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 in | Journal of applied physiology (1985) Vol. 100; no. 2; pp. 512 - 518 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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United States
Am Physiological Soc
01.02.2006
American Physiological Society |
Subjects | |
Online Access | Get full text |
ISSN | 8750-7587 1522-1601 |
DOI | 10.1152/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 2436 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) |
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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 2436 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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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16239610$$D View this record in MEDLINE/PubMed |
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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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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" |
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