Maximal handgrip strength can predict maximal physical performance in patients with chronic fatigue, 2020, Jammes et al

Skeletal Muscle Weakness Often Occurs in Patients with Myalgic Encephalomyelitis / Chronic Fatigue Syndrome ME/CFS

https://www.scientificarchives.com/...phalomyelitis--chronic-fatigue-syndrome-mecfs

 

Hope this is the right thread to post this information (feel free to move it moderators)
copied to the News from the Netherlands thread.

 

Interesting. From personal experience it would probably be relevant, I don't know how generalizable it would be. I actually have to pace my self-massages, usually focused on legs and neck and shoulders, because after 10-15 seconds I simply can't go on, my muscles burn and basically can't apply any force anymore. They feel tingly and weak (and I feel overall a bit weak too), I can't even make a solid fist afterward (though that's pretty common). It usually lasts a few minutes but I don't do repeats so I don't know how well this could apply in a standardized test.

Definitely worth trying. Fatigability is much more accurate than fatigue. The description that some have brought forward, of an illness where you can rather easily lift 20kg once but not lift 2kg 10 times is much more realistic to any tests using a single measure. Force is still mostly there, it's resistance and endurance that are gone.

 

If handgrip strength is reduced on the second day, it strongly suggests central fatigue due to reduced cortical excitability. Which in turn is usually due to inhibition due to feedback from muscle afferents or reduced adrenergic drive.

 

A bit of a tangent, but I believe this might fit with some of my ME illness experiences.

No invigorating effects from exercise, reduced resting and maximal heart rate in spite of deconditioning (secondary to ME), panic attacks with mild ME that dissipated as illness turned more severe, stimulants producing no or paradoxical effects. Think those could be related via the same mechanism?

Always intuitively figured those were adrenergic problems, but I never had the biomedical knowledge to properly expound on the thought. Unfortunately, I found it a lot harder to coerce my doctor into taking a brain biopsy, to confirm that it's a central problem rather than something in the periphery, than into doing bloodwork.

 

I was actually suggesting more of the former (afferent stimulation) than the latter.
But low resting heart rate can be due to elevated parasympathetic activation of the vagus nerve innervating the sinoatrial node (the 'pacemaker') (though there is obviously a balance between parasympathetic and sympathetic activity).
Increased sympathetic activity has several sources - the baroreflex for example, to maintain the balance between blood pressure and flow. If you have impaired blood pressure regulation, then you may have a peripheral neuropathy along these lines.

There is also key coupling between respiratory drive and motor drive - which is in part regulated by sympathetic nerve activity and chemoreflex sensitivity. The obvious consequence being that retarding the motor drive (while maintaining the same ventilatory rate) will lead to higher oxygen availability for a given motor drive, hopefully leading to less variation in the force output of the motor units (due to metabolic factors) and thus less hysteresis in cortical drive for a given force output.

The heart rate in turn follows the change in ventilation rate (with a little bit of latency). I guess I should also mention the other key sympathetic response that leads to hyperventilation in response to low blood PH (due to metabolic reasons at high workrates - 90% of VO2Max), known as the respiratory compensation point (or the second ventilatory threshold) triggered due to chemoreceptor feedback.