The aims of this investigation were 1) to determine whether endurance exercise training could reverse impairments in insulin-stimulated compartmentalization and/or activation of aPKC/ and Akt2 in skeletal muscle from high-fat fed rodents, and 2) assess if the PPAR agonist rosiglitazone could reverse impairments in skeletal muscle insulin signaling typically observed after high fat feeding. Sprague-Dawley rats were placed on chow (NORCON, n=16) or high-fat (n=64) diets for 4 wk. During a subsequent 4 wk experimental period, high fat-fed rats were allocated (n=16/group) to either sedentary control (HFC), exercise training (HFX), rosiglitazone treatment (HFRSG), or a combination of both exercise training and rosiglitazone (HFRX). Following the 4 wk experimental period, animals underwent hind limb perfusions. Insulin-stimulated plasma membrane-associated aPKC and protein concentration, aPKC/|*lambda* activity, GLUT4 protein concentration and cytosolic Akt2 and aPKC activities were reduced (p<0.05) in HFC compared to NORCON. Cytosolic Akt2, aPKC and aPKC protein concentrations were not affected in HFC compared to NORCON. Exercise training reversed the deleterious effects of the high-fat diet such that insulin stimulated compartmentalization and activation of components of the insulin signaling cascade in HFX were normalized to NORCON. High-fat diet-induced impairments to skeletal muscle glucose metabolism were not reversed by rosiglitazone administration, nor did rosiglitazone augment the effect of exercise. Our findings indicate chronic exercise training, but not rosiglitazone, reverse high fat-diet induced impairments in compartmentalization and activation of components of the insulin signaling cascade in skeletal muscle.