The myocardial metabolism of free fatty acids, glucose and catecholamines is reviewed in relation to current trends in the therapy of experimental myocardial infarction. Major modifications in the metabolism of free fatty acids, glucose and catecholamines have already been found after acute myocardial infarction in man, and animal experimental data suggest that such metabolic changes might play a role in the modification of infarct size and sometimes in the development of arrhythmias. However, animal experiments often represent extreme situations and the therapeutic use in man of agents to modify the metabolism of free fatty acids, glucose or catecholamines after myocardial infarction needs intensive investigation before general application. The sum total of the evidence from animal experiments suggests that increased circulating concentrations of free fatty acids and catecholamines, if sufficiently high, may be harmful rather than helpful to the outcome of acute myocardial infarction, and that increased provision of glucose (as glucose, insulin and potassium) may be beneficial. Reservations to these conclusions are that the concentrations used appear to be important factors in catecholamine and free fatty acid effects, and that the mechanism of action of glucose-insulin-potassium is more complex than originally thought.