Dear Wiggo said:
A
My question to you, Almesian, is this: approaching it from an analytical, "correlation is not causation" POV. If muscle fibre types are determined via myosin expression and a change in myosin expression is used as evidence of change in muscle fibre type, is it possible to change myosin expression without changing the fibre type?
But muscle type isn't defined by myosin expression, is it?
It is defined by how the tissue appears under the microscope. I don't know all the staining techniques developed for different muscle types beyond myofibrillar ATPase staining and what pitfalls they may all have.
Maybe they measure myoglobin concentration nowadays, I don't even know.
If you define muscle type based on myosin concentration or the dominant variant of myofibrillar ATPase, then you don't define it based on myosin.
Is is possible angiogenic etc manipulation (?) via EPO usage, not to mention testosterone and HgH could also have an impact on myosin expression without any corresponding muscle fibre type changes?
Anything can be a subtle expression factor without us knowing it. EPO and HGH are triggers for receptors, so who knows what all the tiny elements in the overall cascade are that could affect myosin expression. Nothing is a one way street in gene expression and not to mention it is kind of a psuedo-zero-sum game; one gene is expressed less if another gene is expressed more.
But we know the overall mechanisms of these drugs.
That said, the body does have a mechanism for changing a tiny bit of type I to type II and more importantly to make type I or type II develop out of stem cells. So whatever enzyme or receptor or hormone is involved there, it can be abused someday as a drug. We just know it isn't EPO or HGH.
And when we look at the more straightforward testosterone, we don't even know which all the genes are it promotes and which genes it would never touch.
And we didn't even touch upon the splicing of all these dozens of enzymes involved in metabolism. of glycogen in muscles.
And even so, if this happened in Armstrong, it doesn't explain why it didn't happen in all these other doped up athletes. It isn't even the doping that he measured. All that improvement would mostly come from being able to use more oxygen, not to use it more efficiently because of completely different ratios of enzyme-variants being expressed.
If that is what happens it would require a lot of evidence to substantiate.