Holy nonsequitur batman, I realize people who are not exercise physiologists tend to occasionally oversimplify things from that are but this is on another level. It is a pet peeve of mine when people in the broader medical community think everything related to training is obviously trivial, sorry if this may come off as rant-y or pedantic but we are talking entry-level science that is completely useless due to the most common of mistakes here.
The patients had a history of excessive general and muscular fatigue over one to 19 years but no evidence of neuromuscular disease on clinical, biochemical, histological, or histochemical examinations. Their functional capacity was hampered severely, to the extent that their lives were greatly disrupted.
The term may be a bit colloquial in practical use, but generally muscular fatigueability does refer to the ability to resist changes through repeated use during a given timeframe. If one is reporting 'excessive muscular fatigue' without evidence of disease it is weird since in context it pretty much has to arise from a pathologic problem - high level of fatigueability is expected in untrained individuals and does normally not have any effect on their day-to-day lives. The majority of the western office population is essentially untrained and we do not see them having trouble using computers. The only scientific conclusion I could possibly think of here is that the measurements did not capture whatever was going on (or expectations on how muscle function should be that are way off-base).
...Patients are often told simply to rest, but resting may aggravate the symptoms by causing cardiovascular unfitness. The patients with effort syndromes in this study had muscle that responded normally to exercise even though they experienced fatigue prematurely. This evidence can be used to reassure patients that it is safe to exercise, even though exercising may make them feel worse. Anxiety about tachycardia and breathlessness can therefore be allayed, and the vicious cycle of unfitness and fatigue4 can be broken by carefully and gradually increasing the amount of activity.
I've allowed myself to bold the key sentence in order to highlight precisely where I'd say everything breaks down.
First of all, cardiovascular unfitness to the point of being disabled in daily living situations does not normally arise even from prolonged bed-rest. There is a difference between being able to meet metabolic demands of daily living and sports. Many many many people cannot walk up a flight of stairs without being out of breath who are completely fine going about their lives in general.
A muscle that has an apparently normal response to exercise (which is nontrivial to capture by the way, with training stimuli we can trigger remodeling effects that last days and possibly weeks which are harder to predict than one would think) does in no way, shape or form allow for the conclusion that a human who is reporting symptoms can safely exercise.
Apart from the lack of evidence that it is beneficial or needed to do so in a given patient population, by that reasoning you could tell anyone without a multiple sclerosis type of disease that training is fine for them. Wanna go for a run with a broken hip? Yeah sure, go ahead, your muscles are fine so you're good to go.
Even ignoring that there are quite a few different exercise modalities which all could have different effects, if something makes you feel worse via aggravating a medical condition you might have it is common sense to at least require a solid evidence base before churning out overly broad recommendations.
Stokes et al used a technique of electrical stimulation of the thumb muscle to demonstrate that the muscles of their patients were "normal".
If this is really all they did it is beyond incompetent. No adult human being could possibly be this stupid. If the quoted part above is true I refuse to believe this is anything but malicious intent. Did they even test for different metabolic demands or was it literally just 'hurr durr muscle responds to stimulation so it is working derp'? Theoretically, a muscle can respond apparently fine to external stimulation but not meet demands during prolonged aerobic activity, not function properly under anaerobic conditions, the motor unit could have trouble being innervated for whatever reason which one would not see when using the external stimulation shortcut - and this is just the first batch of things that immediately come to mind while completely ignoring any systemic effects.
Either absolutely no one in the field who recommended exercise based on this paper alone has read it, or worse, they have read it and did not see the jumps in logic as problematic.
Edit: I looked through the paper and no, the thumb muscle stimulation was not everything they did but, in my opinion, that does not save the purported conclusions. The jump from what was measured to what was concluded is gigantic.
I would also argue that the way those measurements were taken ignores what we today would agree on as important features of ME, but this may more be to put the results into context than a failure of the paper per se.
I will not quote the entire paper as I go through it from the top as it is not overly long anyway and am unfortunately unfamiliar with the interpolation technique so I cannot comment on these parts competently.
First of all, I think the slant of the paper is a bit unscientific.
It is stated confidently that bouts of tachykardia during everyday activities stem from poor cardiovascular fitness which is either tautological or unproven in this context (per definition, not going into tachykardia would constitute 'CV fitness' but the way it is worded the more colloquial definition of fitness was probably intended).
Abnormal electrophysiological activity is quoted as occuring through atrophy via disuse as well - again, actual relevant atrophy of muscle tissue requires prolonged and severe disuse when we are not talking about losing glycogen and water storage, so realistically we are talking more about motor units being less efficiently used in conjunction after a period of disuse. We need a lot of tissue atrophy for it to be more relevant than how the tissue is used.
I realize this may be a bit pedantic again and time constraints when writing things up may make it uncomfortable to type out the entire history of every word used (apart from making everything virtually unreadable), but clear thinking tends to lead to clear writing.
