Abstract

0055 Quantification of skeletal muscle damage in response to injurious stretch-shortening cycles (SSC's) would be beneficial in elucidating the effect of different biomechanical exposures on the amount of muscle damage. Purpose: To investigate the effect of stretch-shortening cycle range of motion (ROM) on skeletal muscle damage in rats. Methods: Testing was performed on the dorsiflexor muscles of Sprague-Dawley rats in vivo. Animals (n = 36) were randomly assigned to a long ROM injury group (L-Inj), short ROM injury group (S-Inj), or isometric group (Iso). The injury protocol consisted of 7sets of 10 SSC's at 500°/s. The S-Inj group received SSC's between 70°-120° ankle angle, whereas the L-Inj group received SSC's between 90°-140° ankle angle. The Iso group received equivalent muscle stimulation at 90° ankle angle. Dorsiflexor muscles were stimulated for 2.8 s each set and administered every minute. Rats were sacrificed at 6 and 48 hours post exposure. Following sacrifice, tissue was excised, weighed, sectioned, quick-frozen, and stored at −80°C. Transverse sections (12 μm) were cut, mounted on pre-coated microscope slides, and stained using a routine procedure with Harris Hematoxylin & Eosin. Tissue sections were evaluated on a Leica DMLB microscope. Stereology was used to quantify the degree of myofiber damage in muscle from each group; and, also was used to measure the volume fraction, surface densities, and average thickness of normal myofibers, degenerative myofibers, and the interstitial space. Results: No degenerative fibers were present in the contra-lateral control tissue, Iso group at 6h or 48h post-injury, nor the S-inj and L-inj at 6h post injury. In contrast, there was an increased volume of degenerative myofibers in the S-inj and L-inj at 48h post injury. The volume of cellular interstitium (cell infiltrates) and non-cellular interstitium (edema) increased (p = 0.0082 and p = 0.0053; respectively) from muscle exposed to the S-inj and L-inj at 48h post injury; and, thus the average thickness of the extracellular matrix increased with these groups. Conclusions: Increased degenerative myofibers, cellular infiltrates, and edema occur temporally in response to both S-inj and L-inj. However, a more dramatic increase occurs with the L-inj at 48h as assessed by the increase in volume of cellular and non-cellular interstitium.

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