Followin exercise, the metabolic rate remains elevated for several hours (up to 24 hours). This rise in metabolic rate is dependent on a variety of factors that include exercise intensity and duration. The main goals of exercise recovery are to re-establish metabolic homeostasis and to contribute to exercise adaptations. Whereas skeletal muscle tends to rely on carbohydrate oxidation for ATP production during exercise, energy provision during the post-exercise period tends to rely on lipid oxidation. This fuel shift is optimal because it allows for the replenishment of carbohydrate stores and the metabolic cost associated with protein synthesis (myofibrillar and/or mitochondrial protein synthesis depending on the exercise protocol). Regulation of the metabolic processes favored during exercise recovery has not been systematically studied; however, the roles of several signaling cascades have been investigated. Evidence suggests that several exercise-responsive signaling cascades are implicated in the regulation of metabolism and gene expression following exercise. It is well accepted that exercise activates AMP-activated protein kinase (AMPK), protein kinase B (PKB/Akt), several branches of the stress and/or mitogen-activated protein kinases (MAPK) as well as calcium/calmodulin-dependent protein kinases such as CaMKII. However, a direct link between activation of any of these signaling intermediates during exercise and alterations in substrate utlization following exercise has not been clearly established. In this presentation, I will summarize data investigating the importance of the AMPK-ACC pathway and the Akt-mTOR pathway in the regulation of muscle metabolism and gene expression during exercise recovery. Coordination of these signaling pathways and their respective metabolic goals will be addressed. The presentation will also address the influence of post-exercise nutritional strategies on cellular signaling and on the eventual return of metabolic homeostasis.