Cartoon illustration of the half sarcomere and a two-state model of myosin crossbridge formation.(A) Those protein connections that span the half sarcomere and are responsible for crossbridge-independent viscoelasticity include most notably titin and collagen (blue). Protein connections responsible for crossbridge-dependent viscoelasticity include myosin and other proteins of the thick and thin filaments and the M- and Z-lines such as actin, α-actinin, etc. (red). Still other proteins, such as myosin-binding protein C, contribute to a transverse stiffness that can play indirect roles in longitudinal viscoelasticity (orange and yellow). (B) The two-state model developed here assumes a non–force-producing detached state and a force-producing attached state. The rate of transition from detached to attached is a function of x, f(x), that signifies the spatial distribution of newly formed crossbridges. This distribution is modeled as Gaussian and, importantly, evenly symmetric about a central point we define as x = 0. Crossbridges in the attached state are spatially distributed according to A(x,t), with a mean displacement that is not symmetric about x = 0 owing to the strain dependence of the detachment rate, g(x). In this example, detachment rate is modeled to be enhanced with positive strain, i.e., stretch, and reduced with negative strain, i.e., compression, as signified by the proportionality constant g₁. Under no strain, the detachment rate is a constant g₀.