Acute Normobaric Hypoxia Stimulates Erythropoietin Release

Mackenzie, Richard W.A.; Watt, Peter; Maxwell, Neil

doi:10.1089/ham.2007.1043

Cited by 30 publications

(31 citation statements)

References 48 publications

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“…Accordingly, also the alveolar partial pressure of oxygen after respiratory muscle training significantly increased by approximately 10% (Esposito et al 2010). In another article published in this journal by Sanchis-Gomar et al (2009), it was previously shown that intermittent hypoxic treatment is at least as effective as the administration of recombinant human erythropoietin to increase the red blood cell mass and, inherently, the aerobic performances, in agreement with the previous findings of Mackenzie et al (2008). Taken together, these data support the hypothesis that normobaric hypoxia might indeed contribute to improving sports performance.…”

supporting

confidence: 87%

Normobaric hypoxia and sports: the debate continues

2010

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We have read with interest the recent letter of SanchisGomar et al. (2010), and we basically agree with the authors who concluded that normobaric hypoxia can significantly modify several hematological parameters tested by anti-doping authorities so that anti-doping organizations should take into account the possibility of including normobaric hypoxia among the doping practices at least as a masking method in sports. Nevertheless, we raise several doubts about the fact that two out of three criteria presented by the World Anti-Doping Agency (WADA) for substances and methods to be considered for placement on the prohibited list (i.e., normobaric hypoxia does not exert significant ergogenic effects, and real or simulated altitude is quite safe and unlikely to injure an athlete) were considered by the authors not applicable to normobaric hypoxia.As regards the biological mechanisms supporting the potential ergogenic effect of normobaric hypoxia, these have been recently reviewed by Lemaître et al. (2010) and include (a) optimization of the stimuli needed to improve oxygen delivery while avoiding the detraining effects associated with chronic hypoxia, (b) the splenic contraction effect which increases both hematocrit and hemoglobin between 2 and 5% independently of hemoconcentration and reduces arterial oxygen desaturation, (c) the reduction of blood acidosis (which is enormously advantageous for exercise performance), oxidative stress, and basal metabolic rate, and (d) and the increase in lung volume. It was also recently observed that although 8 weeks of respiratory muscle training did not increase maximum oxygen uptake ð _

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supporting

confidence: 87%

Normobaric hypoxia and sports: the debate continues

2010

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“…Eckardt and Kurtz 2005;Jelkmann 2007). This hypoxia-induced EPO production is well established (Erslev 1997;Faura et al 1969;Ge et al 2002;Mackenzie et al 2008). Eckardt et al (1989) have also shown that the EPO response has a dose-dependent nature, since single exposures to simulated altitudes corresponding to 3,000 and 4,000 m above sea level for 5.5 h caused transient increases in EPO levels equivalent to 1.8 and 3.0-fold, respectively.…”

Section: Introductionmentioning

confidence: 64%

“…Increased [EPO] intensifies the red bone marrow progenitor cells activity in red blood-cell production and can subsequently lead to augmented hematocrit and total hemoglobin mass (Levine and Stray-Gundersen 1997;Stray-Gundersen et al 2001). While short periods (90-120 min) of hypoxic exposure have been shown to augment endogenous EPO production (Mackenzie et al 2008;Rodriguez et al 2000), a distinct dose-related response has also been observed. In particular, Eckardt et al (1989) observed a dose-dependent response in EPO release with DPO 2 stimuli of 62 and 80 hPa, resulting from exposures to simulated altitudes, corresponding to 3,000 and 4,000 m, respectively.…”

Section: Discussionmentioning

confidence: 99%

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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“…85 An increase in EPO levels has been observed after acute exposure to HA. 86 However, after prolonged exposure to hypoxia, EPO does not increase further; on the contrary, its level tends to decrease. 87 In addition, serum EPO levels do not increase further in men with EE at HA.…”

Section: Testosterone and Erythropoiesismentioning

confidence: 97%

Serum testosterone levels and excessive erythrocytosis during the process of adaptation to high altitudes

Gonzales

2013

Asian J Androl

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Populations living at high altitudes (HAs), particularly in the Peruvian Andes, are characterized by a mixture of subjects with erythrocytosis (16 g dl 21 ,haemoglobin (Hb)f21 g dl 21 ) and others with excessive erythrocytosis (EE) (Hb.21 g dl 21 ). Elevated haemoglobin values (EE) are associated with chronic mountain sickness, a condition reflecting the lack of adaptation to HA. According to current data, native men from regions of HA are not adequately adapted to live at such altitudes if they have elevated serum testosterone levels. This seems to be due to an increased conversion of dehydroepiandrosterone sulphate (DHEAS) to testosterone. Men with erythrocytosis at HAs show higher serum androstenedione levels and a lower testosterone/androstenedione ratio than men with EE, suggesting reduced 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activity. Lower 17beta-HSD activity via D4-steroid production in men with erythrocytosis at HA may protect against elevated serum testosterone levels, thus preventing EE. The higher conversion of DHEAS to testosterone in subjects with EE indicates increased 17beta-HSD activity via the D5-pathway. Currently, there are various situations in which people live (human biodiversity) with low or high haemoglobin levels at HA. Antiquity could be an important adaptation component for life at HA, and testosterone seems to participate in this process.

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Acute Normobaric Hypoxia Stimulates Erythropoietin Release

Cited by 30 publications

References 48 publications

Normobaric hypoxia and sports: the debate continues

Normobaric hypoxia and sports: the debate continues

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

Serum testosterone levels and excessive erythrocytosis during the process of adaptation to high altitudes

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