We developed a mathematical model specific to rat ventricular myocytes that includes electrophysiological representation, ionic homeostasis, force production, and sarcomere movement. We used this model to interpret, analyze, and compare two genetic manipulations that have been shown to increase myocyte relaxation rates, parvalbumin (Parv) de novo expression and Serca2a over-expression. The model was used to seek mechanistic insights on: 1) the relative contribution of two mechanisms by which Serca2a over-expression modifies calcium sequestration, i.e. more pumps and an increase in Serca2a/phospholamban ratio, 2) the mechanisms behind post rest potentiation, and how Parv and Serca2a influence this response, 3) the reasons why Parv myocytes retain their fast kinetics when endogenous Serca2a is partially impaired by thapsigargin (a condition used to mimic diastolic dysfunction). The model was also utilized to make predictions on the possibility of modifying Parv metal-binding characteristics to improve diastolic and systolic functions, and on the effects of Parv or Serca2a on diastolic calcium levels and myocyte energetics. One outcome of the model was to demonstrate that Serca2a myocytes had a higher peak and total ATP consumption, while Parv myocytes distributed ATP use more evenly throughout the cardiac cycle. This may have implications for failing hearts that are energetically compromised.