I agree I think the issue here seems to be one of feedback. I think it's been proven that the mitochondria are fully functional in people with CFS/ME once the mysterious blocking agent is removed?
If the mitochondria have switched to producing ATP from fatty acid and amino acid etc then does this mean that the muscles glycogen stores are also defunct? It's probably not an either or thing I'm guessing more an efficiency variance?
When glycogen stores are depleted in normal people they get fatigued, rest and then recover once they lay down more glycogen from the CHO in their diet up until a glycogen saturation point. This I belive has a feedback loop to insulin release etc. When fully topped up they can resume their activity and the fatigue goes away
In our case the glycogen stores are presumably already mostly topped up since we haven't used them we just can't keep up with just fatty acid and amino acids we've got shunting around. hence there must be a shut down mechanism/feedback signal to encourage us to rest rather than start digesting muscle and fat tissue for energy ( starvation). I think with the amount of fat I've laid down that would be a long time, but the signal is quite persuasive.
This would explain why PEM can occur after large burst of activity (aerobic or sudden heavy lifting etc) or equally if you keep on going for longer than your body can supply.
I'm not sure if this gels with what's been said. It does make me wonder whether the cell danger response also causes the ongoing problems and that slowly other systems start getting confused as it goes on too long (endocrine, circulatory, digestion).
Sorry this is a bit off topic and a bit rambley with a lot of assumptions....but it would be interesting to have a marker for glycogen depletion fatigue vs what we have if that is any different.
If the mitochondria have switched to producing ATP from fatty acid and amino acid etc then does this mean that the muscles glycogen stores are also defunct? It's probably not an either or thing I'm guessing more an efficiency variance?
When glycogen stores are depleted in normal people they get fatigued, rest and then recover once they lay down more glycogen from the CHO in their diet up until a glycogen saturation point. This I belive has a feedback loop to insulin release etc. When fully topped up they can resume their activity and the fatigue goes away
In our case the glycogen stores are presumably already mostly topped up since we haven't used them we just can't keep up with just fatty acid and amino acids we've got shunting around. hence there must be a shut down mechanism/feedback signal to encourage us to rest rather than start digesting muscle and fat tissue for energy ( starvation). I think with the amount of fat I've laid down that would be a long time, but the signal is quite persuasive.
This would explain why PEM can occur after large burst of activity (aerobic or sudden heavy lifting etc) or equally if you keep on going for longer than your body can supply.
I'm not sure if this gels with what's been said. It does make me wonder whether the cell danger response also causes the ongoing problems and that slowly other systems start getting confused as it goes on too long (endocrine, circulatory, digestion).
Sorry this is a bit off topic and a bit rambley with a lot of assumptions....but it would be interesting to have a marker for glycogen depletion fatigue vs what we have if that is any different.