Acute normobaric hyperoxia transiently attenuates plasma erythropoietin concentration in healthy males: evidence against the ‘normobaric oxygen paradox’ theory

Keramidas, Michail E.; Kounalakis, Stylianos N.; Debevec, Tadej; Norman, Barbara; Gustafsson, Thomas; Eiken, Ola; Mekjavic, Igor B.

doi:10.1111/j.1748-1716.2011.02262.x

Cited by 19 publications

(23 citation statements)

References 42 publications

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“…Compared to the placebo, the IHH protocol induced a transient reduction in [EPO] within the initial 8 h following the IHH protocol. Our results thus present further evidence against the existence of NOP and concur with the findings of Keramidas et al (2011), McGuire et al (2006, and Momeni et al (2011).…”

Section: Discussionsupporting

confidence: 95%

“…In particular, subsequent studies either did not find augmented EPO production following an acute normobaric hyperoxic exposure (McGuire et al 2006;Momeni et al 2011) or have even shown a suppressive effect on EPO production (Keramidas et al 2011). This is in line with the results of previous studies showing the suppression of erythropoietic activity following normobaric hyperoxia in humans (Kokot et al 1994a, b).…”

Section: Introductionsupporting

confidence: 59%

“…On the other hand, our data support the already reported suppressive effect of the normobaric hyperoxia on EPO release (Kokot et al 1994a, b). This hyperoxic suppressive effect on EPO production was recently confirmed by (Keramidas et al 2011), demonstrating that 2 h of O 2 breathing leads to a transient attenuation of plasma EPO levels during the initial 8 h following the exposure.…”

Section: Discussionmentioning

confidence: 64%

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Acute short-term hyperoxia followed by mild hypoxia does not increase EPO production: resolving the “normobaric oxygen paradox”

et al. 2011

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Recent findings suggest that besides renal tissue hypoxia, relative decrements in tissue oxygenation, using a transition of the breathing mixture from hyperoxic to normoxic, can also stimulate erythropoietin (EPO) production. To further clarify the importance of the relative change in tissue oxygenation on plasma EPO concentration [EPO], we investigated the effect of a consecutive hyperoxic and hypoxic breathing intervention. Eighteen healthy male subjects were assigned to either IHH (N = 10) or CON (N = 8) group. The IHH group breathed pure oxygen (F(i)O(2) ~ 1.0) for 1 h, followed by a 1-h period of breathing a hypoxic gas mixture (F(i)O(2) ~ 0.15). The CON group breathed a normoxic gas mixture (F(i)O(2) ~ 0.21) for the same duration (2 h). Blood samples were taken just before, after 60 min, and immediately after the 2-h exposure period. Thereafter, samples were taken at 3, 5, 8, 24, 32, and 48 h after the exposure. During the breathing interventions, subjects remained in supine position. There were significant increases in absolute [EPO] within groups at 8 and 32 h in the CON and at 32 h only in the IHH group. No significant differences in absolute [EPO] were observed between groups following the intervention. Relative (∆[EPO]) levels were significantly lower in the IHH than in the CON group, 5 and 8 h following exposure. The tested protocol of consecutive hyperoxic-hypoxic gas mixture breathing did not induce [EPO] synthesis stimulation. Moreover, the transient attenuation in ∆[EPO] in the IHH group was most likely due to a hyperoxic suppression. Hence, our findings provide further evidence against the "normobaric O(2) paradox" theory.

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Section: Discussionsupporting

confidence: 95%

Section: Introductionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 64%

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Acute short-term hyperoxia followed by mild hypoxia does not increase EPO production: resolving the “normobaric oxygen paradox”

et al. 2011

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“…We instead analyzed the variation of serum EPO expressed as percent of baseline value to exclude any individual circadian EPO variations. Recently, Keramidas et al (2011) did not Wnd any diVerence between EPO levels after 2 h administration of oxygen or air in a single blinded counterbalanced crossover study protocol. They only found, like Balestra and our group, that 100% oxygen was followed by a transient decrease in EPO level, after a period between 3 and 8 h.…”

Section: Discussionmentioning

confidence: 98%

Effect of N-acetyl-cysteine and hyperoxia on erythropoietin production

et al. 2011

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Previous studies in healthy subjects have shown an increase in erythropoietin (EPO) production after administration of N-acetyl-cysteine (NAC). These authors hypothesized that NAC increases intracellular reduced glutathione, decreasing reactive oxygen species and enabling EPO production. We investigated if EPO production could be stimulated with a single dose of NAC, after 90 min of pure oxygen breathing. Thirty-eight healthy volunteers were randomized into either the control (C) group or the NAC group, which received 600 mg NAC PO dissolved in a glass of orange juice, 60 min before breathing 15 L/min of 100% normobaric oxygen. Orange juice was administered to both groups. Blood samples for EPO measurement were taken at T0, before the orange juice administration, and T1, T2, T3 and T4, respectively, 8, 24, 32 and 48 h after the orange juice. The EPO concentrations of the NAC group decreased significantly at T1, followed by a significant increase compared to baseline, which was obvious until T4. The EPO concentrations of the C group did not show any significant variations. In this study, a significant increase of EPO production was observed after a short-term hyperoxic stimulus only when preceded with the administration of a single dose of NAC.

