Isolated rat hearts were studied by 31 P NMR and 13 C NMR. Hyperpolarized [1-13 C]pyruvate was supplied to control normoxic hearts and production of [1-13 C]lactate, [1-13 C]alanine, 13 CO 2 and H 13 CO 3 ؊ was monitored with 1-s temporal resolution. Hearts were also subjected to 10 min of global ischemia followed by reperfusion. Developed pressure, heart rate, oxygen consumption, [ Myocardial oxygen consumption is sensitive to the ratio of fatty acid versus carbohydrate metabolism (1-3). Fatty acid utilization increases oxygen consumption. This is considered insignificant to physiology in the normoxic heart, but in the setting of ischemia or ischemia-reperfusion, increased metabolism of fatty acids impairs contractility and recovery (1,2). Diverse metabolic (4,5) and pharmacologic (6 -8) interventions share a common featureincreased oxidation of carbohydrates relative to fatty acids improves outcome after myocardial ischemia. Although these benefits have been demonstrated repeatedly, the mechanism is poorly understood and the clinical utility of increased carbohydrate oxidation remains controversial (9).Glucose, pyruvate, and lactate are important substrates for oxidation by the heart. The product of lactate and glucose metabolism, pyruvate, is decarboxylated by pyruvate dehydrogenase (PDH) to produce acetyl-CoA for subsequent oxidation in the citric acid cycle. The other major substrates for energy production, fatty acids and ketones, are metabolized through  oxidation and bypass PDH for generation of acetyl-CoA. Because of the importance of PDH in cardiac metabolism, the classic radiotracer method for assessing PDH flux, 14 CO 2 release from [1-14 C]pyruvate (10 -13), has been extensively developed and widely accepted. Applications, however, are limited in vivo because of radiation containment requirements and the difficulty of collecting blood from the vessels draining the ischemic region. Consequently, there is considerable interest in direct metabolic mapping using hyperpolarized [1-13 C]pyruvate (7,14). 13 C MR images of [1-13 C]lactate, [1-13 C]alanine and H 13 CO 3 Ϫ ([ 13 C]bicarbonate) were relatively homogeneous in the normal myocardium, but reduced signal from [ 13 C]bicarbonate compared with the normal myocardium was observed 2 hr after transient ischemia (15). In the presence of [1-13 C]pyruvate, the appearance of H 13 CO 3 Ϫ in heart tissue is due exclusively to PDH flux (16). When carbohydrates are the only source of acetyl-CoA for oxidation in the TCA cycle, the rate of production of H 13 CO 3 Ϫ is proportional to citric acid cycle flux. However, the heart can derive much of its acetyl-CoA from long chain fatty acids or ketones. It would be expected that reduced bicarbonate signal may be due to reduced flux through the TCA cycle, a switch to oxidation of fats or ketones, or a combination of these two factors.In the present study, oxidation of hyperpolarized [1-13 C]pyruvate was examined in a model widely used for evaluation of tracer kinetics in ischemia and reperfusion, the isolated rat heart...