We examined, in muscle of lean and obese Zucker rats, basal, insulin- and contraction-induced fatty acid transporter translocation, and fatty acid uptake, esterification and oxidation. In lean rats, insulin and contraction induced the translocation of FAT/CD36 (43% and 41%) and FABPpm (19% and 60%), and increased fatty acid uptake (63 and 40%). Insulin and contraction increased lean muscle palmitate esterification and oxidation by 72% and 61%, respectively. In obese rat muscle, basal levels of sarcolemmal FAT/CD36 (+33%) and FABPpm (+14%), and fatty acid uptake (+ 30%) and esterification (+32%) were increased, while fatty acid oxidation was reduced (-28%). Insulin stimulation of obese rat muscle increased plasmalemmal FABPpm (+15%) but not plasmalemmal FAT/CD36, blunted fatty acid uptake and esterification, and failed to reduce fatty acid oxidation. In contracting, obese rat muscle, the increases in fatty uptake, esterification and FABPpm translocation were normal, but FAT/CD36 translocation was impaired and fatty acid oxidation was blunted. There was no relationship between plasmalemmal fatty acid transporters and palmitate partitioning. In conclusion, fatty acid metabolism is impaired at several levels in muscles of obese Zucker rats; specifically, they are 1) insulin-resistant with respect to FAT/CD36 translocation, and fatty acid uptake, esterification and oxidation, and 2) contraction-resistant with respect to fatty acid oxidation and FAT/CD36 translocation, but conversely, 3) obese muscles are neither insulin-, nor contraction- resistant at the level of FABPpm. Finally, 4) there is no evidence that plasmalemmal fatty acid transporters contribute to the channeling of fatty acids to specific metabolic destinations within the muscle.