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“…Keramidas et al. () observed diurnal variation of a nadir in values of EPO in the morning hours and zenith levels during the evening and night hours. Additional hematological measurements prior to the experimental period would provide a more accurate baseline interpretation.…”

Section: Discussionmentioning

confidence: 99%

The time course of endogenous erythropoietin, IL‐6, and TNFα in response to acute hypoxic exposures

Turner

Gibson

Watt

et al. 2016

Scandinavian Med Sci Sports

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21Erythropoietin (EPO) rapidly decreases on return from chronic altitude exposure. Acute hypoxia may 22provide an additional stimulus to prevent this decline in EPO. Optimal normobaric hypoxic exposure 23 has not been established; therefore, investigation of methods eliciting the greatest response, whilst 24 not causing any addition stress is required. Eight physically active males (age 27 ± 4 yrs, body mass 25 77.5 ± 9.0 kg, height 179 ± 6 cm) attended the laboratory on four separate occasions, in a 26 randomised order, and rested passively in a hypoxic chamber for 2 h whilst exposed to four 27 simulated altitudes [FiO 2 : 0.209 (SL) 4,800 m [EPO] increased from 5.9 ± 1.5 to 8.1 ± 1.5 mUmL -1 (P = 0.009) and 6.0 ± 1.4 to 8.9 ± 2.0 32 mUmL -1 (P = 0.037), respectively, with the mean increase in [EPO] peaking at 4h (2h post-exposure). 33,Results indicate there were no differences found in IL-6 or TNFα during or post-exposure. An 34 increase in endogenous [EPO] was found two hours post-hypoxic exposure as result of two hours of 35 normobaric hypoxia, equivalent to 4,200 m and above. There was no dose-response relationship in 36[EPO] between the severity of simulated hypoxia. 37Key words: hypoxia, EPO, altitude, cytokines, inflammation, 38 39 2 Introduction 1Exercise performance and haematological responses have been shown to be variable in response to 2 altitude exposures (Chapman et al. 1998;Chapman 2013). Practitioners and coaches should 3 therefore consider individualising an athlete's post-altitude training strategy in order to fully 4 optimise the benefits of the camp. Elite coach, Dick (1992), discussed training at altitude in practice 5 and suggested that on return from altitude, time was needed to reach a stage were performance 6 shows a clear sign of benefit. Although these assumptions were based upon the training status of 7 the athlete, there is haematological evidence to suggest there is a 're-acclimatisation' that occurs 8 when returning to sea level from altitude. Garvican et al. (2012) observed a 1.5% decrease in 9 tHbmass within 3 days of decent from a 3 week natural altitude training camp, which persisted when 10 measured 10 days after decent and Pottgiesser et al. (2012) found that 9 days after completing at 26 11 day simulated altitude training camp there was a 3.0% decrease in tHbmass. Brugniaux et al. (2006) 12 andHeinicke et al. (2005) both found tHbmass in increased after 3 days at sea level but returned to 13 baseline levels after 16 and 15 days, respectively. 14 Prommer et al. (2009) found that when natural altitude dwellers reside at sea level for sustained 15 durations, a reduction in tHbmass occurs. The study found tHbmass remained stable within the first 16 2 weeks at sea level followed by a reduction of ~2% per week before levelling off around 5-6 weeks 17 post-altitude. The reduction in tHbmass was attributed to transiently suppressed erythropoietin 18 (EPO) as a result of returning to a normoxic environment . The removal of the 19 altitude stimulus appear to result in...

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Acute normobaric hyperoxia transiently attenuates plasma erythropoietin concentration in healthy males: evidence against the ‘normobaric oxygen paradox’ theory

Cited by 19 publications

References 42 publications

Acute short-term hyperoxia followed by mild hypoxia does not increase EPO production: resolving the “normobaric oxygen paradox”

Acute short-term hyperoxia followed by mild hypoxia does not increase EPO production: resolving the “normobaric oxygen paradox”

Effect of N-acetyl-cysteine and hyperoxia on erythropoietin production

The time course of endogenous erythropoietin, IL‐6, and TNFα in response to acute hypoxic exposures

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