We examined whether the increased rates of protein catabolism (proteolysis and leucine oxidation) associated with moderate insulinopenia in subjects with IDDM would be accentuated by prior bicycle exercise (53% VO2max for 82 min). Insulin infusions maintained plasma glucose concentrations on one study day in “tight” control (TC: 6 mmol/l) and on a separate day in “loose” control (LC: 12 mmol/l). Elevations in serum ketone body, plasma NEFA, and whole-blood branched-chain amino acid concentrations on the loose control day during the basal period persisted throughout the post-exercise recovery period. Amino acid kinetics were estimated during a primed, constant infusion of l-[1-13C]leucine from plasma dilution of α-[1-13C]KIC and expired air 13CO2 enrichments. Loose control was associated with increased rates of whole-body leucine oxidation (LC 25±7 vs TC 21±8 μmol · kg−1 · h−1) and protein degradation (LC 127±12 vs TC 118±18 μmol · kg−1 · h−1) (both p<0.05). During the 2-h post exercise recovery period, there were significant decreases in rates of leucine oxidation (LC 21±7, TC 16±7) and protein degradation (LC 112±13, TC 107±11), compared to the basal period (both p<0.05, basal vs recovery). Rates of wholebody protein synthesis were unchanged by prior exercise. In conclusion, moderate insulinopenia is associated with significantly higher rates of protein degradation and leucine oxidation in the basal state. Following exercise, net protein catabolism is diminished due to reduced rates of protein degradation in the presence of maintained rates of protein synthesis. The significantly increased concentrations of fat-derived substrates (ketone bodies, NEFA) may have prevented the predicted increases in protein catabolism which we anticipated would follow acute exercise during periods of relative insulin deficiency.