Mitochondrial Fatty Acid Binding Protein Content is not Altered in Human Skeletal Muscle during Prolonged Aerobic Exercise: 2800

PURPOSE: The transport of long chain fatty acids (LCFA) across mitochondrial membranes is considered a rate-limiting step in fatty acid oxidation. Traditionally, mitochondrial LCFA transport was believed to be solely regulated by carnitine palmitoyltransferase I (CPTI) activity. Although CPTI activity remains an integral part of mitochondrial LCFA transport, it is becoming increasingly clear that additional proteins influence LCFA transport. Recently, the plasma membrane (PM) proteins fatty acid translocase (FAT)/CD36 and fatty acid binding protein (FABP) have been found on skeletal muscle mitochondria. While it has been shown that both PM proteins follow an oxidative heirarchy, are involved in PM LCFA transport and increase following chronic training, only FAT/CD36 has previously been studied in humans with respect to the mitochondrial fraction. It has been shown that FAT/CD36 translocates from an intracellular depot to the mitochondria in exercising skeletal muscles, however the role of FABP with respect to mitochondrial LCFA transport and oxidation in human skeletal muscle during exercise remains unknown. We hypothesized that exercise induced increases in fatty acid oxidation result from an increased mitochondrial FABP content, similar to the translocation of FAT/CD36 that has previously been observed. METHODS: Participants cycled at ∼60% VO2peak for 120 min, and blood and ventilatory data were collected at rest and every 30 minutes during exercise. Purcutaneous needle biopsies were taken from the vastus lateralis at rest, 30 min and following 120 min. Mitochondria were immediately isolated, and used to measure the content of mitochondrial FABP through Western blotting (n=12). RESULTS: Whole body fat oxidation rates increased (P<0.05) during exercise by ∼100% (15 min; 10.1 ± 1.2 vs 120 min; 20.5 ± 2.5 KJ/min). Associated with the exercise induced increase in whole body fat oxidation was ∼200% increase (P<0.05) in plasma free fatty acid concentration (15 min; 0.32 ± 0.03 vs 120 min; 0.91 ± 0.11 mM). However, despite increases in fatty acid oxidation mitochondrial FABP protein content did not change (Rest; 2.62 ± 0.54, 30 min; 2.48 ± 0.49, 120 min; 2.75 ± 0.45 arbitrary units), and as a result did not correlate with whole body fat oxidation rates (r=0.23). CONCLUSIONS: It is concluded that during 120 min of cycling, the content of FABP on mitochondria does not change, despite large increases in whole body fat oxidation. While it appears that FABP exists on mitochondria, the exact role of this subcellular fraction remains to be elucidated.