I'm able to exercise but am still disabled

[Murph]

A better answer would be that having ME/CFS doesn't make one immune to deconditioning and deconditioning will contribute to some degree to how people are feeling.

The concept of deconditioning was abused to deny the existence of an underlying illness and the suffering of patients and that's why it's not popular among patients, but it's certainly occurring to some degree.

I agree with this, we will not be afforded the luxury of being immune to deconditioning. It's not the number one cause of our problems, not by a long shot. And even if it is there, doesn't mean doing exercise is worth it. The short-run symptom cost of exercising is for most people greater than the upside of exercising. Add in the risk of a drop in baseline and the risk of exercising becomes far greater than any upside from exercising for most pwme.

But it is there, in the background, meaning that even on the best, lowest-symptom day, we are going to have less capacity than before we got sick.

is this chart helpful?




I find benefit from exercising, from being stronger, and I think that's because of two factors in my me/cfs. 1. I'm mild. 2. POTS is a big issue for me. I suspect people for whom POTS is a tiny part of their symptom constellation are less likely to experience any upside from exercise.

I'd also make a strong argument that for anyone with even the faintest amount of POTS, walking is a super bad choice. it just shakes all the blood to your legs, and it doesn't do much to make you stronger. The famous Jen Brea story of decline is a story of walking too far. Everyone perceives walking as the most gentle exercise, its the go-to for the sickly and faint, but my feeling is its kryptonite for anyone whose mecfs includes pots.

The controversial extension of this observation is that there are probably higher and lower risk types of exercise. If I had to guess at what is lowest risk it would be brief bursts of strength exercise on small muscles, that terminate well below threshold and are done sitting down/recumbent. bicep curls a good example.

One idea I sometimes consider is that pacing is to mecfs what the banana diet was to coeliac disease. It helps enormously but we haven't grasped why. When we zero in on why pacing is so good, and why aggressive rest can sometimes even lead to a lift in baseline, then we might actually be able to define higher and lower risk types of exercise with precision. Until then we're splashing round in ignorance and exercise is very risky.

 

[Murph]

I regularly ride my e-bike and am fitter than some other people I've spent time with, yet I still consider myself disabled because I can't tolerate a whole day of activity in the same way a normal person can. I end up feeling bad, stressed and overstretched by the end of the day and it's not sustainable even when what I'm doing is not considered tiring by normal standards.

This matches my experience too. Even though my strength is okay (can lift my 20kg child easily), and my fitness is okay (could do a ten minute bike ride right now). I can't do a full day of activity, or even a half day, or even an hour on my feet really, without big PEM.

I need to intersperse heavy rests with any activity to have a chance to endure it:

• Something that builds up needs to be given a chance to be broken down;
• or perhaps something that is used up needs to be given a chance to recover,
• or perhaps some receptor that is pushed towards its trigger point needs to be given a chance to move back.

I've considered a lot of theories for this over time, but recently i've been taking a POTS-centric view and asking: if the brain is starved of blood flow for a short time, perhaps it recovers well enough, but perhaps there's a threshold. Perhaps if you leave your brain with 40-70%* blood flow for a certain amount of time, without a nice long respite where you lie down and hydrate, it decides to triggers some sort of immune response with metabolic features.

*figures made up to illustrate, point is not about this specific level, it's a story about the possibility of reduced cerebral flow being a key PEM trigger. Would explain why we all love a good lie down.

 

[Snow Leopard]

I can exercise on the bike, walk for quite a while (with PEM the next few days), my VO2Max is okay but I cannot run or even jog for more than a very short distance. Exercise also causes OI as a PEM symptom. My 6mwmd is like ~850m.

 

[Sean]

I'm tired of people telling me how fit I look when I tell them I'm disabled.

After more than 40 years of dealing with it all I still don't know what to say when somebody says 'you are looking good/well', when in reality I can barely stand and am heading directly home to crash.

 

[Hoopoe]

I've considered a lot of theories for this over time, but recently i've been taking a POTS-centric view and asking: if the brain is starved of blood flow for a short time, perhaps it recovers well enough, but perhaps there's a threshold.

I agree with this. I don't consider myself to have POTS but it feels like one significant barrier to continued activity is that feeling of decreased blood flow to the brain. I know this from when I had real POTS and more marked OI. It's the same sensation. It seems that the body gets tired after a while and can no longer provide optimal blood flow to the brain and this causes some of the intolerance of activity, perhaps because operating in this state is abnormally stressful.

