Long bouts of estivation (6-9 months) in green-striped burrowing frogs led to a 28% atrophy of cruralis oxidative fibres (p<0.05) and some impairment of in vitro gastrocnemius endurance (p<0.05), but no significant deficit in maximal twitch force production. These data suggest the preferential atrophy of oxidative fibres at a rate slower than, but comparable to, laboratory disuse models. We tested the hypothesis that the frog limits atrophy by modulating oxidative stress. We assayed various proteins at the transcript level and verified these results for antioxidant enzymes at the biochemical level. Transcript data for ND1 (71% downregulated; p<0.05) and ATP synthase (67% downregulated; p<0.05) are consistent with mitochondrial quiescence and reduced oxidant production. Meanwhile, UCP2 transcription (p=0.31), thought to reduce mitochondrial ROS leakage, was maintained. The total antioxidant defence of water-soluble (22.3 ± 1.7 control and 23.8 ± 1.5 µM/µg estivator total protein; p=0.53) and membrane bound proteins (31.5 ± 1.9 and 42.1 ± 7.3 µM/µg total protein; p=0.18) was maintained, equivalent to a bolstering of defence relative to oxygen insult. This probably decelerates muscle atrophy by preventing the accumulation of oxidative damage in static protein reserves. Transcripts of the mitchondrially-encoded antioxidant SOD2 (67% downregulated; p<0.05) paralleled mitochondrial activity while the nuclear-encoded catalase and glutathione peroxidase were maintained at control values (p=0.42; p=0.231) suggesting a dissonance between mitochondrial and nuclear antioxidant expression. PDK4 transcription was 4-fold lower in estivators (p=0.11) implying that, in contrast to mammalian hibernators, this enzyme does not drive the combustion of lipids that helps spare hypometabolic muscle.