Background: An important role of CD36 in muscle fatty acid (FA) uptake has been shown in CD36-knockout or CD36-overexpressed mice. FA is a predominant substrate in energy production during light exercise below the anaerobic threshold (AT). We studied whether aerobic exercise capacity in humans could be affected by CD36 deficiency.
Methods: We investigated the ventilatory threshold (VT) and serum FA changes in normal participants (n = 22) and participants with CD36 deficiency (n = 12) during pedalling on a cycle ergometer.
Results: In participants with CD36 deficiency, FA levels were not reduced at peak work rate, whereas FA levels decreased by about 50% in normal participants. Participants with CD36 deficiency showed significantly lower VT than normal participants. A significant correlation was observed between VT and percentage changes in FA at peak work rate.
Conclusion: This study found reduced FA utilisation and an attenuated aerobic exercise capacity in CD36 deficiency, indicating that CD36-mediated FA oxidation is an important determinant for aerobic exercise capacity in humans.