Background: We developed a single stretch injury model to create damage near the musculotendinous junction\n(MTJ) of the gastrocnemius muscle in mice. Our hypothesis was that magnitude of muscle injury could be\ncontrolled by stepped shortening of the Achilles tendon (AT) prior to a lengthening contraction. Increased\nshortening would result in a greater isometric torque deficit and morphological damage 24 hours post-injury.\nMethods: Sixteen mice were randomly assigned to sham or injury predicated on stepped increases in AT\nshortening. The AT was exposed and placed in a customized stainless steel roller-clamp system to achieve a specific\nlevel of shortening; 0 mm (resting length), 0.7 mm or 1.4 mm. Plantar flexors were stimulated to tetany with a\nneedle electrode and then actively lengthened at 450�°/sec from neutral to 75�° of dorsiflexion. Passive and isometric\ntorques were measured pre- and immediately post-injury. Isometric torque was measured again 24 h post-injury.\nPeak isokinetic torque was recorded during eccentric injury.\nResults: Injury resulted in decreased passive and immediate absolute isometric torque only when induced with AT\nshortening. The percentage of pre-injury isometric torque was significantly lower in the AT shortened groups\nimmediately and 24 h post-injury, but was unaffected by the level of shortening. Relative isometric torque deficits\nwere noted in the 0 mm group only 24 h post-injury. Peak isokinetic torque during injury was similar in all groups.\nHistological evaluation 24 h post-injury revealed increased morphological damage near the MTJ in the AT shortened\ngroups.\nConclusion: Single stretch with AT shortening created morphological damage near the MTJ and isometric torque\ndeficits immediately and 24 h post-injury, but the magnitude of damage could not be titrated with stepped\nincreases in AT shortening. This model provides an opportunity to utilize transgenic mice in order to elucidate\ninflammatory mediators that promote regeneration and inhibit fibrosis in order to optimize therapeutic interventions\nfor complete functional recovery.
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