Exercise significantly influences the progression of atherosclerosis. Oxidized-LDL (ox-LDL), as a stimulator of oxidative stress, facilitates monocyte-related atherogenesis. This study investigates how exercise intensity impacts ox-LDL-mediated redox status of monocytes. Twenty-five sedentary healthy men exercised mildly, moderately, and heavily (i.e., 40%, 60% and 80% VO_2max, respectively) on a bicycle ergometer. Reactive oxygen species (ROS) production, cytosolic and mitochondrial superoxide dismutase (c-SOD and m-SOD) activities, and total and reduced-form -glutamylcysteinly glycine (t-GSH and r-GSH) contents in monocytes mediated by ox-LDL were measured. This experiment obtained the following findings: (1) ox-LDL increased monocyte ROS production and was accompanied by decreased c- and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium (DPI) (a NADPH oxidase inhibitor) or rotenone/2-thenoyltrifluoroacetone (TTFA) (mitochondrial complex I/II inhibitors) hindered ox-LDL-induced monocyte ROS production; (2) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise; and, (3) heavy exercise augmented the inhibition of ox-LDL-induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA-mediated monocyte ROS productions were unchanged in response to mild and moderate exercise. We conclude that heavy exercise increases ox-LDL-induced monocyte ROS production, possibly by decreasing m-SOD activity and r-GSH content in monocytes. However, mild and moderate exercise likely protects individuals against suppression of anti-oxidative capacity of monocyte by ox-LDL.