Progressive Muscle Loss: Dystrophy (Contractile-Contact Fatigue) and Sarcopenia

Two ways muscle loses force, both perturbations of the contractile contact number (§3). Muscular dystrophy is dystrophin-loss fragility: each contraction tears load-bearing contacts, a cyclic fatigue whose rate is set by the reading-frame rule — Duchenne (null) retains only 0.46 of force at the test cycle count versus Becker (partial) 0.85 and normal 1.00. Sarcopenia is a gradual multi-axis ageing decline. Both verified [V].

Dystrophin couples the contractile lattice to the membrane; its loss makes fibres fragile, so a Paris/Basquin law removes contacts per contraction with rate ∝ (1−dystrophin)². The reading-frame rule (Monaco 1988) sets severity, NOT a fit: DMD (null) declines far faster than BMD (in-frame, partial). The loss is structural and NON-recovering, distinct from the reversible metabolic fatigue of T5/T10. Sarcopenia declines max force and fatigue τ together along motor-unit, fibre and endurance axes. Mechanism [V]; reading-frame ordering [L]; absolute timeline/force [O].

Dystrophy: fragility as contractile-contact fatigue

The contractile apparatus is a load-bearing lattice (the same contact-number order parameter as the length-tension test T2). Dystrophin anchors that lattice to the sarcolemma and ECM; without it, the membrane and cytoskeleton are mechanically FRAGILE, so every forceful contraction tears a few load-bearing contacts. That is a cyclic fatigue process — the same Paris/Basquin law used for OA (§12) — with the per-contraction damage rate set by fragility = (1 − dystrophin). The force loss is STRUCTURAL and does not recover on rest, which is what distinguishes it from the reversible metabolic fatigue of T5 and T10.

The reading-frame rule sets severity (no fit)

Severity is CITED from the dystrophin reading-frame rule (Monaco 1988): out-of-frame / nonsense deletions abolish dystrophin → Duchenne (severe); in-frame deletions leave a partial, shortened but functional dystrophin → Becker (mild). Mapping that to a fragility (null ≈ 0, partial ≈ 0.5, normal = 1.0), retained force at the test cycle count falls monotonically as dystrophin falls:

Normal stays at full force (1.00), Becker declines slowly (0.85) and Duchenne collapses (0.46), and the Duchenne trajectory is progressive across contraction count — the documented severity order, reproduced from the genotype rule alone.

Sarcopenia: gradual multi-axis ageing

Ageing muscle loss is different in character: not a fast fibre-tearing defect but a gradual decline along several axes at once — motor-unit dropout (recruitment), type-II fibre atrophy (the contact number) and reduced fatigue resistance (a shorter T5 τ). Scaling all three with an age parameter:

Maximum force falls AND fatigue onsets earlier with age, simultaneously across axes — the sarcopenia direction. The cited direction is ~1 %/yr strength loss after ~50; the absolute force and rate are not fixed by the substrate [O].

What is NOT claimed

For dystrophy the absolute age-at-milestone (loss of ambulation, etc.) is not fixed by the substrate [O]; the reading-frame ORDER and the progressive shape are the result. For sarcopenia the DIRECTION is claimed; absolute force and the rate of loss are [O].

Analgesic lever map (cross-reference)

Exertional and overuse muscle pain carries an L1 and an L2 lever that both lower the crossing rate by DIRECTION, but there is no discrete contact-loss lesion to run the coupled/decoupled cross-check, so it is graded DIRECTION-only (honest partial). See §25 the three-lever threshold logic for the inherited technique (concept DOI 10.5281/zenodo.20733420), and §28 limits / honest partial for the worked lever sweeps. The analgesic axis adds no new physics: pain is a threshold-crossing rate on the same R19 barrier this chapter already uses.