RLC phosphorylation and cMyBP-C loss alter viscoelasticity and crossbridge kinetics under maximally activated conditions (pCa 4.8). (A–D) Elastic moduli (A and B) and viscous moduli (C and D) values plotted against frequency for AP- and MLCK-treated strips from WT and cMyBP-C KO mice. (E and F) Frequency of the minimum viscous modulus represents a relative measure of crossbridge recruitment rate (fixed effects: genotype: P = 0.015; treatment: P = 0.001; genotype*treatment: P = 0.012; E) and frequency of the maximal viscous modulus represents a relative measure of the crossbridge detachment rate (fixed effects: genotype: P = 0.011; treatment: P = 0.001; genotype*treatment: P < 0.001; F). Averages represent mean ± SEM, with individual data points shown for each fiber where applicable. The number of biological and technical replicates is listed in Table 1.
Figure 5.

RLC phosphorylation and cMyBP-C loss alter viscoelasticity and crossbridge kinetics under maximally activated conditions (pCa 4.8). (A–D) Elastic moduli (A and B) and viscous moduli (C and D) values plotted against frequency for AP- and MLCK-treated strips from WT and cMyBP-C KO mice. (E and F) Frequency of the minimum viscous modulus represents a relative measure of crossbridge recruitment rate (fixed effects: genotype: P = 0.015; treatment: P = 0.001; genotype*treatment: P = 0.012; E) and frequency of the maximal viscous modulus represents a relative measure of the crossbridge detachment rate (fixed effects: genotype: P = 0.011; treatment: P = 0.001; genotype*treatment: P < 0.001; F). Averages represent mean ± SEM, with individual data points shown for each fiber where applicable. The number of biological and technical replicates is listed in Table 1.

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