During ischemic and cardiomyopathic conditions, carbohydrate (glucose) metabolism in cardiomyocytes predominates over use of free fatty acids. The shift to glucose metabolism is a physiologic response to ischemia, which in many patients, particularly diabetics or those who are insulin-resistant, is blunted. Free fatty acid metabolism during ischemia produces higher levels of lactate and hydrogen ions within the ischemic cells. This in turn degrades myocardial contractility, induces diastolic dysfunction, and reduces the arrhythmogenic threshold of the cardiomyoctye. Suppression of free fatty acid uptake and oxidation by any means will increase myocardial glucose substrate utilization in ischemia. Theoretically, then, an insulin-glucose solution that can augment GLUT-1 and GLUT-4 translocation to the sarcolemmal membrane can assist cardiomyocyte survival during ischemia; however, study results have not supported metabolic therapy. It is essential for any investigation of glucose, insulin, potassium therapy to separate out the effect of hyperglycemia and glucose toxicity to make any meaningful comment on the effectiveness of metabolic support in myocardial infarction.