We hypothesized that deficits in the maximal force generation (Po) of muscles observed after repair of injured nerves are caused by lengthening contractions. The specific hypothesis tested was that, compared with control muscle, muscles that have been denervated and reinnervated are more susceptible to a single bout of lengthening contractions and recover less well from contraction-induced injury. In adult rats, the peroneal nerve was divided and repaired with either all (NR=non-reduced) or a reduced number (DR=drastically reduced) of motor axons from the proximal nerve stump included in the repair. Sham-operated animals served as controls. After a recovery period of 4 months, Po of the EDL muscles was measured in situ at optimal muscle length by supramaximal stimulation of the peroneal nerve. The muscles were then subjected to 225 lengthening contractions with 20% strain. Po was re-measured at either 3 days when the Po deficit is maximal or 2 months when the recovery is complete. Results are shown in the Table. Data are means ± SEM; * different from sham (p<0.05). Compared with sham muscles, reinnervated muscles (NR and DR groups) generated a lower Po. There were no significant differences observed in the Po deficit at 3 days between sham, NR and DR muscles. Two months following the contraction-induced injury protocol, sham, NR and DR muscles recovered to pre-injury levels. Based on these data, we reject our hypothesis and conclude that on the whole muscle level, reinnervated muscles are not more prone to a single bout of contraction-induced injury and recover equally well from contraction-induced injury compared with sham muscles.