Myostatin (GDF-8) is a TGF-β-superfamily myokine secreted by muscle itself. It binds the ActRIIB receptor, which phosphorylates SMAD2/3; phospho-SMAD2/3 enters the nucleus and represses genes needed for protein synthesis and satellite-cell fusion — an autocrine brake on muscle growth. Resistance exercise activates the opposing pathway (IGF-1/PI3K/Akt → mTORC1), which drives ribosome biogenesis and protein synthesis. Net fiber growth is the balance of the two:
SMAD(t) = Hill( myostatin · (1 − inhibitor) )
mTOR(t) = Hill( baseline + training )
dCSA/dt = k_syn · mTOR(t) − k_deg · SMAD(t) [%/day]
CSA(t+dt) = CSA(t) + dCSA/dt · dt
This 2D-native companion renders the exact same ODE two genuinely distinct ways instead of a camera angle on a 3D bundle: a hex-packed fiber field drawn directly in 2D pixel space (left), where each of 109 myofiber cross-sections is colour-coded live by its own instantaneous growth/shrink direction; and a dose-response phase plot (right) tracing both Hill curves in full — the same sigmoids the 3D model only ever evaluates at one point — with the live operating point marked on each, plus a mass-vs-time strip chart the 3D view has no room to show at all.
- Myostatin slider — baseline circulating GDF-8 level; higher values raise SMAD2/3 signaling and suppress growth.
- ActRIIB inhibitor — models an anti-myostatin antibody or ActRIIB decoy receptor; scales the effective myostatin that can bind, exactly as in the mouse myostatin-knockout and Belgian Blue "double-muscling" phenotype.
- Training stimulus — resistance-exercise intensity feeding IGF-1/Akt/mTORC1 activation; the anabolic counterweight to the myostatin brake.
- Each of the 109 myofibers carries a small individual gain (satellite-cell recruitment variance), so the field thickens or thins unevenly, the way real hypertrophy and atrophy are heterogeneous across fibers.
Real-world relevance: myostatin-null cattle (Belgian Blue, Piedmontese) and a documented human infant with a myostatin-pathway mutation show ~2× muscle mass. Anti-myostatin/ActRIIB biologics are in clinical development for muscular dystrophy, sarcopenia and cancer cachexia — this is the exact signaling arithmetic those drugs are designed to shift.