Clearly then you are not a severe patient.
Two years ago, I was MUCH worse than I am now - sleeping 16 hours a day and brain fogged most of the time. I have been gradually improving, with the use of extensive lab work, to identify a plethora of problems, which match many of the ones the leading researchers have been finding, and applying a variety of treatments to successfully address the abnormal lab results. It has not been easy, but it is possible, with curious doctors and modern treatments, to improve.
One of the first things my doctor did was to test adrenal, thyroid, and sex hormones, which were all severely impacted, and to get me on doses of pregnenolone, DHEA, hydrocortisone, testosterone, estriol, progesterone, T3 and T4.
I fought the hydrocortisone at first, but my doctor made me take it, and it raised me from a sleepy heap in the floor after 20 minutes. It has been a help ever since. However, I have tried taking more when I have PEM and it does nothing.
But for those who are, one-off occasional use of corticosteroids in the way some patients have described may be an enabling approach that allows severe patients to perform vigorous exercise, which in turn may help with conditions like POTS, and may be useful for maintaining general conditioning.
As in my case, it can be a help to improve functioning. But ability to exercise also involves B12, amino acids, oxygen, CoQ10, carnitine, etc.
If we become depleted in these nutrients, our muscles break down. Feeding the body to support the needs for exercise is wise and I believe one thing that is missing from ME/CFS exercise programs.
Perhaps if GET were performed by first giving patients corticosteroids, it would not lead to the worsening of ME/CFS that some patients have reported this exercise regimen results in.
And vitamins, minerals, lipids, antioxidants, and mitochondrial nutrients. DHEA and testosterone are helpful, too.
If your doctors' theory is that ROS generated by mitochondria are the cause of PEM, or a factor in PEM, which is a reasonable theory, then you could perhaps test this theory by taking an antioxidant which directly targets mitochondrial superoxide, the primary ROS generated during mitochondrial operation. Other ROS produced by mitochondria arise as a downstream consequence of the superoxide. In the mitochondria H2O2 is the next downstream ROS to superoxide.
Superoxide dismutase (SOD) is the antioxidant which targets superoxide, but taking a superoxide dismutase supplement like Glisodin is not going to help, as this will not get into the mitochondria, where the superoxide is found.
There is a special SOD that works exclusively in the mitochondria, called MnSOD (aka: SOD2). The spin trap antioxidant
tempol is a potent SOD2 memetic, so taking tempol as a supplement will boost mitochondrial antioxidant capabilities against superoxide. If your theory is right, you might expect tempol to reduce or prevent PEM.
Although you would probably also want to ramp up mitochondrial antioxidants which deal with H2O2, as MnSOD or tempol will breakdown superoxide into H2O2.
This is exactly what we've been doing with a great deal of success. Lipid replenishment therapy has been helpful at repairing damage and increasing my function. NAD+ has been helpful, too.