Overtraining syndrome (OTS) as PEM for healthy people?

It took 9 days this time to recover from a long trip, a bit longer than usual: 8 hours spent lying down, then 5 and then finally back down to 2-3. Now that I got my brain back, I thought I'd throw this one up for discussion even though there doesn't seem to be much interest in overtraining syndrome (OTS) in ME/CFS community. It is however of interest to me since I developed ME/CFS after repeated episodes of OTS.

It was my annual therapy trip. I rarely suffer PEM when I live on the road these days, so it became my therapy. I'm also more exertion-tolerant when I'm in a new place where I can wander about, so I often combine the two together and make a cross-country trip to NYC. I ended up spending 2 months walking all over NYC exploring the city and looking for an apartment. On the way back, I stopped at national parks and forests for hiking and backpacking.

I got to Phoenix late in the afternoon, but I still had a little bit of sunlight left. As usual, I got greedy and over-reached: I decided to squeeze in a hike up Superstition Mountains. I practically ran up the hill for 1.5 miles so that I could get to the cave before it got too dark to see, and then came down on the pitch-dark trail. The next a few days, my performance drastically shrank. I struggled to walk 5 miles on flat when I was able to hike 13-15 miles up and down the mountains in prior days. It happened a few times before and I've been calling it PEM. But it also occurred to me that it fits the classical definition of overtraining syndrome: dramatically reduced performance and mood change.

OTS after an athletic over-exertion as a form of post-exertional malaise seems to make an intuitive sense. Except that it happens at much higher threshold, obviously since healthy people don't get knocked out for days after a minor household work. It's just that ME/CFS people are super hypersensitive to exertion, or whatever exertion produces, that they keel over much sooner. And they constantly struggle because the sickness smolders rather than getting snuffed out when PEM is over, as it does when OTS is over. Again, ME/CFS people are super duper sensitive, that they could be reacting to a tiny bit of exertion-byproduct that are around constantly.

That is my unified theory of OTS, PEM and ME/CFS anyway. I think researchers should pay more attention to OTS as it may hold a clue or two for ME/CFS. Nobody calls athletic OTS a functional disorder, so unifying OTS and PEM may also make people, at least some of them, think twice before giving ME/CFS patients an effort preference test.

 

The first problem is that OTS doesn't seem to have a very good definition. Some authors seem to define it as undergoing hard training without adequate rest and the developing a range of unpleasent symptoms that hinder performance, whilst others seem to define it as a plateauing or decrease in physical performance when training loads can't be handled https://journals.lww.com/nsca-jscr/...g__a_review_of_the_signs,_symptoms_and.6.aspx. In most definitions the symptoms described are very different to those described to PEM (elevated resting heart rate, changes in blood pressure, weight loss, excessive thirst, burnout etc none of which are associated with ME/CFS).

How in your case would you differentiate OTS from overreaching (vaguely defined as hard training that decreases subsequent training performance but eventually after a period of rest or detraining leads to higher than previous levels)? Additionally there can be many things that explain a reduced physical performance following exertion none of which would have to do anything with OTS which has a more specific definition, similar to how PEM has a different somewhat specific definition. What about the experience you describe here would make it OTS specifically?

I think generally, unless done with lots of ingenuity, it is rather hopeless to describe something that isn't well understood in terms of something else that isn't well understood. In a sense, a unifying theory is supposed to explain everything fully, rather than to group together things one hasn’t fully understood. One major difference between OTS and ME/CFS and PEM seems to be that the solution presented to OTS is simply to adapt your training regimen. We know that that doesn't work for ME/CFS and PEM otherwise they wouldn't exist anymore as people would simply have found a way to adjust their regimen. If one was to equate PEM to “OTS for people with a much lower threshold” it would appear to me that the whole concept of OTS would anyways become rather irrelevant to ME/CFS as one would just try to figure out the pathology that leads to such a difference in threshold and fix that?

Does it matter much what one calls something when the solution that is commonly presented for it is to simply adjust the training regimen which can be suggested to not work for ME/CFS?

 

There are a couple of athletic phenomena that could share some similarities with ME/CFS.

Over trainign syndrome is one: My understanding of this term is it refers to a long period of feeling weak, perhaps months or weeks of reduced performance that is alleviated only by rest. A sort of temporary pseudo-mecfs. I'm extra interested in that because my own mecfs came on at a time when I was doing some very big athletic efforts, and then I caught a virus.

The other athletic phenomenon is delayed onset muscle soreness. The delay in timing is very similar to what we describe in PEM, athough the symptoms are much more tightly circumscribed: local pain ratehr than systemic everything.

