Glucose transport is an essential physiologic process that is characteristic of all eukaryotic cells, including skeletal muscle. In skeletal muscle, glucose transport is mediated by the Glut-4 protein under conditions of increased carbohydrate utilization. The three major physiologic stimuli of glucose transport in muscle are insulin, exercise/contraction and hypoxia. Here, the role of reactive oxygen species (ROS) in modulating glucose transport in skeletal muscle is reviewed. Convincing evidence for ROS involvement in insulin- and hypoxia-mediated transport in muscle is lacking. Recent experiments, based on pharmacological and genetic approaches, support a role for ROS in contraction-mediated glucose transport. During contraction, endogenously produced ROS appear to mediate their effects on glucose transport via AMP-activated protein kinase.