Histological, enzymohistochemical and biomechanical observation of skeletal muscle injury in rabbits.

OBJECTIVE

To explore the pathophysiological and biomechanical features of skeletal muscular injury for providing a rational basis for its treatment, prevention and rehabilitation.

METHODS

In 70 adult rabbits, the left tibialis anterior (TA) muscle was stretched to injury, while the right TA muscle served as control. Histological, enzymohistochemical and biomechanical changes were observed on days 0, 1, 2, 3, and 7 after injury. Cytochrome oxidase (CCO), acid phosphatase (ACP), ATPase, succinate dehydrogenase (SDH), malate dehydrogenase (MDH), NADH-diaphorase (NADHD), glutamatedehydrogenase (GDH), alpha-glycerophosphate dehydrogenase (alpha-GPD) and lactate dehydrogenase (LDH) were measured. The examined biomechanical parameters included maximal contractile force, ultimate load, length, energy absorption, tangent stiffness, and rupture site.

RESULTS

Partial or complete rupture of TA muscle occurred near the muscle-tendon junction. There was an intense inflammatory reaction on day 1 and 2 after injury. Endomysium fibrosis and myotube formation were observed on day 3, and developed further on day 7. The activity of cell oxidases (CCO, ATPase, MDH, alpha-GPD, SDH, NADHD and GDH) showed a significant drop from day 0 to 2, and resumed with different levels on day 3. The increment of enzymatic activities continued on day 7 and the levels of NADHD and alpha-GPD reached to the levels of control muscle. Maximal contractile force was 70.17%+/-3.82% of controls immediately after injury, 54.82%+/-3.09% at 1 day, 66.41%+/-4.36% at 2 days, 78.39%+/-4.90% at 3 days and 93.64%+/-5.02% at 7 days. Ultimate load was 85.78%+/-7.54% of controls at the moment of injury, 61.44%+/-5.91% at 1 day, 49.17%+/-4.26% at 2 days, 64.43%+/-5.02% at 3 days, and 76.71%+/-6.46% at 7 days.

CONCLUSIONS

Endomysium fibrosis and scar formation at the injured site are responsible for frequent recurrence of skeletal muscle injury. Recovery of tensile load slower than that of maximal contractile force may be another cause. Whether the injured muscle returns to normal exercise is mainly determined by the tensility on which the muscle-tendon can bear rather than the maximal contractile force.