FemHab: The effects of bed rest and hypoxia on oxidative stress in healthy women

Independently, both inactivity and hypoxia augment oxidative stress. This study, part of the FemHab project, investigated the combined effects of bed rest-induced unloading and hypoxic exposure on oxidative stress and antioxidant status. Healthy, eumenorrheic women were randomly assigned to the following three 10-day experimental interventions: normoxic bed rest (NBR; n = 11; PIO2 = 133 mmHg), normobaric hypoxic bed rest (HBR; n = 12; PIO2 = 90 mmHg), and ambulatory hypoxic confinement (HAMB; n = 8: PIO2 = 90 mmHg). Plasma samples, obtained before (Pre), during (D2, D6), immediately after (Post) and 24 h after (Post + 1) each intervention, were analyzed for oxidative stress markers [advanced oxidation protein products (AOPP), malondialdehyde (MDA), and nitrotyrosine], antioxidant status [ superoxide dismutase (SOD), catalase, ferric-reducing antioxidant power (FRAP), glutathione peroxidase (GPX), and uric acid (UA)], NO metabolism end-products (NOx), and nitrites. Compared with baseline, AOPP increased in NBR and HBR on D2 (+ 14%; + 12%; P < 0.05), D6 (+ 19%; + 15%; P < 0.05), and Post (+ 22%; + 21%; P < 0.05), respectively. MDA increased at Post + 1 in NBR (+ 116%; P < 0.01) and D2 in HBR (+114%; P < 0.01) and HAMB (+ 95%; P < 0.05). Nitrotyrosine decreased (-45%; P < 0.05) and nitrites increased (+46%; P < 0.05) at Post + 1 in HAMB only. Whereas SOD was higher at D6 (+ 82%) and Post + 1 (+ 67%) in HAMB only, the catalase activity increased on D6 (128%) and Post (146%) in HBR and HAMB, respectively (P < 0.05). GPX was only reduced on D6 (- 20%; P < 0.01) and Post (- 18%; P < 0.05) in HBR. No differences were observed in FRAP and NOx. UA was higher at Post in HBR compared with HAMB (P < 0.05). These data indicate that exposure to combined inactivity and hypoxia impairs prooxidant/antioxidant balance in healthy women. Moreover, habitual activity levels, as opposed to inactivity, seem to blunt hypoxia-related oxidative stress via antioxidant system upregulation.