Long‐term intermittent hyperoxic exposures do not enhance erythropoiesis (original) (raw)
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Acta Physiologica, 2011
Aim: The purpose of the present study was to evaluate the 'normobaric oxygen paradox' theory by investigating the effect of a 2-h normobaric O 2 exposure on the concentration of plasma erythropoietin (EPO). Methods: Ten healthy males were studied twice in a single-blinded counterbalanced crossover study protocol. On one occasion they breathed air (NOR) and on the other 100% normobaric O 2 (HYPER). Blood samples were collected Pre, Mid and Post exposure; and thereafter, 3, 5, 8, 24, 32, 48, 72 and 96 h, and 1 and 2 weeks after the exposure to determine EPO concentration. Results: The concentration of plasma erythropoietin increased markedly 8 and 32 h after the NOR exposure (approx. 58% and approx. 52%, respectively, P £ 0.05) as a consequence of its natural diurnal variation. Conversely, the O 2 breathing was followed by approx. 36% decrement of EPO 3 h after the exposure (P £ 0.05). Moreover, EPO concentration was significantly lower in HYPER than in the NOR condition 3, 5 and 8 h after the breathing intervention (P £ 0.05). Conclusion: In contrast to the 'normobaric oxygen paradox' theory, the present results indicate that a short period of normobaric O 2 breathing does not increase the EPO concentration in aerobically fit healthy males. Increased O 2 tension suppresses the EPO concentration 3 and 5 h after the exposure; thereafter EPO seems to change in a manner consistent with natural diurnal variation.
Erythropoietin production in normoxic and hypoxic rats with increased blood O2 affinity
Respiration physiology, 1985
Effects of an acute increase in blood O2 affinity on erythropoietin production were studied in normoxic and hypoxic male rats. Blood O2 affinity was increased by exchange-transfusion with blood from sodium cyanate treated rats. P50 was lowered to 27.6 torr (pH 7.4, PCO2 = 40 torr, 37 degrees C) in the recipients compared to 41.8 torr in control rats exchange transfused with normal blood. Hypoxia was induced by exposure to simulated high altitude (4750 or 7000 m) for 16 h. Erythropoietin was determined by in vivo bioassay. In rats with normal blood O2 affinity, plasma erythropoietin was undetectable at 300 m, 0.26 +/- 0.10 U/ml at 4750 m (mean +/- SEM; n = 7), and 3.52 +/- 0.58 U/ml at 7000 m (n = 10). Plasma erythropoietin titers were significantly enhanced in rats with high blood O2 affinity at 300 m (0.05 +/- 0.01 U/ml; n = 4) and moderately increased at 4750 m (0.57 +/- 0.12 U/ml; n = 7), but unchanged at 7000 m (3.88 +/- 0.74 U/ml; n = 10). These results indicate that a high blo...
2012
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Acute Normobaric Hypoxia Stimulates Erythropoietin Release
High Altitude Medicine & Biology, 2008
MacKenzie, Richard W. A., Peter W. Watt, and Neil S. Maxwell. Acute normobaric hypoxia stimulates erythropoietin release. High Alt. Med. Biol. 9:28-37, 2008.-Investigations studying the secretion of EPO (erythropoietin) in response to acute hypoxia have produced mixed results. Further, the errors associated with the various methods used to determine EPO are not well documented. The purpose of the current study was to determine the EPO response of 17 trained male subjects to either an acute bout of normobaric hypoxia (Hy; n ϭ 10) or normoxia (Con; n ϭ 7). A secondary aim was to determine the error associated with the measurement of EPO. After baseline tests, the treatment group (Hy) underwent a single bout of hypoxic exposure (F I O 2 ϳ 0.148; 3100 m) consisting of a 90-min rest period followed by a 30-min exercise phase (50%V O 2max ). Venous blood samples were drawn pre (0 min) and post (120 min) each test to assess changes in plasma EPO (⌬EPO). The control (Con) group was subjected to the same general experimental design, but placed in a normoxic environment (F I O 2 ϳ 0.2093). The Hy group demonstrated a mean increase in EPO [19.3 (4.4) vs. 24.1 (5.1) mU/mL], p Ͻ 0.04, post 120 min of normobaric hypoxia. The calculated technical error of measurement for EPO was 2.1 mU/mL (9.8%). It was concluded that an acute bout of hypoxia, has the capacity to elevate plasma EPO. This study also demonstrates that the increase in EPO accumulation was 2 times greater than the calculated measurement of error.
Frontiers in Physiology, 2021
The "Normobaric Oxygen Paradox" (NOP) is a physiologic mechanism that induces an increase of endogenous erythropoietin (EPO) production by creating a state of relative hypoxia in subjects previously exposed to hyperoxia, followed by a rapid return to normoxia. Oxygen exposure duration and inspired oxygen fraction required to observe a significant increase in EPO or hemoglobin are not clearly defined. Consequently, we here study the effect of one model of relative hypoxia on EPO, reticulocytes and hemoglobin stimulation in patients after surgery. Patients were prospectively randomized in two groups. The O 2 group (n = 10) received 100% oxygen for 1 h per day for eight consecutive days, via a non-rebreathing mask. The control group (n = 12) received no oxygen variation. Serum EPO, hemoglobin and reticulocyte count were measured on admission and postoperatively on days seven and nine. Percentage EPO at day nine with respect to the baseline value was significantly elevated within the groups [O 2 group: 323.7 (SD ± 139.0); control group: 365.6 (SD± 162.0)] but not between them. No significant difference was found between the groups in terms of reticulocytes count and hemoglobin. Our NOP model showed no difference on EPO increase between the two groups. However, both groups expressed separately significant EPO elevation.