[LisaS]

and here's a little intro from a study which gives a simple overview of the process in muscle

Glycogen phosphorylase is the rate-limiting enzyme of glycogen breakdown. In muscle, glycogen serves mainly to provide glucose for energy production during exercise, although it is also consumed in the resting state. During exercise muscle glycogenolysis is triggered by the dual control of contractile activity and epinephrine(1) . These stimuli result in the release of Ca and an increase in cyclic AMP, respectively, which in turn lead to the phosphorylation and activation of glycogen phosphorylase by phosphorylase kinase(2) .
During exercise, glucose uptake and metabolism are greatly increased in muscle despite low physiological concentrations of insulin. Indeed, it has been shown that insulin is not required to mediate glucose uptake during contractions (3, 4) and that contractile activity augments glucose uptake by muscle even in severely insulin-deficient diabetic rats(5) . Furthermore, in exercised muscle, glucose uptake and disposal are enhanced independently of insulin(6) . Insulin sensitivity of glucose uptake and glycogen synthesis are increased in exercised muscle, in normal humans and insulin-deficient type I diabetic patients (7, 8) . The mechanism by which exercise increases basal and insulin-stimulated muscle glucose uptake remains to be elucidated. The system accounting for such effects appears to be located at a post-receptor level, because exercise does not affect the amount of insulin receptors or insulin-stimulated kinase activity(9, 10) . Breakdown of glycogen stores (11, 12, 13) or the activation of glycogen synthase (9) have been suggested as possible mediators of this phenomenon. On the other hand, even though these studies are consistent with the fact that glucose uptake is limited by glucose metabolism, other studies suggest that it is glucose transport that limits glucose uptake(14, 15) .