The effect of reinnervation on force production and power output in skeletal muscle

Failure to fully restore contractile function after denervation and reinnervation of skeletal muscle engenders significant disability in patients suffering peripheral nerve injuries. This work tested the hypothesis that skeletal muscle denervation and reinnervation result in a deficit in normalized power (W/kg), which exceeds the deficit in specific force (N/cm2), and that the mechanisms responsible for these deficits are independent. Adult Lewis rats underwent either transection and epineurial repair of the left peroneal nerve (denervation-reinnervation, n = 13) or SHAM exposure of the peroneal nerve (SHAM, n = 13). After a 4-month recovery period, isometric force, peak power, and maximum sustained power output were measured in the left extensor digitorum longus (EDL) muscle from each animal. Isometric force measurements revealed a specific force deficit of 14.3% in the reinnervated muscles. Power measurements during isovelocity shortening contractions demonstrated a normalized peak power deficit of 25.8% in the reinnervated muscles, which is accounted for by decreases in both optimal velocity (10.5%) and average force during shortening (13.7%). Maximum sustained power was similar in both groups. These data support our working hypothesis that both whole 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 production appear to be independent of those that result in changes in peak power output. The measurement of muscle power output may represent a clinically relevant variable for studies of the recovery of mechanical function after motor nerve injury and repair.