Surviving replacement muscle stays weak because too few myosin motors become active
Contractile enzyme stateIn surviving replacement muscle fibers, inhibited myosin motors limit force despite adequate activation and adenosine triphosphate (ATP).
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SCOUT 2—molecular enzymology: Surviving replacement fibers retain an abnormally large, slowly recruitable population of enzymatically inhibited myosin motors after inactivity. Neural recruitment, membrane excitation, calcium delivery, and ATP availability are adequate, but too few motors enter force-producing cycles during physiological activation. The persistent state is myosin activation kinetics, not tissue quantity or matrix mechanics. Resetting motor availability restores output and stabilizes SPV_9 without renewal.
Weak graft fibers have normal action potentials and calcium transients but reduced force under matched physiological calcium activation.
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Permeabilized fibers retain abnormal nucleotide-turnover kinetics and delayed force recruitment despite clamped ATP, calcium, and sarcomere length. A validated manipulation of myosin regulatory state normalizes both motor kinetics and force without altering membrane excitability, heteroplasmy, or mass. Normal motor-state kinetics, or failure of verified motor-state correction to restore force, rejects this hypothesis.
In aged muscle-replacement animals, pair attempted movements with selective graft-afferent stimulation while preventing graft contraction during training.
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Correctly phased pairing, but not phase-scram
Graft-specific repetitive-force failure tracks increasing deletion heteroplasmy and impaired oxidative flux within surviving fibers. In a mechanistic arm with a characterized, selectively targetable d
Across pre-illness, post-illness, and rehabilitation assessments, the graft's causal contribution to matched-task torque remains within a prespecified equivalence band, even while whole-limb performan
Post-illness graft fibers show impaired action-potential propagation and a shifted sodium-channel inactivation curve despite preserved motor-axon conduction. Calcium-clamped permeabilized fibers gener