But the same is true with someone who trained heavy for most of his training life. Once he performs higher rep training, hypertrophy ensues since the CNS is no longer in a rep range that’s neurologically efficient. Ed Coan is a perfect example of this phenomenon.
I’m not sure I understand… if you do higher reps you stimulate fibers that are stimulated by low reps anyways - type 1s and type 2as since their recruitement threshold is lower and the intensity is high -, so what does it change? Maybe the CNS is less effective in that range but what matters for hypertrophy is just that the fibers be stimulated to receive a TUT.
What’s more, you increase the TUT of the type 1s and type 2as, but at the same time you decrease the load very much. So how can you be sure that those fibers are more damaged in the end?
Valid questions you asked. In fact, I was going to delve into what you mentioned, but I was pressed for time. Here goes.
First off, heavy training primarily recruits FF motor units that possess Type IIB fibers. FFR motor units that possess Type IIA fibers also come into play (as you mentioned). But the primary focus is on Type IIB muscle fibers when you perform heavy, short-duration (<10s) sets. But, if a trainee primarily stimulates these fibers through his training life, hypertrophy gains will be subpar. Why? Because Type IIA fibers also have growth potential. Since they aren’t preferentially recruited with heavy, short sets, then they don’t get maximum stimulation. For maximum stimulation of Type IIA fibers, you must also hit the higher rep ranges.
This phenomenon isn’t solely based on “muscle damage,” instead it’s based on preferential recruitment of various motor unit pools for complete hypertrophy.
I mentioned Ed Coan because he experienced newfound hypertrophy once he switched over to higher rep training. The reasoning is based on my explanation.