Repetitive lengthening contractions have been predicted as a mechanism causing injury, pain, and delayed soreness in the hyperactive masticatory muscle. This mechanism was examined by the mechanical lengthening of the contracted superficial masseter (SM) muscle in anesthetized rats. Repetitive stimulation of the left SM to tetanic tension was followed by mechanical lengthening, which stressed contracted muscle. The contralateral muscle was passively lengthened repetitively. Contractile tension in response to a varying frequency of stimulation was measured in pre- and post-lengthened SM muscles. A selective loss of force at all frequencies up to 100 Hz occurred in the muscles subjected to lengthening contractions. Low-frequency fatigue did not occur in SM muscles passively lengthened. All animals recovered without loss of weight or dehydration. They were killed at 24 or 72 h post-lengthening. The SM muscles were collected, and no significant differences were found in mean weight, length, or cross-sectional area when the right and left SM muscles were compared at 24 or 72 h. Two observers independently examined histological secretions of SM muscles and graded the localized inflammatory sites on a scale of 1-4. A non-parametric statistical test was used so that the inflammatory scale for each muscle could be ranked. There were significantly more injured sites in SM muscles subjected to lengthening contractions, compared with the lengthened (but relaxed) SM muscles. The SM muscles of anesthetized rats were internally injured by repetitive lengthening contractions, and they exhibited low-frequency fatigue. These findings support the hypothesis that repetitive lengthening contractions in the masticatory muscle could be a mechanism for the pain and dysfunction of masticatory muscles in humans with certain parafunctional habits.

The etiology of myofascial tenderness and pain of masticatory muscles in humans is difficult to understand. Parafunctional oral habits such as tooth grinding or vigorous chewing are thought to be factors. The objective of this study was to determine if masticatory muscles are susceptible to weakness and injury induced by repetitive, dynamic, forced-lengthening contractions. Results would support the hypothesis that contraction-induced injuries could occur in hyperactive masticatory muscles of humans in response to parafunctional oral habits. Mice were anesthetized and randomly assigned to three groups: non-treated controls, treated by repetitive passive jaw opening, or treated by repetitive isometric tetanic contractions with lengthening by jaw opening. In each treatment group, masticatory muscle injury was evaluated by contractile tension, plasma creatine kinase, and muscle glycogen. Contractile tension was determined at different stimulation frequencies and was significantly decreased 5 min, 4 h, and 72 h after repetitive contraction/lengthening. Plasma creatine kinase was significantly elevated at 4 but not at 72 h post-treatment in mice subjected to repetitive contraction/lengthening. Masticatory muscle glycogen was not significantly different in any groups at 4 or 72 h post-treatment. These results indicate that contraction injuries can be induced in masticatory muscle of mice by forced lengthening contractions which simulate eccentric contractions.