Short-Term Ingestion of Virgin Coconut Oil Improves Endothelial-Dependent Dilation but not Exercise-Mediated Hyperemia in Healthy Young Adults

Abstract

Nitric oxide (NO), a powerful vasodilator produced in the endothelium, can be rapidly converted into toxic peroxynitrite by reactive oxygen species (ROS). Virgin coconut oil (VCO) is high in antioxidants (polyphenols) that reduce the action of ROS, and may subsequently increase flow-mediated dilation (FMD) and exercise-mediated hyperemia. This has never been assessed in humans. We investigated whether 30 ml·day-1 VCO for 4 weeks would improve popliteal artery (PA) FMD, improve the PA hyperemic response to moderate-intensity cycling, and alter plasma total antioxidant content (TAC) in healthy adults (10♂, 22±2 years). Short-term VCO ingestion increased FMD (Pre-VCO, 4.9±0.9%; Post-VCO, 5.7±1.2%; p < 0.001), but not five-minute mean post-exercise hyperemia (Pre-VCO, 102±75 ml·min-1; Post-VCO, 124±83 ml·min-1; p = 0.28), or plasma TAC (Pre-VCO, 96.0±15.1 ng·ml-1; Post-VCO, 96.8±17.0 ng·ml-1; p = 0.88). These results indicate that VCO may increase NO bioavailability, and that NO contributes relatively little to the exercise-mediated hyperemic response.