Large forces are the primary mechanism of injury in muscular dystrophy, and muscular dystrophy is especially damaging to type IIB muscle fibers. It was hypothesized that post-tetanic potentiation (PTP) would be down-regulated to prevent damage in Xlinked muscular dystrophy (mdx) mice since PTP increases force and PTP effects are greatest in IIB fibers. PTP experiments were performed on the extensor digitorum longus (EDL) of 50 day old mdx (YM) and C57BL/10 (YC) mice and 10 month old mdx (OM) and C57B1710 (OC) mice. Twitch and tetanic forces were lower in mdx than controls and lower in younger than older mice. Contrary to the hypothesis, PTP was higher in both mdx groups compared to controls. OM potentiated more than any other condition (OM: 29.8%, OC: 23.2%, YM: 21.9%, YC: 17.2%). In accordance with literature PTP increased in the older groups. To explain PTP changes, fiber typing and Western blots for myosin light chain kinase (MLCK) were performed. YM and YC had similar fiber type profiles (2% I, 58% IIX/D and 40% IIB). In accordance with literature but contrary to expected conditions for elevated PTP, OM had a slower fiber type profile (1.7% I, 69% IIX/D and 29% IIB) than OC (0.4% I, 61% IIX/D and 38% IIB). No differences were found in MLCK expression. It seems that PTP is up-regulated to maintain muscle function rather than being down-regulated to prevent muscle damage. Ca""^ transient and myosin phosphorylation measurements would be beneficial in explaining increased PTP seen in this study.
Muscular dystrophy., Musculoskeletal system
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