Enhanced skeletal muscle and whole body insulin sensitivity can persist up to 24-48 hours after one exercise session. This review focuses on potential mechanisms for greater post-exercise, insulin-stimulated glucose uptake (ISGU) by muscle in individuals with normal or reduced insulin sensitivity. A model is proposed for the processes underlying this improvement. (1) Triggers are initiating events that activate subsequent (2) memory elements which store information that is relayed to (3) mediators which translate memory into action by controlling (4) an end-effector that directly executes increased insulin-stimulated glucose transport. Several candidates are potential triggers or memory elements, but none has been conclusively verified. Regarding potential mediators, in both normal and insulin resistant individuals, elevated post-exercise ISGU with a physiologic insulin dose coincides with greater Akt Substrate of 160 kDa (AS160) phosphorylation without improved proximal insulin signaling at steps from insulin receptor binding to Akt activity. Causality remains to be established between greater AS160 phosphorylation and improved ISGU. The end-effector for normal individuals is increased GLUT4 translocation, but this remains untested for insulin resistant individuals post-exercise. Following exercise, insulin resistant individuals can attain ISGU values similar to non-exercising healthy controls, but after a comparable exercise protocol performed by both groups, ISGU for the insulin resistant group has been consistently reported to be below post-exercise values for the healthy group. Further research is required to fully understand the mechanisms underlying the improved post-exercise ISGU in individuals with normal or subnormal insulin sensitivity and to explain the disparity between these groups after similar exercise.