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Prolonged muscle exposure to low PO 2  conditions may cause oxidative stress resulting in severe muscular injuries. We hypothesize that PO 2  cycling preconditioning, which involves brief cycles of diaphragmatic muscle exposure to a low oxygen level (40 Torr) followed by a high oxygen level (550 Torr), can reduce intracellular reactive oxygen species (ROS) as well as attenuate muscle fatigue in mouse diaphragm under low PO 2 . Accordingly, dihydrofluorescein (a fluorescent probe) was used to monitor muscular ROS production in real time with confocal microscopy during a lower PO 2  condition. In the control group with no PO 2  cycling, intracellular ROS formation did not appear during the first 15 min of the low PO 2  period. However, after 20 min of low PO 2 , ROS levels increased significantly by ∼30% compared to baseline, and this increase continued until the end of the 30 min low PO 2  condition. Conversely, muscles treated with PO 2  cycling showed a complete absence of enhanced fluorescence emission throughout the entire low PO 2  period. Furthermore, PO 2  cycling-treated diaphragm exhibited increased fatigue resistance during prolonged low PO 2  period compared to control. Thus, our data suggest that PO 2  cycling mitigates diaphragm fatigue during prolonged low PO 2 . Although the exact mechanism for this protection remains to be elucidated, it is likely that through limiting excessive ROS levels, PO 2  cycling initiates ROS-related antioxidant defenses.

PO2 Cycling Reduces Diaphragm Fatigue by Attenuating ROS Formation