title: Persistent suppression of resting energy expenditure after acute hypoxia.
abstract: Resting energy expenditure (REE) is known to be influenced by various ambient conditions such as oxygen supply. Investigations in healthy subjects during acute hypoxia revealed a drop in REE, but persistent effects after hypoxia had ended have not been examined so far. Although indirect calorimetry is a well-established method to measure REE, it may lead to false conclusions when hyperventilation, rise in lactate or catecholamines, and decrease of food intake accompany hypoxia. Therefore, we determined REE in healthy men after hypoxia had ended and under conditions of controlled energy supply during a glucose clamp. In a double-blind crossover study design, we induced hypoxia for 30 minutes by decreasing oxygen saturation to 75% (vs 96% in a control session) in 13 healthy men. Indirect calorimetry was performed at baseline and 150 minutes after hypoxia had ended. Plasma glucose was held stable between 4.5 and 5.5 mmol/L, and lactate as well as catecholamine concentrations were monitored. In parallel, we measured alterations in hormones of the hypothalamic-pituitary-thyroid axis, which is one known factor mediating changes in REE. Resting energy expenditure was decreased after hypoxia (from 1656+/-80 to 1564+/-97 kcal/d) as compared with the normoxic control condition (1700+/-82 to 1749+/-79 kcal/d, P=.037), whereas the respiratory quotient remained stable (P=.79). Plasma lactate, catecholamine levels, and the pituitary thyroid secretory activity were unchanged after hypoxia (P>.2). Our data demonstrate that the REE decrease persists 150 minutes after acute hypoxia, indicating an adaptation of energy metabolism. This should be valued as an additive pathogenic factor in diseases with disturbed energy metabolism.
authors.affiliation: Department of Psychiatry, University of Luebeck, 23538 Luebeck, Germany. oltmanns@medinf.mu-luebeck.de
authors.forename: Kerstin M
authors.initials: KM
authors.lastname: Oltmanns
authors.forename: Hartmut
authors.initials: H
authors.lastname: Gehring
authors.forename: Sebastian
authors.initials: S
authors.lastname: Rudolf
authors.forename: Bernd
authors.initials: B
authors.lastname: Schultes
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schweiger
authors.forename: Jan
authors.initials: J
authors.lastname: Born
authors.forename: Horst L
authors.initials: HL
authors.lastname: Fehm
authors.forename: Achim
authors.initials: A
authors.lastname: Peters
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004734:Energy Metabolism / Q000502:physiology*; D004837:Epinephrine / Q000097:blood; D015309:Glucose Clamp Technique; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism; D000860:Hypoxia / Q000097:blood / Q000378:metabolism*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D010913:Pituitary-Adrenal System / Q000378:metabolism; D012119:Respiration; D013954:Thyroglobulin / Q000097:blood; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D001786:Blood Glucose; D014284:Triiodothyronine; D019344:Lactic Acid; D013972:Thyrotropin; D013954:Thyroglobulin; D013974:Thyroxine; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine