The aim of this study was to establish why oxidative type muscles (soleus muscle, SM) are resistant to muscle cachexia induced by dexamethasone disodium phosphate overload (2 mg/kg b.w. day(-1) during 5 consecutive days). DEX treatment was associated with the dramatic drop in total antioxidant status, that was partially corrected by the supplementation with antioxidants. The relationships between the expression of selected proteins (phospho-Ser473-Akt [P-PKB] and Akt [PKB], nucleus encoded subunit IV of mitochondrial cytochrome-c oxidase [NCOIV]) and the activity of selected enzymes (lactate dehydrogenase - LDH, phosphofructokinase - PFK, isocitrate dehydrogenase - ICDH) in SM vs. gastrocnemius muscle (GM) Were examined in rats additionally treated with antioxidants (sodium ascorbate, ASC, or ascorbic acid phosphate, ASC-P). No changes were observed in the expression of PKB, P-PKB, NCOIV in soleus muscle. The activity of LDH was not affected, either. Interestingly, PFK activity in SM was elevated in experimentally treated annuals (P<0.05) and the highest value was observed after ASC-P (P<0.01). In turn, ICDH activity peaked in SM after dexamethasone treatment (P<0.05) and dropped during the co-treatment with ascorbate (DEX/ASC). The average expression of NCOIV was significantly higher in GM in contrast to SM, although it decreased considerably after DEX treatment or co-treatment. DEX was also shown to reduce significantly the expression of P-PKB in GM. Anyway, the rise in the activity of PFK suggests that SM started to utilize excess glucose during DEX-induced hyperglycemia. In contrast to SM, the activity of PFK in GM Was significantly lower after treatment or co-treatment with antioxidants. Taken together, these results pointed to the metabolic profile of the skeletal muscle that determines the resistance of SM to steroid diabetes-induced muscle cachexia. Antioxidants significantly affect the metabolic profiles of examined muscles.