Adverse remodeling after a myocardial infarct has been linked to the elevated wall stress in the myocardium adjacent to the infarct (i.e. border zone). Perturbed metabolism in this region could drive the transition from compensated to adverse remodeling. To evaluate regional metabolism this study compared the uptake and intracellular conversion of [1-13C]pyruvate using hyperpolarized 13C. An infarct model of ventricular remodeling was used to investigate region metabolism. Pharmacologic stress produced an increase in remote metabolite flux compared to border zone region which may provide a metabolic mechanism for the established association of mechanical stress and adverse cardiac remodeling following infarct.