The SRX state of myosin assessed in skinned PMs from 7–10-mo-old mouse models of hypertrophic (HCM-A57G) and restrictive (RCM-E143K) cardiomyopathy and in a near-physiological Δ43 ELC model compared with WT-ELC mice. (A) Fluorescence decay curves and simulated single-exponential curves of mant-ATP release. (B) Comparison of fluorescence decay curves for WT-ELC (11 mice, 5 M and 6 F), HCM-A57G (8 mice, 4 M and 4 F), Δ43 (10 mice, 5 M and 5 F), and RCM-E143K (7 mice, 4 M and 3 F) animals (left), redistribution of cross-bridges (in %) between the DRX (P1) state (middle) and the SRX (P2) state (right). Open symbols depict female mice, and closed symbols depict male mice. Data are mean ± SD; *, P < 0.05 for mutant versus WT-ELC; $, P < 0.05 for E143K versus A57G; and &, P < 0.05 for Δ43 versus A57G calculated with one-way ANOVA with Tukey’s multiple comparison test. Note that the percentage of DRX is increased in HCM-A57G compared with WT-ELC, Δ43, and RCM-E143K mice, and this increase is coupled with a decrease in percentage of SRX for HCM-A57G mice. (C) Myosin head redistribution between the DRX (P1) versus SRX (P2) states plotted as a function of genotype and sex. Data are mean ± SD of male or female mice analyzed by two-way ANOVA with two nominal variables (genotype, sex) followed by Tukey’s or Sidak’s multiple comparison test.