Then the definition of fatigue in the context of
exercise physiology [this part is inaccurate, see below] is given and that is all fine and well, but we run into the problem we had with the psychiatric concept of 'recovery' - central fatigue here means mostly lessened neural drive. In the sense that one can measure less neural output. It has no real bearing on cognitive or affective states a person would notice. Peripheral fatigue is usually how well muscles respond to stimuli and gets a bit muddled all the time.
Edit2: Please have a look at post#14 for clarification, I did not even know there was a difference between neurological and other kinds of definitions here. I assumed it was basically the same thing using different words.
Not finding fatigue in this context has absolutely no bearing on people feeling tired or brainfogged or exhausted, these phenomena really just tell you how hard it is to push something at a given moment. Increased peripheral fatigue would usually mean the CNS needs to increase its output to innervate motor units and this can subsequently lead to feeling a bit off if one tries to do that a lot as it has effects on neurotransmitter availability but that is getting off-topic - the point is, you can bench press to failure repeatedly and induce peripheral and central fatigue without having anything that resembles PEM. I can personally attest to this as I have done this pre and post ME onset and it just feels differently, assuming my experiences can be extrapolated (which, again, is not necessarily the case as I may be muddling something, misremembering etc).
Not making all of this very, very clear is the same as not stating psychiatric recovery is meant to communicate 'you are recovered as far as was possible using our approach' - it may be fine when communicating within a field, it needs to be made very clear when talking to a laypopulation. I imagine this aspect has not been harped on too much when this very paper was cited?
I cannot see anything that remotely resembles coherent information on how probands were selected. It is quoted that they had a history of excessive general fatigue (there it is again, here fatigue doesn't mean central/peripheral fatigue at all but the colloquial usage would be required?) but not very much beyond that is mentioned apart from not finding much wrong via traditional testing. Again, this may be fine when one is looking for points to start more research but it makes extrapolating results to patient populations with different and unknown etiological entities impossible.
A pretty standard exercise test panel is run and as far as I can tell this part is in and of itself okay, but I am not confident in my assessment here as I am not up to date at all on how those methods are viewed today. There are limitations inherent in those methods, e.g. everyone always measures quadriceps strength because it is easy to do with available equipment but that obviously does not give clues at how efficiently said quadriceps is used during things like squats. Which is what you want when measuring whether a muscle responds to stimuli, but it does not tell you if you have problems with movements and coordination and so on.
Patients only reaching about 90% of a predicted heart rate does not necessarily mean much since the models used to inform what kind of heart rate would be the proper one are heavily contested. These parts are a bit like measuring inflation for an economic body - it is almost impossible to to completely objectively in the most meaningful way since what you value as being meaningful changes the discussion and several ways may be objectively correct. Being within 10ish %s of a rate reached at exhaustion is actually pretty good to my mind for untrained people (most inexperienced probands subjectively rate their perceived effort as a '9-10/10' when they are objectively at a '7' when looking at actual VO2max as a rule of thumb).
I am missing a short mention of people who are most likely untrained individuals being unable to reach theoretical maxima is to be expected. A number that was thrown around a decade ago was '40-50%' for what a completely untrained individual can use voluntarily from the available motor unit pool. Weakness in this regard is not only not unusual, it is the norm. Like I said, I am not familiar enough with the interpolation or the occlusion methods to comment on them but I would assume this was all done competently in and of itself.
All of this seems to point to the problem not being in the contractility of muscles which is a statement that probably still holds true to this day. I do not know if the conclusion that is has to be a central mechanism if voluntary movement is impaired is completely true but for the sake of discussion I'd say we can assume this to be correct or at least close enough.
It is normal for untrained individuals to be way behind in what can be achieved in a voluntary contraction vs external stimulation, but I've already said that. Considerable variety on repeated testing with normal strength would point to a problem that could be interesting to to research on. I'd look at something something electrolytes first and go from there.
It is completly, entirely, utterly off base to state that exercise is safe for patients with a condition one does not understand based on those few tests.
Just to type up a non-exhaustive list of was
not done here: Prolonged aerobic exercise, looking at responses to increased exercise volume or frequency,
looking at anything on day 2, comparing results on subjectively good/bad days, actual response to training stimulus after weeks&months, reporting changes in any symptoms whatsoever, recording effects of any training intervention in any of the patient population, recording effects of different training regimes, etc etc
All of this is ignoring any problems with study structure (lowish number of probands, how appropriate is the control group really, does doing a couple reps on some quad machine really measure the most interesting things and so on).
It is apparently just assumed that this patient population probably responds to training normally and that training will probably fix something along the lines. Which is an abhorrent response when it is completely unclear where reported symptoms are coming from.
I do want to quote one sentence though:
Great caution is needed in interpreting the results of this study and drawing conclusions about treatment as the findings clearly point to lack of central drive or motivation.
Yeah, well, you know. Saying that it is necessary to be careful when drawing conclusions about treatment and then implicitly stating that the conclusions are obviously to put people through a training regime is a bit saying one thing and doing another. I'd wager any scientist worth his salt would've been intrigued to coax out why people seem to struggle with central drive and why repeated results during strengthtesting seemed to be all over the place. This is interesting. What it is decidedly not is 'yeah well probably something something motivation or other lets just make them somehow train something or other yadda dadda'.
