Glycolysis is greatly stimulated in the ischaemic/hypoxic heart as ATP production by oxidative metabolism becomes impaired. The end product of glycolysis, lactic acid, must leave the cell if the intracellular pH is not to drop. This process is mediated by members of the monocarboxylate transporter (MCT) family – monocarboxylate/proton symporters with a broad substrate specificity that includes L-lactate, pyruvate and the ketone bodies acetate, acetoacetate and β-hydroxybutyrate. Hence MCTs may also be used to import such substrates as metabolic fuels for the heart under normoxic conditions. There are fourteen members of the MCT family, but only MCTs 1-4 have been shown to transport lactate, each with subtly different kinetics that fit the different requirements of the tissues in which they are expressed. The major MCT isoform in heart is MCT1, but some species may also express lower amounts of the higher affinity MCT2 or the lower affinity MCT4. However, the latter isoform is expressed strongly in neonatal heart cells, whose energy metabolism is more glycolytic than adult heart cells, and is up-regulated by hypoxia through a Hypoxia Inducible Factor 1α (HIF-1α) mediated increase in gene transcription. By contrast, MCT1 is up-regulated in response to increased work load by mechanisms involving both transcriptional and post-transcriptional mechanisms. MCT1 expression is confined to the plasma membrane and is not detected in Percoll-purified mitochondria that possess a separate mitochondrial pyruvate carrier. MCTs require a single transmembrane ancillary protein, with extracellular immunological domains, for expression and function at the plasma membrane. This can be either Basigin or Embigin, the contribution of each depending on the species. Organomercurials inhibit lactate transport into cardiomyocytes by binding to a reactive thiol group on basigin, with residual inhibitor-insensitive transport reflecting the MCT1-embigin complex. Very recently, a novel class of MCT1 specific inhibitors (K_i values ~ 1nM) have been described and the effects of these on lactate transport into heart cells and on the haemodynamic behaviour of the heart under normoxic conditions and following ischaemia/reperfusion will be described.