title: Correlation between biomechanical and structural changes during the regeneration of skeletal muscle after laceration injury.
abstract: A standardized and reliable model for muscle laceration injuries was developed. The biomechanical and morphological changes during the process of muscle repair after injury were analysed, and the reproducibility of the methods was evaluated. The soleus muscles of Sprague-Dawley rats were completely transected and were allowed to heal for 5, 7, 10, 14, 21, 28, or 56 days, when the muscles either were pulled to failure to measure different parameters of tensile strength or were removed for morphological analysis. During the repair process, the regenerating myofibers penetrated into the connective-tissue scar and formed new myotendinous junctions, thus restoring the functional continuity across the muscle stumps. The muscle atrophied significantly during the recovery period. Mechanical failure occurred in the scar until day 10, and thereafter it occurred within myofibers. Until day 10, the failure load, strain, and specific energy increased to as much as 46, 59, and 36% of the control level, respectively; thereafter, there were only minor changes. Stress (tensile strength per cross-sectional area) reached 86% of the control level by day 21 and further increased to as much as 96% of the control level until day 56. These results indicate that the scar becomes stronger than muscle within 14 days; thereafter, the weakest point is the atrophic muscle. The fact that the stress value was most rapidly normalized suggests that, qualitatively, the regenerated muscle had virtually regained its pretrauma strength by day 56 and that the low values of failure load, strain, and specific energy were mainly due to atrophy of the muscle. Thus, further increase in the tensile strength of the regenerated muscle-tendon unit may require active exercise to reverse muscle atrophy.
authors.affiliation: Medical School and Institute of Medical Technology, University of Tampere, Finland. blmioi@uta.fi
authors.forename: M
authors.initials: M
authors.lastname: Kääriäinen
authors.forename: J
authors.initials: J
authors.lastname: Kääriäinen
authors.forename: T L
authors.initials: TL
authors.lastname: Järvinen
authors.forename: H
authors.initials: H
authors.lastname: Sievänen
authors.forename: H
authors.initials: H
authors.lastname: Kalimo
authors.forename: M
authors.initials: M
authors.lastname: Järvinen
mesh_terms: D000818:Animals; D002921:Cicatrix / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D008297:Male; D018482:Muscle, Skeletal / Q000293:injuries* / Q000473:pathology / Q000502:physiology*; D009210:Myofibrils / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000502:physiology*; D015203:Reproducibility of Results; D013718:Tensile Strength; D016474:Weight-Bearing