Skeletal muscle reinnervation by reduced axonal numbers results in whole muscle force deficits

Patients sustaining a peripheral nerve injury: will frequently experience r esidual muscle weakness after muscle reinnervation, even if the nerve repai r is performed under optimal circumstances to allow rapid muscle reinnervat ion. The mechanisms responsible for this contractile dysfunction remain unc lear. It is hypothesized that after peripheral nerve injury and repair, a r educed number of axons are available for skeletal muscle reinnervation that results in whole muscle force and specific force deficits. A rat model of peroneal nerve injury and repair was designed so that the number of axons a vailable for reinnervation could be systematically reduced. In adult rats, the peroneal nerve to the extensor digitorum longus muscle was either left intact (sham group, n = 8) or divided and repaired with either 50 percent ( R50 group, n = 7) or 100 percent (R100 group, n = 8) of the axons in the pr oximal stump included in the repair. Four months after surgery maximal teta nic isometric force was measured and specific force was calculated for each animal. Mean tetanic isometric force for extensor digitorum longus muscles from R50 rats (2765.7 +/- 767.6 mN) was significantly lower than sham (408 2.8 +/- 196.5 mN) and R100 (3729.0 +/- 370.2 mN) rats (p < 0.003). Mean spe cific force calculations revealed significant deficits in both the R100 (24 2.1 +/- 30 kN/m(2)) and R50 (190.6 +/- 51.8 kN/m(2)) rats compared with the sham animals (295.9 +/- 14 kN/m(2)) (P < 0.0005). These data support our h ypothesis that after peripheral nerve injury and repair, reinnervation of s keletal muscle by a reduced number of axons results in a reduction in tetan ic isometric force and specific force. The greater relative reduction in sp ecific force compared with absolute force production after partial nerve re pair may indicate that a population of residual denervated muscle fibers is responsible for this deficit.