 

[PrairieLights]

I don't have POTS but have a different form of dysautonomia that the doctor won't further classify. I asked why he hasn't diagnosed it as inappropriate sinus tachycardia and he said he doesn't diagnose that as the goal posts for it's criteria keep changing and no one agrees what it is.

Anyhow, that gets in the way of me being able to do things I might otherwise have had the energy for... but doing stuff that gets my heart up more just gives me more fatigue.

This thread is very interesting to me hearing how others do or don't do activities. I haven't wrapped my head around how me/cfs doesn't seem to be a spectrum like my mind expects it to be. For example, someone sounds a lot like me but then says they can do this long hard activity in this certain time frame and it blows my mind how that is possible.

 

[Utsikt]

is this chart helpful?

That’s how I think about it. Although the deconditioning probably tapers off over time, it will only increase to the level that is maintained by your current activity level. The delta between your conditioning and activity decreases with time, so the change rate decreases as well.

 

[Creekside]

For example, someone sounds a lot like me but then says they can do this long hard activity in this certain time frame and it blows my mind how that is possible.

We still don't have the right theory for what's going on, but instead have lots of theories that are wrong, but people are stuck on because those theories fit their individual experiences. I mostly dismiss theories based on mitochondrial dysfunction, because my experience is that I'm not seeing any signs of inadequate ATP production, even when my symptoms are at their worst. Likewise, my physical PEM triggering seemed to not be by muscle exertion, but by unaccustomed muscle strain. Do we have different mechanisms, or is there another theory that would fit the wide variety of experiences? I think we could do with some more out-of-box ideas.

Maybe the right theory will involve certain brain cells involved with tail wagging, which aren't working properly due to our atrophied tails.

 

[PrairieLights]

Likewise, my physical PEM triggering seemed to not be by muscle exertion, but by unaccustomed muscle strain.

What do you mean by unaccustomed muscle strain? Is this how PEM is triggered now or how it has always been even in the beginning?

Mine is exertion period be it regular or unaccustomed. I don't really know if one or the other is worse as I haven't thought about it or observed.

I feel like I went from normal to losing the ability to do normal exertion to normal levels.

 

[jnmaciuch]

mitochondrial dysfunction, because my experience is that I'm not seeing any signs of inadequate ATP production

I also think certain issues in the mitochondria themselves (e.g. non-functional ETC proteins) have been well ruled out at this point. But it would be quite a fallacy to boil down all of metabolism to "inadequate ATP production"--that's what I've been trying to get at with a theory involving malate-aspartate shuttle function. With all the various ways that ATP production can be compensated for, you wouldn't expect to see a big "lack" of ATP at any point, that's just going to end up with cell death. But plenty of ways for things to go wrong with consequences like you might see in ME/CFS with a metabolic theory, at least for some parts of the illness

 

[Creekside]

What do you mean by unaccustomed muscle strain?

My example was that I could do a 40 km bike ride in hilly terrain without triggering PEM (after getting accustomed to long rides), but climbing a few steps up a ladder (unaccustomed muscle usage) or washing a window (also unaccustomed muscle usage) for maybe a minute would trigger PEM. Based on that, my theory is that muscle cells were damaged, which in turn activated immune cells, which in turn activated glial cells, resulting in PEM. It's possible that there's some non-immune-related signalling caused by unaccustomed muscle usage, but I haven't found any suspects. That could be one of those things that is still undiscovered by science.

I think PEM has multiple possible triggers, so some (most?) PWME trigger on something from duration and/or magnitude of exertion, while I didn't have that trigger, but instead triggered on a muscle damage signal. It would be interesting if people did notice a difference between PEM from different types of muscle activity, but might be hard to set up as a controlled experiment, or even to differentiate from observation of daily activities.

If you can climb a set of stairs without triggering PEM, would climbing them backwards use the same amount of ATP but strain the muscles differently? Can anyone think of an experiment that would keep exertion level the same but change the amount of muscle cell damage?

 

[PrairieLights]

Makes me want to try stairs backwards for a day.

 

[jnmaciuch]

My example was that I could do a 40 km bike ride in hilly terrain without triggering PEM (after getting accustomed to long rides), but climbing a few steps up a ladder (unaccustomed muscle usage) or washing a window (also unaccustomed muscle usage) for maybe a minute would trigger PEM. Based on that, my theory is that muscle cells were damaged, which in turn activated immune cells, which in turn activated glial cells, resulting in PEM. It's possible that there's some non-immune-related signalling caused by unaccustomed muscle usage, but I haven't found any suspects. That could be one of those things that is still undiscovered by science.

