useful.

Those studies were a major red-herring that set the field of ME/CFS back decades!

The fact is the very same result as found in ME/CFS "central activation failure" was found in ALL other diseases, including mitochondrial diseases, peripheral neuropathies and muscular dystrophy.

In fact the only diseases which showed clear peripheral fatigue were glycogen storage diseases.

Which means that the supramaximal twitch interpolation studies tell us NOTHING about fatigability of of aerobic metabolism, they only tell us something about whether there is sufficient glycogen remaining, or I guess hypothetically, if the nerve somehow was damaged after repeated stimulation.


We now know from studies as I cited in the first part of my comment that "central activation failure" aka central fatigue is itself due to afferent feedback that reduces motor cortex excitability.

 

I understand that it can be over interpreted but I was using it in a combined argument with the fact that first day CPET in ME/CFS tends to be unremarkable. The fact that the twitch data are similarly normal in other conditions is important, I agree. But a first day CPET would presumably be abnormal.

If I remember rightly the point I was trying to make is that there is a real decline in function in ME/CFS but we do not yet have evidence for a simple mechanism such as simple loss of muscle power to contract (which would for instance be the case in late dystrophy or myositis) or an ongoing metabolic block (which should make the first day CPET abnormal in someone with ongoing disease).

In my view we should be looking at what is wrong with the signalling between muscle and brain, which might have a biochemical basis at either end or both. Maybe that is your view as well?

 

Compared to what? There is is no controlled basis to compare it with.

Having said that, invasive CPET studies by Systrom et al. are suggestive that things might not be normal on the first day.

edit - there are also other ways of measuring EMG, MMG fatigue thresholds and also brain activation patterns that may indicate differences on the first CPET.

But I agree that my focus right now is the signalling between muscle and brain.

 

They may be linked in a relatively simple way, but that doesn't mean that there aren't other complexities that could be involved. CF could be triggered by other mechanisms, or the trigger from periphery (or its feedback) could be miscommunicated or misprocessed. Even a "simple" communication link between muscle and brain involves a lot of complexity in each cell and between cells and probably involving other organs, so that simplicity is just a very limited perspective.

 

I dont know if this will be usefull but from my 25 years observation (I have mild ME/CFS and I am ex profesional sportman):
1. the muscle weakness came immediately after getting ME/CFS (the problem with stamina, not strength)

2. the high heart rate came immediately after getting ME/CFS

3. why there is muscle strength but very bad stamina (I tried to improve the stamina of some muscles by regular exercising but I could improve the stamina only a bit)

4. I can do stacionar bike for 20 minutes if the heart rate is down (maybe 80 - 100 beats per minute is OK), if I do 2 minutes with high intensity I start to feel dizy, kind of heart weakness and I will probably get PEM (I get PEM only occasionaly)

5. I saw that i can do one hour walk without a problem so I was thinking that I try to swim and if I will keep my heart rate down, which is easier if you exercise in horizontal position, maybe I can do it. But I was disappointed that even if I was able to keep my heart rate around 80 beats per minute, I started to feel dizy and I got PEM

So with the points 4 and 5 I ask myself if there is not an important problem in our muscles in all this puzzle - if they have to work more it´s somehow problematic. After walking and swimming I feel the same fatigue and it´s quiet Ok if I respected my limits. But why I dont get PEM after walking but I get PEM after swimming when I was able to keep my heart rate down? Maybe the muscles use too much oxygen or there is an oxygen problem and that´s what is problematic. How I said if I dont use too much my muscles and I dont walk too fast I can walk 1 hour without a problem, but if I bike too fast (fast heart rate) I feel dizy already after a short time and also if I swim (big muscles use) I start to feel dizy even if I am able to keep my heart reat down and I will probably get PEM. So at least in my case what is bad is fast heart rate and big muscles use, the worst is the combination of fast heart rate and big muscles use. So is there not a problem if we use too much oxygen or something else which is happening with fast heart rate and big muscles use?

6. also i live uphill and so I am used to have higher heart rate. I feel that it doesnt make me good to walk too much uphill. Sometimes I walk with my friends and many of them have to breath very fast, even we have to stop sometimes because they have to take a small break. For me i dont need a break but I breath generally slowly and flat and often I feel like I miss oxygen and I feel that it doesnt make me good to go uphill. So I am used to go uphill, but heart rate is very high and if I go too much I will again start to feel dizy and can get PEM.

 

Sure, we can come up with many hypotheses, but the burden of proof is on actually demonstrating any of those hypotheses is actually true.

 

Even before me/cfs and I mean throughout childhood swimming was the most exhausting thing I could do - and I did most other sports so it wasnt fitness then. I think it is that it gets every part of your body due to the water and there is no other way of advantage to bouncing or striding out or being small etc it’s absolutely about strength rather than generation of power.

but yes the water didn’t help i would feel absolutely like a drowned rat after - the closest I felt to having me/cfs (before I had it, or when I wasn’t ill with something else serious) is probably actually those times after leisurely messing about in the pool swims as a kid and being sat after eating chips. And being exhausted everywhere

when I tried gym after first diagnosis thd PT put rowing on the routine and I had to knock it off completely (ie not just number of minutes/distsnce) after two goes be i realised that was the activity that was absolutely blasting past all my limits in PEM and leaving my whole body totally screwed ie it was really obvious how harmful it was even to someone who assumed they’ve get fitter at running (as I had in past)

so I think those whole body activities are a real problem for PEM and overall exhaustion where eg weights or walking you can negotiate it a bit more … however by six months remember it didn’t matter it had all caught up and I was worse anyway.

 

My PEM depended not on overall exertion level or duration, but how abnormal the muscle usage was. My leg muscles were used to the movements of pedaling, so it might have required a strenuous 40 km ride to trigger PEM, but climbing a 10' ladder once would trigger PEM, because the muscles were strained in different ways. I think it was activity that resulted in some muscle cell tears, which in turn triggered immune cells to clean up the debris, and that immune signalling triggered the PEM mechanism. It's possible that some non-immune signalling was responsible, but my PEM had a very consistent 24 hr delay, and the immune system is known for precise delay timing.

Another example: I could dig soil for hours without triggering PEM if I did the usual movements (stomp shovel into soil, pry and lift into wheelbarrow), but a few shovels done with different movements (stab horizontally into side of the hole) would trigger PEM.

If you didn't swim regularly, going for a swim would have triggered that sort of muscle damage and immune activation.

 

For what it's worth, I used to get PEM just by squatting down and getting back up a couple of times. This was when I was able to walk at 90 steps/min for 30 minutes or longer.

This is why I'm generally not for controlling PEM by keeping the HR down. It may work for steady and even exercises like walking on flat terrain, but it doesn't work for high intensity in a short burst. HR has to do with energy consumption, and it hardly changes for a squat or two because the glucose/ATP in your muscles and stream is enough to power it. But it still can damage the muscle fiber and cause inflammation next day. Slow walking, on the other hand, burns a lot more calories but causes little damage.

 

I still think it's a decent enough call that it could do with being excluded.

Trouble is, until you find what could be a completely novel genetic mutation OR a disease process that causes secondary channelopathy, it's not easy to exclude. Some people with periodic paralysis appear to have potassium shifts that are so tiny they don't show up on tests, even though in their case doctors know what they're looking for.

 

True. In fact, my wife is normokalemic, and her channelopathy has had its gene - KCNJ2 - identified and verified.