I tend to think we do not strictly have a mitochondrial problem. We have a problem in ramping up mitochondrial function, possibly as Myhill suggests due to limitations on the transfer rate of key substances across the mitochondrial membrane. So this problem in moderate or mild patients probably will not show up at rest, only under challenge. However I think the worst moderate patients and all those severe or worse, probably cannot ramp up enough to do basic chores for most of the time.
When we try to push mitochondria beyond their limits, the first thing seen is lactic acid buildup. If in our case there are substrate limitation, or cofactor limitations, or whatever, then this might damage the mitochondria, or alternatively send a signal to the body that says STOP.
Such limitations fit with the deconditioning hypothesis only under resting conditions. Lying down resting we kind of resemble deconditioned people. As soon as stress is put on the system though, the energy production goes into crisis. This also fits with the CPET studies.
Also there is a possibility of damage to key enzymes in the mitochondria if oxidative stress levels spike. Some have low replacement rates if damaged or destroyed. NO inactivates aconitase (needed to process citric acid for the Krebs cycle) for example, but ONOO destroys it. If destroyed it has to be imported from the rest of the cell, as mitochondria do not make their own aconitase. Folding of aconitase to a useful form requires glutathione. In conditions of prolonged oxidative stress and aconitase damage it would take time to replace it. This is of course only one of many possible mechanisms.