Urbanchek MG1, Van der Meulen JH1, Aydin MA2, Cederna PS1, Eguchi T3, and Kuzon WM1. (1) Surgery, University of Michigan, Section of Plastic Surgery, 300 North Ingalls Street, Ann Arbor, MI, USA, (2) Plastic Surgery, Suleyman Demirel University, Isparta, Turkey, (3) Department of Plastic and Reconstructive Surgery, University of Tokyo, Tokyo, Japan
Reinnervated skeletal muscle generates lower maximal force (P0). As a result of contraction-induced injury, skeletal muscle has an immediately reduced force capacity which is reportedly fully recovered by 60 days. It is unknown whether force deficits following contraction-induced injury are attributable to muscle atrophy and muscle fiber denervation after recovery from contraction-induced injury. The specific hypothesis tested was that, denervated-reinnervated muscle force deficits following contraction induced injury are attributable to muscle atrophy and muscle fiber denervation. Adult rat peroneal nerve was either sham operated (SHAM) or divided and repaired with all (NR- non-reduced) or a reduced number (DR=drastically reduced) of proximal axons stumps included in the repair. Following a recovery period of 4 months, extensor digitorum longus muscle P0 was measured in situ at optimal muscle length by supramaximal stimulation of the peroneal nerve. For some rats this was the endpoint (no injury subgroup). For others muscle testing continued with an EDL contraction-induced injury protocol (injury subgroup) consisting of 225 muscle lengthening contractions at 20% strain. P0 was re-measured at 60 days. Muscle cross-sections were labeled to identify neural cell adhesion molecule, a marker for cell denervation, and fiber denervation was quantified. For reinnervated muscle groups exposed to no injury, both the NR (3261 ± 636) and DR (2590 ± 975) demonstrated force deficits (mN) when compared with the Sham muscle group (3994 ± 346). When the no injury subgroup force was normalized to muscle cross sectional area (CSA) (sP0), the DR group continued to show a sP0 deficit (Sham 283± 30, NR 267 ± 43, DR 233± 60 (kN*m2); however when their sP0 was corrected to eliminate the contribution on denervated fibers, there was no longer a significant force deficit (Sham 293± 31, NR 292± 50, DR 280± 88 (kN*m2). At 60 days post injury, DR group denervated-reinnervated muscles had lower P0 (2522 ± 540 mN) compared with SHAM ( 3608± 485 mN) and NR ( 2767 ± 531 mN) group muscles. Force normalized to muscle CSA (sP0) for the SHAM, NR, and DR groups was 260 ± 86, 221 ± 52, and 208 ± 35 kN*m2 respectively. When injured muscle sP0 was corrected to eliminate denervated fiber contribution, the corrected sP0 (kN*m2) for each group was 210 ± 31 (SHAM), 231 ± 11 (NR), and 239 ± 26 (DR). These preliminary data find force differences following contraction-induced injury attributable to muscle atrophy but not to muscle fiber denervation.