A hypothesis involving maintenance and restorative processes in ME/CFS

[Hoopoe]

PEM is generally the main cause of disability in ME/CFS and it is typically delayed with respect to the activity that triggered it.

It seems possible that PEM is closely related to maintenance and restorative processes that occur in the body. More activity during the day would lead to more maintenance and restoration work later on. Much of this work is performed at night and the brain coordinates these processes, which include removal of metabolic waste, synaptic homeostasis, memory consolidation, reset of the ANS. Unrefreshing sleep seems like it would fit well with this idea.

PEM may be a form of sickness response that is triggered when brain senses that the repair and maintenance is going badly, and that more activity would dangerously exceed the repair and maintenance capacity. The symptoms of PEM would then force the person to reduce activities to the minimum necessary and to learn how to better stay within their limits. That the recovery from PEM is prolonged seems consistent with the general idea.

We don't know what exactly could be going wrong in the maintenance and restorative processes. As DecodeME suggests it may involve the brain and the immune system. This idea doesn't seem incompatible with a "faulty signal" hypothesis either.

Unfortunately much of ME/CFS research has not studied the biology of patients before, during and after PEM.

I remember there were two papers that did, and which found a post-exercise non-response pattern in ME/CFS patients compared to controls, one in the protein signature, the other I can't remember. I have focused on other things than ME/CFS science in the mean time and can't remember enough to locate these papers. The interpretation was that the usual processes triggered by exercise were blunted in patients.

If this idea lacks detail, it is because I'm an amateur that struggles to come up with something more detailed. I think the idea may have some merit because it focuses on, arguably, the biggest problem and attempts to explain the unusual and characteristic delay of PEM in the simplest way. It's not an attempt to explain everything.

 

[Kitty]

PEM may be a form of sickness response that is triggered when brain senses that the repair and maintenance is going badly, and that more activity would dangerously exceed the repair and maintenance capacity.

Either that, or signals that sign off those processes don't get sent? So there is no damage, no risk of harm, but the production manager can't allow the lighting crew on the scaffolding without a scaff tag.

 

[Hoopoe]

Either that, or signals that sign off those processes don't get sent? So there is no damage, no risk of harm, but the production manager can't allow the lighting crew on the scaffolding without a scaff tag.

The idea is roughly that the brain senses that the maintenance isn't proceeding at the rate that is sustainable with current activity levels and that the only option is to limit further activity and dedicate more time to rest. It achieves this via PEM.

 

[EndME]

In which part of the body do you postulate that repair and maintenance are not happening? Is it something happening in the muscles (say related to T-cells) or something happening directly in the brain (say synaptic homeostasis)? In the first case, is the repair and maintenance system really not working locally or is it perhaps that it's working as it should but some signal is sent that it's not (T-cells are doing their thing inside muscles but the T-cell management team has told the higher ups that they are off duty for the day).

(Edit: I just saw that the last question is what @Kitty already asked, but the answer doesn't quite make sense to me. Why does the body have to produce symptoms of pain, malaise etc if things are not sustainable with current activity levels? This to me sounds like a "lack of ATP theory" but that doesn't make much sense to me, why not just tell the person "have a snickers and I'll keep busy repairing and maintaining"?)

 

[Creekside]

More activity during the day would lead to more maintenance and restoration work later on.

My experience is contrary to this theory. A 40 km bike ride did not trigger PEM, but climbing a few rungs of a ladder did. The difference seems to be straining (causing microtears) muscles in unusual ways rather than usual. The former would trigger a different immune response.

Resting extra-long or having an unusually deep sleep never seemed to reduce my ME or PEM symptoms, nor did shorter or disrupted sleep make those symptoms worse. I don't feel that sleep, or even rest, is closely connected to ME's mechanism.