L-carnitine is an essential cofactor for the transport of fatty acids across the mitochondrial membranes. L-carnitine can be provided by food products or biosynthesized in the liver. After intestinal absorption or hepatic biosynthesis, L-carnitine is transferred to organs whose metabolism is dependent upon fatty acid oxidation, such as the skeletal muscle and the heart. The intracellular transport of L-carnitine into the cell requires specific transporters and today, several of these have been characterized. Most of them belong to the solute carrier family. Heart is one of the major target for carnitine transport and use, however basic properties of carnitine uptake by heart cells have never been studied. In this paper, the transport of L-carnitine by rat heart explants has been examined and the kinetic properties of this transport determined and compared to data obtained in skeletal muscle explants. As in muscle, L-carnitine uptake by heart cells was shown to be dependent on sodium and was inhibited by L-carnitine analogues. Molecules known to interact with the skeletal muscle L-carnitine transport were studied in the heart. While trimethyl hydrazinium propionate (THP) was shown to fully inhibit the L-carnitine uptake by muscle cells, it remained inefficient in inhibiting the L-carnitine uptake by heart cells. On the other hand, compounds such as verapamil and AZT were both able to inhibit both the skeletal muscle and the cardiac uptake of L-carnitine. These data suggested that the muscle and heart systems for L-carnitine uptake exhibited different systems of regulation and these results have to be taken in consideration while administrating those compounds that can alter l-carnitine uptake in the muscle and the heart and can lead to damage to these tissues.