No Evidence For The "Normobaric Oxygen Paradox"

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PURPOSE: Renal tissue hypoxia is an established trigger of de novo erythropoietin (EPO) production. It has recently been suggested that EPO synthesis may be stimulated also by relative hypoxia, induced by an acute exposure to hyperoxia followed by a return to normoxia. This phenomenon has been termed the "normobaric oxygen paradox". The purpose of this study was to evaluate whether such relative hypoxia, induced by acute and successive exposures to hyperoxia and hypoxia can stimulate EPO synthesis. METHODS: [EPO] was measured in ten healthy males before, in the middle, and after a 2 hr hyperoxic/hypoxic (HH) protocol comprising breathing oxygen (FiO2=1.0) for 60 minutes, followed by breathing a hypoxic mixture (FiO2=0.15) for 60 minutes. Values were compared with those obtained during the trial in which eight matched subjects breathed a normoxic air mixture for 2 hrs (Normoxic trial). Thereafter, blood samples were taken 3, 5, 8, 24, 32 and 48 hours after the cessation of HH and Normoxic exposures. RESULTS: There were no significant differences in absolute [EPO] between the HH and Normoxic trials. Significant within group differences in [EPO] were observed; [EPO] was significantly higher at 8 (+ 60%) and 32 h (+ 49%) in the Normoxic, and at 32 h (+ 49%) in the HH trial, compared to values before the trials. In addition, the relative Δ[EPO] values were significantly lower in the HH trials compared to the Normoxic 5 and 8 hours following the exposure. CONCLUSION: Successive and acute periods of breathing hyperoxic and hypoxic gas mixtures did not augment [EPO] synthesis, which in both the HH and Normoxia seems to follow a circadian rhythm. The present results do not support the theory of a "normobaric oxygen paradox". ACKNOWLEDGEMENTS: Supported, in part, by the Slovene Research Agency (Slovenia) and b-Cat (The Netherlands).