This thesis examined the translocation of fatty acid (FA) transport proteins to the plasma membrane (PM) in human and rat skeletal muscle during moderate intensity exercise. The responses to the post-exercise period and to acute moderate intensity exercise after 6 weeks of high intensity interval training (HIIT) were also examined in humans. The overall hypotheses were that 1) FAT/CD36 and FABPpm would translocate to the PM in human skeletal muscle during 120 min of moderate intensity exercise, 2) FAT/CD36 and FABPpm would translocate to the PM in rat skeletal muscle during 120 min of moderate intensity exercise and this would correlate to an increase in palmitate uptake, 3) FAT/CD36 and FABPpm would translocate to the PM during 120 min of moderate intensity exercise, but return to basal levels by 45 min post-exercise, 4) six weeks of HIIT would increase PM content of FABPpm but not FAT/CD36 in resting skeletal muscle, 5) six weeks of HIIT would cause a further increase in the translocation of FAT/CD36 and FABPpm to the PM during moderate intensity exercise and this would correspond to an increase in whole body fat oxidation compared to exercise pre-training, and 6) six weeks of HIIT would increase whole muscle content of FATP1 and FATP4. In human skeletal muscle, PM FAT/CD36 and FABPpm increased 75% and 20% respectively after 120 min of cycling at ~60% VO2 peak which corresponded to a 110% increase in whole body fat oxidation. In rat skeletal muscle, PM FAT/CD36 and FABPpm increased 20% and 30% respectively, which correlated to a 30% increase in palmitate uptake following 120 min of treadmill running at ~65% VO2 peak. The PM content of FAT/CD36 increased further to 120% of resting values by 45 min of post-exercise following 120 min of cycling at ~60% VO2peak, which correlated with a heavy reliance on fat as a fuel during the post-exercise period. FABPpm returned to resting levels of PM content by 15 min post-exercise. After 6 wk of HIIT, whole muscle FAT/CD36 (50%), FABPpm (21%) and FATP4 (25%) were increased in human skeletal muscle, while FATP1 remained unchanged. There were no changes in PM content of FAT/CD36 or FABPpm at rest following training. FAT/CD36 and FABPpm were also measured before and after 120 min of cycling at ~60% of pre-trainingVO2 peak following training, but no differences in the magnitude of the PM content increases were seen compared to pre-training, despite a 27% increase in fat oxidation. These studies demonstrate that FA transport proteins translocate to the PM during moderate intensity exercise, which correlates with increased FA uptake and whole body fat oxidation. This relationship does not appear to hold during the post-exercise period, as further increases in the PM content of FAT/CD36 does not correspond with the decrease in fat oxidation. The PM content of FAT/CD36 and FABPpm were not increased at rest following training, and there was no effect of training on the translocation of FAT/CD36 or FABPpm to the PM during moderate intensity exercise at the same absolute power output, however there may be a further increase at a relative power output. / Natural Sciences and Engineering Research Council, Canadian Institute of Health Research, Ontario Graduate Scholarship