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Figure 1 | Skeletal Muscle

Figure 1

From: Oxidative stress, mitochondrial damage, and cores in muscle from calsequestrin-1 knockout mice

Figure 1

EDL muscles from CASQ1-null mice exhibit impaired force output and slowed kinetics of contraction. (A) Maximal grip strength (normalized to body weight) is significantly reduced across all ages in CASQ1-null mice compared to WT. (B) Peak-specific force measured during maximal fused isometric tetanic contractions in excised EDL muscles is significantly reduced in 14- and 22- to 24-month-old CASQ1-null mice compared to WT and in CASQ1-null mice from 4 to 6 months to 14 months of age. (C) Time-to-peak isometric twitch force is significantly increased in CASQ1-null mice across all ages compared to WT and increases both in WT and CASQ1-null mice up to 22 to 24 months. Number of animals tested for grip strength test: WT, n = 175, 31, and 9 for 4 to 6, 14, and 22 to 24 months of age, respectively; CASQ1-null, n = 157, 51, and 9 for 4 to 6, 14, and 22 to 24 months of age, respectively. Number of animals tested for force and contraction kinetics: WT, n = 5, 8, and 10 for 4 to 6, 14, and 22 to 24 months of age, respectively; CASQ1-null, n = 5, 5, and 6 for 4 to 6, 14, and 22 to 24 months of age, respectively. Data are given as means ± SEM (*P < 0.05, **P < 0.01). EDL, extensor digitorum brevis; CASQ1, skeletal isoform of calsequestrin; WT, wild type.

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