Atrial Fibrillation (AF) is the most common arrhythmia with a complex pathophysiology. In experiments, it becomes quite challenging to dissect the key mechanisms behind the AF induced remodeling effect. Using the power of computational modeling, we have developed a chronic atrial fibrillation version of our recently developed human atrial electromechanical cardiomyocyte model. Using an incremental approach, the model incorporates the remodeling effect in parameters related to electrical/ionic currents, Ca2+-handling, the myofilament and the CaMKII effect. Based on this model, we have identified that at basal rate AF induced raised diastolic Ca-transient level is due to loss of SERCA function. Similarly, reduced cross-bridge cycling rate also contributes to elevated level of diastolic phase of contractility. Using this model, we extended the simulation for higher rates, and we found that under chronic AF (cAF) condition, the biphasic trend of contractility with rate was lost. Though the percentage change in Ca2+ and force was large due to raised diastolic levels. Thus, the model is a useful tool for future understanding cellular level mechanisms of other arrhythmias.