A model for creating a single stretch injury in murine biarticular muscle.

BACKGROUND

We developed a single stretch injury model to create damage near the musculotendinous junction (MTJ) of the gastrocnemius muscle in mice. Our hypothesis was that magnitude of muscle injury could be controlled by stepped shortening of the Achilles tendon (AT) prior to a lengthening contraction. Increased shortening would result in a greater isometric torque deficit and morphological damage 24 hours post-injury.

METHODS

Sixteen mice were randomly assigned to sham or injury predicated on stepped increases in AT shortening. The AT was exposed and placed in a customized stainless steel roller-clamp system to achieve a specific level of shortening; 0 mm (resting length), 0.7 mm or 1.4 mm. Plantar flexors were stimulated to tetany with a needle electrode and then actively lengthened at 450°/sec from neutral to 75° of dorsiflexion. Passive and isometric torques were measured pre- and immediately post-injury. Isometric torque was measured again 24 h post-injury. Peak isokinetic torque was recorded during eccentric injury.

RESULTS

Injury resulted in decreased passive and immediate absolute isometric torque only when induced with AT shortening. The percentage of pre-injury isometric torque was significantly lower in the AT shortened groups immediately and 24 h post-injury, but was unaffected by the level of shortening. Relative isometric torque deficits were noted in the 0 mm group only 24 h post-injury. Peak isokinetic torque during injury was similar in all groups. Histological evaluation 24 h post-injury revealed increased morphological damage near the MTJ in the AT shortened groups.

CONCLUSION

Single stretch with AT shortening created morphological damage near the MTJ and isometric torque deficits immediately and 24 h post-injury, but the magnitude of damage could not be titrated with stepped increases in AT shortening. This model provides an opportunity to utilize transgenic mice in order to elucidate inflammatory mediators that promote regeneration and inhibit fibrosis in order to optimize therapeutic interventions for complete functional recovery.