Failure to fully restore contractile function after denervation and reinner
vation of skeletal muscle engenders significant disability in patients suff
ering peripheral nerve injuries. This work tested the hypothesis that skele
tal muscle denervation and reinnervation result in a deficit in normalized
power (W/kg), which exceeds the deficit in specific force (N/cm(2)), and th
at the mechanisms responsible for these deficits are independent. Adult Lew
is rats underwent either transection and epineurial repair of the left pero
neal nerve (denervation-reinnervation, n = 13) or SHAM: exposure of the per
oneal nerve (SHAM, n = 13). After a 4-month recovery period, isometric forc
e, peak power, and maximum sustained power output were measured in the left
extensor digitorum longus (EDL) muscle from each animal. Isometric force m
easurements revealed a specific force deficit of 14.3% in the reinnervated
muscles. Power measurements during isovelocity shortening contractions demo
nstrated a normalized peak power deficit of 25.8% in the reinnervated muscl
es, which is accounted for by decreases in both optimal velocity (10.5%) an
d average force curing shortening (13.7%). Maximum sustained power was simi
lar in both groups. These data support our working hypothesis that both who
le muscle force production and power output can be impaired in reinnervated
muscle and that the relative deficits in power output exceed the deficits
in force production. The mechanisms responsible for the deficits in force p
roduction appear to be independent of those that result in changes in peak
power output. The measurement of muscle power output may represent a clinic
ally relevant variable for studies of the recovery of mechanical function a
fter motor nerve injury and repair. (C) 1999 Academic Press.