Figure 2: Muscle physiology from 12 month old mice.
From: Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophy
(a–d) Ex vivo EDL muscle function. (a) dKO muscles produce ∼27% less force than mdx controls (mdx – 171.0 mN, dKO – 126.2 mN, One-way ANOVA, P<0.001). (b) When corrected for cross-sectional area, dKO muscles produce significantly less maximum specific force than mdx. (c) dKO muscles suffer less damage than mdx controls following a series of three 15% eccentric contractions (mdx - 71% drop in force following eccentric contractions, dKO - 47%, One-way ANOVA, P<0.01). (d) dKO show significantly greater recovery from fatigue compared with WT, and mdx. (e,f) In situ TA muscle function replicates the phenotype seen in the EDL. (e) dKO muscles produce ∼25% less force than mdx controls (mdx - 1613 mN, dKO-1221 mN, One-way ANOVA, P<0.01), (f) After correction for cross-sectional area, dKO show reduced specific force compared with mdx. Both are significantly reduced compared with WT. (g) Both mdx and dKO muscles are significantly injured compared with WT by eccentric contractions of increasing strain (Multiple T-test, FDR 1% #P <0.01), but dKO muscles suffer less damage than mdx between 25-30% LO (0–35%; mdx – 80% drop in force following eccentric contractions, dKO 65%, Multiple T-test, FDR 1%, P<0.05). Data shown as mean±s.e.m., One-way ANOVA, *P<0.05, **P<0.01, ***P<0.001, WT n=5, mdx n=6, dKO n=6.
