Urbanchek MG1, Van der Meulen JH1, Aydin MA2, and Kuzon Jr WM1. (1) Surgery, University of Michigan, 300 NIB Room 1060, Section of Plastic Surgery, Ann Arbor, MI, USA, (2) Plastic Surgery, Suleyman Demirel University, Isparta, Turkey
Introduction: Skeletal muscle contracts with lower maximal isometric force following neurovascular transfer. The force deficit is not due solely to atrophy as a specific force deficit can also exist. A comparison of the contractile properties of rat muscle single fibers may determine whether the whole muscle force decrements are reflected by the contractile proteins within the myofiber. The hypothesis is: the mean absolute and specific isometric forces for maximally activated single permeabilized muscle fibers from neurovascular muscle transfers show deficits when the number of motor axons available to reinnervate the muscle is limited. Methods: The extensor digitorum longus (EDL) muscle was orthotopically transferred without vascular disruption in the adult rat. Proximal and distal tendons were transected and repaired in all groups. The peroneal nerve was either sham operated (SHAM) or divided and repaired with all (TOTAL) or approximately 30% (LIMITED) of proximal axons included in the repair. Following a 4 month recovery period, whole EDL muscle force was measured in situ at optimal muscle length by supramaximal stimulation through the peroneal nerve. The muscle was removed and bundles of fiber segments were stored in a membrane permeabilizing solution. The maximum calcium-activated force was measured from randomly selected muscle fibers. Results: The whole EDL muscle force was lower for both the TOTAL and LIMITED groups compared to the SHAM and for the LIMITED group compared to the TOTAL group. Estimated “specific” force normalizes force to whole muscle or single fiber cross sectional area (CSA) and thus adjusts for muscle atrophy. Whole muscle specific force for the LIMITED group was lower compared to the SHAM group. Single fibers from the LIMITED group produced less absolute isometric force compared with fibers from muscles from SHAM and TOTAL animals. There was no specific force deficit at the whole or single fiber level for the TOTAL group. After accounting for muscle atrophy, single fibers from the LIMITED group produced 31% less specific force than that produced by SHAM group single fibers. Conclusion: The hypothesis is tenable as muscle fibers from the LIMITED group showed quantitatively reduced ability to generate absolute and specific isometric force. The 31% force deficit observed for the LIMITED group single fibers explains the 32% whole muscle specific force deficit observed for the same group.
This work was supported by the National Institute of Neurological Disorders and Stroke Grant S 34380.