Serum erythropoietin levels in healthy humans after a short period of normobaric and hyperbaric oxygen breathing: the "normobaric oxygen paradox"

1 Divers Alert Network Europe Research Division, 2 Université Libre de Bruxelles Institut Supérieur d'Éducation Physique et de Kinésithérapie; 3 Department of Environmental & Occupational Physiology, Haute Ecole Paul Henri Spaak; and 4 Center for Hyperbaric Oxygen Therapy, Military Hospital...

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Published inJournal of applied physiology (1985) Vol. 100; no. 2; pp. 512 - 518
Main Authors Balestra, Costantino, Germonpre, Peter, Poortmans, Jacques R, Marroni, Alessandro
Format Journal Article
LanguageEnglish
Published United States Am Physiological Soc 01.02.2006
American Physiological Society
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Online AccessGet full text
ISSN8750-7587
1522-1601
DOI10.1152/japplphysiol.00964.2005

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Abstract 1 Divers Alert Network Europe Research Division, 2 Université Libre de Bruxelles Institut Supérieur d'Éducation Physique et de Kinésithérapie; 3 Department of Environmental & Occupational Physiology, Haute Ecole Paul Henri Spaak; and 4 Center for Hyperbaric Oxygen Therapy, Military Hospital Queen Astrid, Brussels, Belgium Submitted 8 August 2005 ; accepted in final form 10 October 2005 Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24–36 h. A 60% increase ( P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the "normobaric oxygen paradox," does not appear to be present after hyperbaric oxygen breathing. erythropoietin stimulus; erythropoietin; hypoxia Address for reprint requests and other correspondence: C. Balestra, Environmental & Occupational Physiology Dept., Haute Ecole Paul Henri Spaak, Pôle Universitaire de Bruxelles Wallonie, 91 Ave. C. Schaller, 1160 Bruxelles, Belgium (e-mail: balestra@daneurope.org)
AbstractList Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24–36 h. A 60% increase ( P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the “normobaric oxygen paradox,” does not appear to be present after hyperbaric oxygen breathing.
1 Divers Alert Network Europe Research Division, 2 Université Libre de Bruxelles Institut Supérieur d'Éducation Physique et de Kinésithérapie; 3 Department of Environmental & Occupational Physiology, Haute Ecole Paul Henri Spaak; and 4 Center for Hyperbaric Oxygen Therapy, Military Hospital Queen Astrid, Brussels, Belgium Submitted 8 August 2005 ; accepted in final form 10 October 2005 Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24–36 h. A 60% increase ( P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the "normobaric oxygen paradox," does not appear to be present after hyperbaric oxygen breathing. erythropoietin stimulus; erythropoietin; hypoxia Address for reprint requests and other correspondence: C. Balestra, Environmental & Occupational Physiology Dept., Haute Ecole Paul Henri Spaak, Pôle Universitaire de Bruxelles Wallonie, 91 Ave. C. Schaller, 1160 Bruxelles, Belgium (e-mail: balestra@daneurope.org)
Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24-36 h. A 60% increase (P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the "normobaric oxygen paradox," does not appear to be present after hyperbaric oxygen breathing.Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24-36 h. A 60% increase (P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the "normobaric oxygen paradox," does not appear to be present after hyperbaric oxygen breathing.
Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24-36 h. A 60% increase (P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the "normobaric oxygen paradox," does not appear to be present after hyperbaric oxygen breathing. [PUBLICATION ABSTRACT]
Author Balestra, Costantino
Germonpre, Peter
Poortmans, Jacques R
Marroni, Alessandro
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Snippet 1 Divers Alert Network Europe Research Division, 2 Université Libre de Bruxelles Institut Supérieur d'Éducation Physique et de Kinésithérapie; 3 Department of...
Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative...
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StartPage 512
SubjectTerms Blood Gas Monitoring, Transcutaneous
Erythropoietin - blood
Female
Hormones
Humans
Hyperbaric Oxygenation
Hyperoxia - blood
Hypoxia
Hypoxia - blood
Kidneys
Male
Oxygen
Oxygen - blood
Respiratory system
Time Factors
Title Serum erythropoietin levels in healthy humans after a short period of normobaric and hyperbaric oxygen breathing: the "normobaric oxygen paradox"
URI http://jap.physiology.org/cgi/content/abstract/100/2/512
https://www.ncbi.nlm.nih.gov/pubmed/16239610
https://www.proquest.com/docview/222161206
https://www.proquest.com/docview/70702979
Volume 100
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