It is snippets like this that cause me to devalue the rest of your posts. You say things with such certitude, but on fronts I know about you leave out quite a bite of information. I would say many times knowingly you leave it out to prove your point.
For instance, most guys that bench over 400lbs are on steroids - were you then?
SteadyGains, you’re free to attach whatever “value” you want to my posts. But your implication that I “knowingly” deceive with my posts is unwarranted balony.
No, I’ve never used steroids.
Did you currently maintain your weight or weigh near as much you did then?
I’m heavier than I was when my max was 180 (172 lbs BW), but lighter than when I hit 435.
Gains equating to strength and size are two different things - correct?
Agreed. It’s possible to gain more size from bodybuilding-type training, and affect mostly sarcoplasmic hypertrophy. Conversely, lower-rep, lower-volume heavy training usually leads more to myofibrillar hypertrophy. I was merely using them in a decompensation paradigm.
The bench is one of the most complicated lifts a normal lifter (non-Olympic lifter) will do. Coordination can easily be 50 to 100lbs of the lift.
While you’re correct about the extreme complexity of the Olympic lifts, I totally disagree with you regarding the bench - which is one of the most simple compound exercises there is - far simpler than power cleans (which football players routinely do), proper barbell squats, etc.
I agree with your comments about vascular increases (for example, a person develops about 1/4 mile of extra capillaries for each additional lb of fat they gain). But I don’t believe you’re asserting that PE gains are merely the result of extra capillaries.
I did more searching about hyperplasia - as I’ve been away from the iron game for a long time. But, the consensus seems the same: muscular hyperplasia has not yet been “confirmed” in humans. There are various instances of other types of hyperplasia in humans, but theses are associated with pathological conditions (illnesses, tumors, disease, etc.).
Also, you wrote, “…Notice how shear stress (stress parallel to the vessel) can increase vessel diameter.”
Yes, I agree with you! In fact, that’s how I explain the EtP model of girth increases (tissue deformation via internally-invoked stressors). Increasing “vessel diameter” is not a model of mitosis, it’s more akin to the model of deformation.