Rainbow trout, Oncorhynchus mykiss, were exercise trained for 28-52 days. Trained fish were 13% larger and swam 12% faster in an aerobic swimming test. Training induced cardiac growth that was isometric with body growth, since ventricle mass relative to body mass was constant. The proportions of compact and spongy myocardia in the ventricle were also unchanged by training. Trained fish had significantly higher levels of citrate synthase, ß-hydroxyacyl CoA dehydrogenase, and hexokinase in both compact and spongy myocardium. Ligation of a 0.5- to 1.0-cm section of the coronary artery produced only a temporary interruption of coronary flow to the compact myocardium because new vessels grew around the ligation site in the majority of fish during the 28- to 52-day experiment. Nonetheless, coronary ligation resulted in a significantly smaller (17%) proportion of compact myocardium with lower levels of citrate synthase, ß-hydroxyacyl CoA dehydrogenase, and hexokinase. Exercise-induced increases in the levels of these enzymes in the compact myocardium were prevented by coronary ligation. The decrease of enzymes in the compact myocardium as a result of coronary ligation was compensated for by a 30% increase in the levels of the aerobic enzymes citrate synthase and ß-hydroxyacyl CoA dehydrogenase and a 32% increase in the mass of spongy myocardium. As a result of these compensations and coronary regrowth, chronic coronary ligation did not affect maximum prolonged swimming speed. These experiments clearly reveal that cardiac plasticity allows compensatory changes that are necessary for the heart to maintain adequate oxygen delivery to exercising skeletal muscle. The compensatory changes were isometric increases in heart mass or proportionately larger increases in heart mass and compact tissue if the coronary artery was ligated and an increase in metabolic enzymes associated with ATP generation, namely, citrate synthase, ß-hydroxyacyl CoA dehydrogenase, and hexokinase.