To me the delayed onset in PEM is a giant clue that should be the main thing we are looking at. I guess the issue is that the medical system finds a signle blood draw conveinent, a provocaiton and longitudinal study is very expensive. We really need to have mdoel that let scientists move to the bench and away from in vivo work.

And when it comes to overtrainign syndrome, that is also hard to study because the onset is unpredictable.

 

Overtraining/overreaching syndrome is relatively rare compared to post-viral syndrome (since its prevalence is usually sports-related), and it usually resolves in days or weeks. (If it doesn't, it becomes reclassified as ME/CFS.) It doesn't have public health implication unlike ME/CFS or Long COVID in other words, so there probably wasn't a lot of effort to rigorously define it outside of sports medicine. If you think about it, it's not that different from the early days of ME/CFS till 1994 definition, as flawed as it was, attempted define it.

I think this is similar to Long COVID that includes anything and everything left over from COVID. OTS may include any/every effect of over-exercising, but it definitely also includes ME/CFS-like subsets.

Personally, I'd define overtraining/overreaching syndrome as drastically reduced physical performance and mental changes unexplained by other factors. That's the parts relevant to ME/CFS, not elevated HR or such, which could be the result of the body working extra-hard to recover. To me, the experience is as distinct as PEM: you know it when you have it. Mine actually includes blacking out. I see stars when I try to push through it.

Same underlying mechanism would unify phenomena. I'm proposing that OTS and PEM (and therefore ME/CFS since I think PEM is the essence of ME/CFS) share the same underlying mechanism, just at different threshold level.

Isn't that same as pacing? At least that is my understanding. I think a more typical recommendation is complete rest, which is same as the solution for PEM.

I don't quite understand what you are saying here. But I'm saying that the pathology that leads to such a difference in threshold could be the key. Why are we keeling over after a minor household work when it takes trail-running 2 days in a row for healthy people? If we figure that out, we may figure out ME/CFS.

 

I've been suspecting some parallel for a long time too. There was a paper that said PEM is not DOMS because they didn't find micro-tear in muscle biopsy. But it's quite possible that the same process happens for lower-level exertion even if there is no micro-tear. Inflammatory cytokines may shoot up twice high the day after a minor exertion rather than 100 times high as it does after maximal exertion, for example. The delay and duration of typical PEM could be explained rather nicely by the hypersensitivity to that low-grade inflammation.

The Effects of Physical Activity on Serum C-Reactive Protein and Inflammatory Markers: A Systematic Review | Journal of the American College of Cardiology studied acute response to strenuous exercise by drawing blood every hour after a maximal pedaling. What was striking to me was that the response matched the waves of post-exercise fatigue that I've been seeing: 30 minutes later, 2 hours later and the next day. It's possible that I was seeing what I wanted to see. But I've read some accounts of similar waves by other patients before.

 

My understanding is that DOMS only affects the affected limbs. This is not the case in delayed PEM which affects all the unused muscles- weakness, fatigue et

 

Yes, DOMS is a local symptom. But the same exercise-response that leads to DOMS could be precipitating PEM in ME/CFS.

 

It does appear to be that way a bit at least looking at the literature. But maybe similar to how we can see that Long-Covid is a meaningless definition for pathological research there are possibly exercise scientists out there who also have a more meaningful definition.

From what I can see that is not how tends to be defined or at least most definitions focus on there being a specific training phase (typically of several weeks). That is why I'm a bit confused by your above example (of going on a one day walk) and also the comparison to ME/CFS (because there's no training phase in ME/CFS). That is to say I don't think anybody would call it overtraining syndrome if someone didn't follow a specific training plan that essentially didn't lead to the desired output and instead just did something one day and feels worse (in some way or another) with worsened performance on the same task in the following days (which can be explained by thousands of different things).

No, the adaption doesn't have to be pacing (or some form of reduction in training), whilst for some the recommendation might be complete rest (as for PEM), for others it might simply mean following a different training regimen (for instance polarized training, which might very much follow a graded exercise regimen, more zone 2 training, training different muscle groups on different days, doing lactacte threshold testing and developing a training program according to laboratory values etc, none of which would have anything to do with reducing the training load per day or only training as much without feeling worse in the following period, which would probably be more similar to pacing).

 

Furthermore repeated DOMS tends to only make healthy people fitter, sort of the pinnacle of GET, whilst the opposite appears to be the case for ME/CFS, the PEM threshold doesn't increase just because PEM was previously induced nor does performance increase after repetitive induction of PEM. Apart from that, exertion whilst experiencing DOMS (whilst experiencing muscles aches following a heavy day of exercise) is possible and even bread and butter for many competitive athletes, whilst pwME report the opposite about PEM and I don't think that can be in any way explained by the purely local nature of DOMS vs more global nature of PEM. I think it would have to involve something else entirely.

