A Spatially Detailed Model of Isometric Contraction Based on Competitive Binding of Troponin I Explains Cooperative Interactions between Tropomyosin and Crossbridges
Fig 8
Tension redevelopment rates in mouse, rat and human.
Panel A shows results for q = 1 (constant crossbridge unbinding rate), and Panel B plot results for q = 0.5 (variable crossbridge unbinding rate). Each plot shows both normal kinetics, and with RU (un)blocking due to TnI-actin binding disabled for mouse, rat, and human parametrizations of the model. The difference in ktr when disabling RU (un)blocking reveals the influence of transient blocking of RU’s on tension redevelopment kinetics. This transient blocking causes a significant difference between the minimum ktr and the ktr at high [Ca2+], the ratio of which is indicated with the results. Note the shift in the minimum ktr is not significant here as it is a direct result of the difference in peak calcium shown in Fig 7A and subsequent parametrization.