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.
Shu
Bin
B
Department of Rehabilitation Medicine, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China. shubin1017@163.com
Shen
Yue
Y
Wang
Ai-min
AM
Fang
Xiang-qin
XQ
Li
Xiang
X
Deng
Hao-yue
HY
Yu
Zi-qin
ZQ
D000135:Acid Phosphatase / Q000032:analysis; D000251:Adenosine Triphosphatases / Q000032:analysis; D000818:Animals; D001696:Biomechanical Phenomena; D008058:Dihydrolipoamide Dehydrogenase / Q000032:analysis; D003576:Electron Transport Complex IV / Q000032:analysis; D005969:Glutamate Dehydrogenase / Q000032:analysis; D005993:Glycerolphosphate Dehydrogenase / Q000032:analysis; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D008291:Malate Dehydrogenase / Q000032:analysis; D018482:Muscle, Skeletal / Q000293:injuries* / Q000473:pathology / Q000502:physiology; D011817:Rabbits; D013385:Succinate Dehydrogenase / Q000032:analysis
D005993:Glycerolphosphate Dehydrogenase; D007770:L-Lactate Dehydrogenase; D008291:Malate Dehydrogenase; D013385:Succinate Dehydrogenase; D005969:Glutamate Dehydrogenase; D008058:Dihydrolipoamide Dehydrogenase; D003576:Electron Transport Complex IV; D000135:Acid Phosphatase; D000251:Adenosine Triphosphatases