Because smooth muscle becomes anelastic, due to more collagen deposition.
(Changes in TA tissue could be as much relevant, of course, if not more. But we are speaking of smooth muscle now.).
Smooth muscle hypertrophy is the first step, hyperplasia the second, fibrosis of smooth muscle the least. Going from one step to the next is not unavoidable, but one has to be very careful. The time needed from an organ to another, or a men to another, or even specific circumstances, can vary a lot. A 20y guy in perfect shape in a warm room maybe will not experience any harm from a 3 hours erection; a 50y, obese man, with an incipient diabetis, in cold day could report significative structural changes.
And at the bottom of this all: how increased SM can increase the size of your penis? There is little doubt that the limiting factor will be tunica albuginea. That’s why you don’t see many proofs of gains among edgers, despite all the yada yada.
Thanks very much for posting that link. I do not have time to read it now (I am supposed to be working), but I will read it sometime this week.
What does SM stand for?
I agree that the tunica is probably the limiting factor. I am considering using Verapamil or some other Peyronie’s Disease Meds to soften the tunica and inhibit collagen formation.