Prof. Chase's research interests are in the physiology and biophysics of striated (cardiac and skeletal) muscles. His primary focus is Ca2+-regulation of contraction by thin filaments that are comprised of proteins actin, tropomyosin and troponin, and alteration of Ca2+-regulation by genetic variants of these thin filament proteins that are associated with cardiomyopathies. Computation is an important complement to our experimental studies on muscle. Diffusion with reaction modeling in the context of biochemical reactions (fixed and diffusible) within the myofilament lattice provides quantitative insights into the roles of product inhibition in muscle fatigue. Monte Carlo simulations provide evidence that evolution has tuned myofilament compliance to optimize muscle force, paralleling macroscopic observations that human running performance can be enhanced by optimizing the compliances of running tracks and running shoes. Ca2+-dependent, isometric muscle kinetics (kTR) and force relationships can be fit to computational models by embedding systems of differential equations within a nonlinear least squares regression (Simplex) algorithm. Thin filament cooperativity can be evaluated at the level of individual filaments through statistical analysis of cryo-EM images.