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Attenuated aerobic exercise capacity in CD36 deficiency

¹ Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo, Japan
² Department of Rehabilitation Medicine and Physical Medicine, Hokkaido University School of Medicine, Sapporo, Japan
³ Laboratory of Human Performance and Fitness, Hokkaido University Graduate School of Education, Sapporo, Japan
⁴ Department of Health Science, Hokkaido University School of Medicine, Sapporo, Japan
⁵ Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Hokkaido, Japan

Correspondence to:
Dr Hidekatsu Yanai
Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo 060-8648, Japan; yanaih{at}jikei.ac.jp] 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.

Abbreviations: AT, anaerobic threshold; CPT I, carnitine palmitoyltransferase I; FA, fatty-acid; UTR, untranslated region; VT, ventilatory threshold

Keywords: CD36; anaerobic threshold; exercise; fatty acid