 

I can experience delayed PEM without exertion just from sitting upright and talking too much the day before. I can not lift my arms because they are too weak and I have chest pressure. It can take 2-3 days to recover.

 

Hi. I made a hypothesis video which you can find on the following link-

https://www.s4me.info/threads/me-hypothesis-noradrenergic-neuron-dysfunction.40280/

At 8.40 in the video I discuss overtraining syndrome. The idea is that there is a problem with regulating extracellular norepinephrine which leads to postsynaptic adrenergic receptor desensitization and downregulation in response to exercise.

 

And my/our interest would be how OTS/LC intersects ME/CFS rather than managing/researching OTS/LC themselves. If we are to wait for satisfactory definition of LC before delving into the intersection, we could wait forever. Likewise for OTS. I think we should just take the portion that is relevant to ME/CFS and jump into it as there could be important clues for ME/CFS in them.

Obviously, they need to define overtraining/overreaching in order to define OTS/NFOS. And that may require specifying the amount of exercise before calling something OTS. In ME/CFS, there also is specific amount of over-exercise that will trigger PEM. Except that the amount is a lot smaller and varies from patient to patient depending on the severity of ME/CFS. As for my cases, they could be in between the healthy and ME/CFS. I just need one day of trail running, not 3 weeks of running 4 days a week, when I'm on the road to provoke "OTS", and 5 min jogging when I'm home to provoke PEM. No, it won't be OTS/NFOS according to the definition even if the symptoms fit. But I'm proposing that there is continuity, or spectrum, with OTS at one end and PEM at the other.

To me, that is still a form of adaptive pacing. Healthy athlete has a lot more latitude than ME/CFS patient. Just switching between one exercise to another could well provide enough headroom to avoid the maladaptive response to excessive exercise. And that's what adaptive pacing is, a way to avoid the response to excessive exertion.

 

I hear you. I can even believe some people experiencing PEM just from being alive and breathing. I believe that is what severely ill people with tubes hanging from their orifices experience. Some people say every activity is exercise; I might even say just being alive is an exercise.

 

A car ride for two hours as a passenger was the worst. All that sensory overload, talking, being upright, going over bumps, cars passing by, and all of sudden I feel dehydrated, stressed, and need to lie down.

 

I would like to reiterate my original post: DOMS and PEM are different. DOMS is adaptive. PEM is pathological. DOMS is local. PEM is systemic. One is a system working. The other is a system failing. That doesn't mean they can't be using similar pathways.

In one the pathway may be working, in the other it would be going haywire. The delay is the clue. There are several biological systems with delays (UPR, antibody production, etc) but this one is sparked by exercise, so it's worth further investigation into any parallels. Among the benefits of such research would be the possibility of funding from outside the me/cfs ecosystem, and the availability of research subjects (as everyone can get DOMS).

 

I get a form of PEM that only affects local muscles - I'm fully bedbound, and if I use my legs a bit for instance to push myself a little way up the bed, or prop them up for about 30 seconds, I can develop shaking in the leg muscles, or a sensation that they are made of concrete, so heavy and sluggish that just laying on my back, it feels as though the weight of them is wrenching my legs off at the hip. Either one of these outcomes can last for months after the exertion.

I also only experience muscle soreness in one muscle: between my thumb and forefinger on my right hand, a muscle I use for pressing buttons and brushing my teeth, etc. This is also the only muscle I experienced pain in when I was milder and still walking and working and dancing.

 

Yes, the thing that I thought made the pathway analogy less fruitful was that I thought it would be possible for someone with ME/CFS to develop PEM without DOMS but also to develop DOMS without PEM. I'm less sure whether the second part has been proven or even is true, but it should be possible to prove or disprove it by doing a very localised exercise that should cause DOMS locally but that shouldn't be too exertive for people on the milder spectrum of ME/CFS to develop PEM (I was thinking of something like repetitive hand-grip strength exercises or something of that sort). Perhaps that would even be a sensible experiment in it's own right, i.e. is it possible to induce DOMS without PEM?

 

I have had DOMS without PEM. From low level activity where I was doing something at an odd angle.

 

And your arm muscles were even sorer the day following that day (since that's how DOMS usually tends to hit)?

I'm guessing one could still argue that the same pathways could somehow be involved but the localization didn't make the phenomenon go haywire or that an additional component is required that is somehow absent in such exercises or something of that sort...