Acute and delayed response to resistance exercise leading or not leading to muscle failure (2016) Fernando Pareja‐Blanco et al

Subtropical Island

Senior Member (Voting Rights)
This is not a study of ME/CFS at all (mods please move if it’s in the wrong place).

I’m interested because of the time factor in the study: they studied physiological effects of exertion over time (6hrs, 24hrs, 48hrs) in relation to level of exertion (defined in proportion to failure = max exertion) for healthy men.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/cpf.12348

Just checking if anyone already has access to this? in order to see if the change over time after the greater intensity exertion follows a different curve/form than the lesser exertion (or if it’s a similar curve but with greater amplitude leading to the longer recovery).
Unfortunately it’s only 10 men. But there is a range of measures taken.

I think it’s important for us to really understand the effects of exertion over time in healthy people - to see if PwME are different in nature or degree.
 
It’s probably obvious that I’m new to really looking into exercise physiology.

I found this article (I’m having a very good reading day) quite interesting:
https://www.painscience.com/articles/delayed-onset-muscle-soreness.php

It’s about DOMS = delayed onset muscle soreness (generally in active healthy people) and essentially talks about how little we do know about this part of our physiology, and a lot of the misconceptions still floating about.

Delayed Onset Muscle Soreness (DOMS), AKA “muscle fever,” is the muscle pain and weakness that starts up to a day after unfamiliar exercise, peaking up to two days later. The strongest trigger is a lot of eccentric contraction (e.g. quadriceps while descending). DOMS is much weaker after the next workout, but the first bout can be so fierce that people avoid starting valuable exercise programs, especially strength training. It’s worse for some people due to genetic factors and other biological stresses (especially sleep trouble).

Medical science can’t explain DOMS, let alone treat it. Many athletes believe that massage helps, but that’s not what the evidence shows. And many take ibuprofen as prevention, but that doesn’t work either. Drugs will only take the edge off the pain. The only promising treatments are heat and Indian food (curcumin), but not confirmed. Excessive DOMS may also be a symptom of other health problems, some of which can be treated, most notably vitamin D deficiency and insomnia.

DOMS is probably not caused by micro-trauma — a popular old idea — although it might be a mild form of “rhabdomyolysis,” which is caused by mucle proteins spilling into the blood. Some kind of “metabolic stress” may be a more likely culprit, and yet there is no clear link between DOMS and any specific biological marker (and definitely not lactic acid). There are even clues that DOMS is neurological. Certainly it is not straightforwardly inflammatory: evidence suggests that inflammation is what reduces DOMS pain as you continue to exercise. Mysterious indeed!

So I’m increasingly wondering if we need to wait for sports science to get a good handle on athlete physiology, ...then normal person physiology, ...then sedentary physiology, ...then people with well-understood conditions, ...then ME.
 
NB I know what DOMS feels like for me (when I was fit and healthy and for a few weeks in a remission) and my illness feels distinct from that - and has a lot more symptoms. I’m not confusing the two, just wanting to get a handle on how much we know about normal before we can identify abnormal.
I've thought for a while that research into DOMS may provide insight into PEM, given the similarities in delayed reaction to exertion.
 
I think it’s important for us to really understand the effects of exertion over time in healthy people - to see if PwME are different in nature or degree.
This!

And I would love to see comparison studies between PwME and healthy but severely overtrained athletes. On the face of it there is significant symptom overlap between overtraining syndrome and (exercise-induced) PEM. The question is this: is the mechanism of (exercise-induced) PEM the same as in overtraining syndrome and our problem is that we for some reason get it at a ridiculously low threshold, or are the mechanisms for the two conditions quite different?

Here is a review article on overtraining syndrome. Note how familiar the various hypotheses attempting to explain it sound: there are the glycogen hypothesis, central fatigue hypothesis, glutamine hypothesis, oxidative stress hypothesis, autonomic nervous system hypothesis, hypothalamic hypothesis and cytokine hypothesis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435910/

@Andy, I agree. Studies comparing PwME in PEM with healthy people with DOMS could also provide valuable insights.
 
Back
Top Bottom