Gordon · Canadian journal of physiology and pharmacology 2004 · narrative review · n=?

The resilience of the size principle in the organization of motor unit properties in normal and reinnervated adult skeletal muscles.

Cited 98 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review of basic physiological mechanism and animal experimental models without human clinical data.

PubMed 15523522 · doi:10.1139/y04-081 · record verified 2026-08-29

What was done

This review evaluates experimental studies addressing the mechanisms of Henneman's size principle in normal adult skeletal muscle and following nerve injury and surgical repair (self-reinnervation or cross-reinnervation). It analyzes structural and functional parameters, including motoneuron size, muscle fiber cross-sectional area, specific force, direct anatomical enumeration of innervation ratios (muscle fibers per motoneuron), and the effect of imposing uniform daily neuromuscular activity via synchronous motor unit activation.

What was found

The abstract provides no numerical data, sample sizes, or statistical significance values. Directionally, it reports that the relationship between motoneuron size and muscle unit size is lost immediately after nerve injury and repair but recovers over time in both self- and cross-reinnervated muscles. This rematching is driven by size-dependent branching of regenerating axons rather than changes in muscle fiber area alone. Additionally, applying identical, synchronous daily activation to all motor units did not disrupt the normal size-dependent matching of motoneuron size to muscle fiber numbers per unit.

Why it matters

These observations indicate that intrinsic size-dependent axonal branching governs motor unit reorganization after peripheral nerve repair, preserving the foundational architecture required for size-ordered recruitment and smooth force gradation during movement.

Limits

The abstract describes a narrative review of animal or physiological models without detailing species, sample sizes, experimental timelines, or quantitative effect sizes. Findings rely on mechanistic reasoning and cannot be directly translated to human clinical nerve repair without dedicated clinical trial data.

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