Between this and some other details you've mentioned, I'm getting the sense that your ME/CFS seem quite unique compared to what I've heard from many other people.

Am I remembering correctly that you also tried cyclosporin at one point and it had no effect? I've been trying to find anybody who has tried cyclosporin due to some other leads.

 

[Trish]

Between this and some other details you've mentioned, I'm getting the sense that your ME/CFS seem quite unique compared to what I've heard from many other people.

I agree. I'm not doubting Creekside's experiences, but they seem completely different from any other ME/CFS descriptions I have come across, including mine.

 

[Mij]

If you can climb a set of stairs without triggering PEM, would climbing them backwards use the same amount of ATP but strain the muscles differently? Can anyone think of an experiment that would keep exertion level the same but change the amount of muscle cell damage?

I think climbing stairs backwards would certainly trigger something? Using an alien force of balance for starters would require another level of maintaining our balance which would be exhausting in itself. Brushing my teeth standing on one leg is exhausting enough.

 

[NelliePledge]

No way I would take the risk of climbing stairs backwards. It is one of the most challenging physical activities I do and I have to hold on with both hands at all times when going up face forward.

I previously had a fall down just a couple of steps and sprained my ankle on one side and foot on the other and it took me a couple of months before my walking was back to normal.

 

[Sean]

No way I could do a 40km bike ride, or any comparable physical activity, without very serious payback, and the real risk of a permanent worsening of my health status.

 

[Snow Leopard]

My example was that I could do a 40 km bike ride in hilly terrain without triggering PEM (after getting accustomed to long rides), but climbing a few steps up a ladder (unaccustomed muscle usage) or washing a window (also unaccustomed muscle usage) for maybe a minute would trigger PEM.

Different tasks have *vastly* different demands regardless of "unaccustomed" or not. When we're "accustomed", we might just pare back our effort because we have more idea of what is too demanding or not.

 

[Creekside]

Between this and some other details you've mentioned, I'm getting the sense that your ME/CFS seem quite unique compared to what I've heard from many other people.

Not totally unique. I've read posts by a few other PWME who were continuing to do bodybuilding at levels way beyond my bike rides. I think outliers like myself are useful for ruling out some theories about ME and PEM. It's not absolute ruling out, since there could be possibilities where a theory is correct, but there are unusual circumstances where an individual has an unusual bypass/correction mechanism, but it still helps decide which theories are more likely to be worth investigating.

No way I could do a 40km bike ride, or any comparable physical activity, without very serious payback, and the real risk of a permanent worsening of my health status.

Yet another variation: even the activities that did trigger PEM never resulted in more than a day or two of feeling lousier. I think food intolerances caused more severe symptoms that PEM did. Microbiome changes (so I assume) caused significant raising of my baseline severity, but could switch off (and on) abruptly. I think that reflects chronic triggering of more severe symptoms, rather than a change in the mechanism that causes the symptoms.

 

[jnmaciuch]

Not totally unique. I've read posts by a few other PWME who were continuing to do bodybuilding at levels way beyond my bike rides. I think outliers like myself are useful for ruling out some theories about ME and PEM. It's not absolute ruling out, since there could be possibilities where a theory is correct, but there are unusual circumstances where an individual has an unusual bypass/correction mechanism, but it still helps decide which theories are more likely to be worth investigating.

Yet another variation: even the activities that did trigger PEM never resulted in more than a day or two of feeling lousier. I think food intolerances caused more severe symptoms that PEM did. Microbiome changes (so I assume) caused significant raising of my baseline severity, but could switch off (and on) abruptly. I think that reflects chronic triggering of more severe symptoms, rather than a change in the mechanism that causes the symptoms.

I think the main concern from a research perspective is: if outlier experiences of a disease without a known biomarker deviate very far from the norm, it may actually be very different disease mechanisms for those outliers, not just that there's an unusual bypass/correction mechanism. Either there are multiple ways to end up with a similar symptom presentation, or the main similarity is something very far downstream.

If it is a case of converging at a far downstream mechanism, that downstream mechanism is obviously important and should be accounted for by a good theory--but a theory should not be discounted because the proposed upstream mechanisms don't match the experience of outliers. Using outliers as a litmus test would really only be useful if we already have a known biological mechanism where all cases must converge.

Also not doubting your experience nor saying you don't have ME/CFS, just cautioning against using more uncommon experiences as a metric for gauging which theories are worth investigating.