Difference between revisions of "Calbet 2003 Am J Physiol Regul Integr Comp Physiol"
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{{Publication | {{Publication | ||
|title=Calbet JA, Boushel RC, Radegran G, Sondergaard H, Wagner PD, Saltin B (2003) Why is VO2 max after altitude acclimatization still reduced despite normalization of arterial | |title=Calbet JA, Boushel RC, Radegran G, Sondergaard H, Wagner PD, Saltin B (2003) Why is VO2 max after altitude acclimatization still reduced despite normalization of arterial O<sub>2</sub> content? Am J Physiol Regul Integr Comp Physiol 284:R304-316. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/12388462 PMID: 12388462 Open Access] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/12388462 PMID: 12388462 Open Access] | ||
|authors=Calbet Jose AL, Boushel RC, Radegran G, Sondergaard H, Wagner PD, Saltin B | |authors=Calbet Jose AL, Boushel RC, Radegran G, Sondergaard H, Wagner PD, Saltin B | ||
|year=2003 | |year=2003 | ||
|journal=Am J Physiol Regul Integr Comp Physiol | |journal=Am J Physiol Regul Integr Comp Physiol | ||
|abstract=Acute hypoxia (AH) reduces maximal | |abstract=Acute hypoxia (AH) reduces maximal O<sub>2</sub> consumption (''V''<sub>O<sub>2</sub>max</sub>), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O<sub>2</sub> saturation that can normalize arterial O<sub>2</sub> concentration ([O<sub>2</sub>]), ''V''<sub>O<sub>2</sub>max</sub> remains low. To determine why, seven lowlanders were studied at ''V''<sub>O<sub>2</sub>max</sub> (cycle ergometry) at sea level (SL), after 9-10 wk at 5260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (''F''<sub>i</sub>O<sub>2</sub> = 0.105) equivalent to 5260 m. Pulmonary and leg indexes of O<sub>2</sub> transport were measured in each condition. Both cardiac output and leg blood flow were reduced by approximately 15 % in both AH and CH (''P'' < 0.05). At maximal exercise, arterial [O<sub>2</sub>] in AH was 31 % lower than at SL (''P'' < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O<sub>2</sub> extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76 % of the cardiac output perfused the legs, in CH the legs received only 67 %. Pulmonary ''V''<sub>O<sub>2</sub>max</sub> (4.1 +/- 0.3 L/min at SL) fell to 2.2 +/- 0.1 L/min in AH (''P'' < 0.05) and was only 2.4 +/- 0.2 L/min in CH (''P'' < 0.05). These data suggest that the failure to recover ''V''<sub>O<sub>2</sub>max</sub> after acclimatization despite normalization of arterial [O<sub>2</sub>] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH. | ||
|mipnetlab=CA Vancouver Boushel RC, ES CN Las Palmas Calbet JAL | |mipnetlab=CA Vancouver Boushel RC, ES CN Las Palmas Calbet JAL | ||
}} | }} | ||
Latest revision as of 18:43, 18 December 2021
| Calbet JA, Boushel RC, Radegran G, Sondergaard H, Wagner PD, Saltin B (2003) Why is VO2 max after altitude acclimatization still reduced despite normalization of arterial O2 content? Am J Physiol Regul Integr Comp Physiol 284:R304-316. |
Calbet Jose AL, Boushel RC, Radegran G, Sondergaard H, Wagner PD, Saltin B (2003) Am J Physiol Regul Integr Comp Physiol
Abstract: Acute hypoxia (AH) reduces maximal O2 consumption (VO2max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]), VO2max remains low. To determine why, seven lowlanders were studied at VO2max (cycle ergometry) at sea level (SL), after 9-10 wk at 5260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FiO2 = 0.105) equivalent to 5260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by approximately 15 % in both AH and CH (P < 0.05). At maximal exercise, arterial [O2] in AH was 31 % lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O2 extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76 % of the cardiac output perfused the legs, in CH the legs received only 67 %. Pulmonary VO2max (4.1 +/- 0.3 L/min at SL) fell to 2.2 +/- 0.1 L/min in AH (P < 0.05) and was only 2.4 +/- 0.2 L/min in CH (P < 0.05). These data suggest that the failure to recover VO2max after acclimatization despite normalization of arterial [O2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.
• O2k-Network Lab: CA Vancouver Boushel RC, ES CN Las Palmas Calbet JAL
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Stress:Ischemia-reperfusion Organism: Human Tissue;cell: Skeletal muscle, Lung;gill Preparation: Intact organism
