A cardiac ischemia-reperfusion injury (heart attack) can be the cause of up to 50% of the damage to the heart for an individual who has suffered from a heart attack. We update the 2004 Kyoto model with a new metabolism model to explore how calcium overload impacts the cardiomyocyte energetics and contractility. The model simulates excitation, contraction, and metabolism of the heart and allows us to run the system such that it mimics calcium overload. We perturb selected parameters and initial conditions individually in an effort to gain perspective of how the parameter affects the model by quantifying how much the perturbation impacts the system; the technique is called local sensitivity analysis. We then tested several hypotheses linking oxidative stress to myocyte function believed to occur in I/R injury. To do this, we added free radical signaling mechanisms to the ECC and calcium handling processes in the model. We found that oxidative-induced modifications of the ryanodine receptor significantly altered electrophysiological and mechanical behavior closely mimicking what was observed in other studies. Oxidative stress dependent effects are then added to explore the damage caused by this addition.