The principal investigator of this clinical trial previously demonstrated that: (1) the skeletal muscle of obese individuals has elevated levels of in vivo ROS compared to that of lean or overweight individuals, (2) in obese individuals, elevated in vivo ROS levels were normalized and local microvascular endothelial dysfunction was reversed by the perfusion of apocynin, an NADPH oxidase inhibitor, and (3) in vivo H2O2 production and microvascular endothelial dysfunction were ameliorated in obese individuals by aerobic exercise [57]. Here, FMO5 is linked to endothelial dysfunction.