Recruitment × tension, then recovery
The two conditions, and why both are non-negotiable
Motor units are recruited in ascending order of size (Henneman). Full recruitment arrives around 90% of maximal unfatigued isometric force — roughly a 5RM — but effort substitutes for load: take a lighter set close enough to failure and fatigue forces the nervous system to call up the same high-threshold units. That is condition one. Condition two is per-fibre mechanical tension, governed by the force-velocity relationship: during fast shortening myosin heads detach before completing their power stroke, so few crossbridges are bound and per-fibre force is low; during slow shortening they accumulate. Only reps satisfying both count — roughly the last five before failure. Everything else is a fatigue tax paid to arrive there.
How tension becomes protein
Load deforms integrin complexes at the costamere, recruiting focal adhesion kinase. The route onward to mTORC1 is genuinely not closed — the defining finding is that mechanical mTORC1 activation is *insensitive to PI3K/Akt inhibition*, so the growth-factor pathway is not the carrier, and the FAK→TSC2→Rheb chain is a leading proposal rather than settled. In parallel, mechanical stimulation activates diacylglycerol kinase-ζ, generating phosphatidic acid, which binds and activates mTOR directly. Downstream, mTORC1 phosphorylates S6K1 and 4E-BP1, raising translational efficiency, while satellite cells donate myonuclei to support a larger cytoplasmic domain.
So the entire programme reduces to one optimisation: maximise the number of stimulating reps delivered in a recovered state per unit time, without accumulating fatigue faster than you can clear it. Volume, frequency, exercise selection and nutrition are all just levers on that one quantity.