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http://hdl.handle.net/10553/6557
Título: | Plasma volume expansion does not increase maximal cardiac output or VO2 max in lowlanders acclimatized to altitude | Autores/as: | Calbet, JAL Radegran, Goran Boushel, R. Sondergaard, H. Saltin, Bengt Wagner, P.D. |
Clasificación UNESCO: | 241106 Fisiología del ejercicio | Palabras clave: | Hypoxia Muscle Cardiac output |
Fecha de publicación: | 2004 | Editor/a: | 0363-6135 | Publicación seriada: | American Journal of Physiology - Heart and Circulatory Physiology | Resumen: | With altitude acclimatization, blood hemoglobin concentration increases while plasma volume (PV) and maximal cardiac output (Qmax) decrease. This investigation aimed to determine whether reduction of Qmax at altitude is due to low circulating blood volume (BV). Eight Danish lowlanders (3 females, 5 males: age 24.0 +/- 0.6 yr; mean +/- SE) performed submaximal and maximal exercise on a cycle ergometer after 9 wk at 5,260 m altitude (Mt. Chacaltaya, Bolivia). This was done first with BV resulting from acclimatization (BV = 5.40 +/- 0.39 liters) and again 2-4 days later, 1 h after PV expansion with 1 liter of 6% dextran 70 (BV = 6.32 +/- 0.34 liters). PV expansion had no effect on Qmax, maximal O2 consumption (VO2), and exercise capacity. Despite maximal systemic O2 transport being reduced 19% due to hemodilution after PV expansion, whole body VO2 was maintained by greater systemic O2 extraction (P < 0.05). Leg blood flow was elevated (P < 0.05) in hypervolemic conditions, which compensated for hemodilution resulting in similar leg O2 delivery and leg VO2 during exercise regardless of PV. Pulmonary ventilation, gas exchange, and acid-base balance were essentially unaffected by PV expansion. Sea level Qmax and exercise capacity were restored with hyperoxia at altitude independently of BV. Low BV is not a primary cause for reduction of Qmax at altitude when acclimatized. Furthermore, hemodilution caused by PV expansion at altitude is compensated for by increased systemic O2 extraction with similar peak muscular O2 delivery, such that maximal exercise capacity is unaffected. | URI: | http://hdl.handle.net/10553/6557 | ISSN: | 0363-6135 | DOI: | 10.1152/ajpheart.00840.2003 | Fuente: | American Journal Of Physiology-Heart And Circulatory Physiology[ISSN 0363-6135],v. 287 (3), p. H1214-H1224 |
Colección: | Artículos |
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