We have shown that chronic intermittent hypoxia – modelling human sleep apnoea – causes rat diaphragm muscle weakness and fatigue (1). Antioxidant treatment prevents the deleterious effects of CIH on diaphragm function. In the present study, we sought to determine if CIH causes oxidative stress in rat respiratory muscle. Adult male Wistar rats were exposed to CIH consisting of 90s normoxia/ 90s hypoxia [5% oxygen at the nadir; SaO2 ~80%], for 8h/day or to sham treatment (air/air) for 2 weeks. Following gas treatments, we determined the concentration of thiobarbituric acid reactive substance (TBARS) in diaphragm homogenates as an index of oxidative stress using commercial kits. In addition, 10 µm transverse sections of diaphragm were prepared and immunohistochemically probed for the lipid peroxidation marker – 4-HNE, using an indirect immunofluorescence approach. In separate sections, nuclei were tagged by Hoescht stain and probed for 8-OHdg – a sensitive marker of DNA oxidation. CIH did not significantly increase diaphragm (1.8±0.6 vs. 3.7±1.4 µM MDA/mg protein; mean±SEM, n=6 for both groups, Student’s unpaired t test) or liver TBARS concentration. Moreover, there was no difference in 4-HNE labelling between sham and CIH diaphragm. Of interest, however, we noted evidence of DNA oxidation in 5 out of 6 CIH diaphragms. Our previous studies suggest that the deleterious effect of CIH on respiratory muscle endurance is due to oxidative stress since antioxidants reverse CIH-induced respiratory muscle fatigue (1). The results of the present study indicate that there may be only mild oxidative stress in respiratory muscle in our model. Therefore, the mechanism underpinning the beneficial effects of antioxidant treatment warrants further investigation especially since we have shown that superoxide scavengers are powerful inotropic agents (2).