Different mechanisms can alter fatty acid transport when muscle contractile activity is chronically altered.

We examined whether skeletal muscle transport rates of long-chain fatty acids (LCFAs) were altered when muscle activity was eliminated (denervation) or increased (chronic stimulation). After 7 days of chronically stimulating the hindlimb muscles of female Sprague-Dawley rats, the LCFA transporter proteins fatty acid translocase (FAT)/CD36 (+43%) and plasma membrane-associated fatty acid-binding protein (FABPpm; +30%) were increased (P < 0.05), which resulted in the increased plasmalemmal content of these proteins (FAT/CD36, +42%; FABPpm +13%, P < 0.05) and a concomitant increase in the LCFA transport rate into giant sarcolemmal vesicles (+44%, P < 0.05). Although the total muscle contents of FAT/CD36 and FABPpm were not altered (P > 0.05) after 7 days of denervation, the LCFA transport rate was markedly decreased (-39%). This was associated with reductions in plasmalemmal FAT/CD36 (-24%) and FABPpm (-28%; P < 0.05). These data suggest that these LCFA transporters were resequestered to their intracellular depot(s) within the muscle. Combining the results from these experiments indicated that changes in rates of LCFA transport were correlated with concomitant changes in plasmalemmal FAT/CD36 and FABPpm, but not necessarily with their total muscle content. Thus chronic alterations in muscle activity can alter the rates of LCFA transport via different mechanisms, either 1) by increasing the total muscle content of FAT/CD36 and FABPpm, resulting in a concomitant increase at the sarcolemma, or 2) by reducing the plasma membrane content of these proteins in the absence of any changes in their total muscle content.