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Articles in PresS, published online ahead of print November 30, 2001
J Appl Physiol, 10.1152/jap.00684.2001
Submitted on July 2, 2001
Accepted on November 6, 2001
1 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, USA; Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
2 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, USA
3 Hematology, Baylor College of Medicine, Houston, Texas, USA
4 Norwegian University of Sport and Physical Education, Oslo, Norway; Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, USA
5 Norwegian University of Sport and Physical Education, Oslo, Norway
* To whom correspondence should be addressed. E-mail: BenjaminLevine{at}TexasHealth.org.
To determine the "dose-response" relationship between altitude exposure and erythropoietin (EPO) production, we measured blood EPO concentration, arterial oxygen saturation (SaO2), urine PO2, and renal blood flow (RBF) in 48 subjects (32 men, 16 women) at simulated altitudes of 1780 m, 2085 m, 2454 m and 2800 m (PB of 612mmHg, 590mmHg, 564mmHg, and 538mmHg respectively). EPO, SaO2 and urine PO2 (an index of renal tissue pO2) were measured at sea level and after 6 hr and 24 hr at each simulated altitude. Each altitude was separated by one week of recovery, with the order determined by balanced randomization (ultimate order was 2454/2800/2085/1780m). Renal blood flow (RBF) was determined at sea level and after 6 hr at each altitude by using Doppler ultrasound. Hb was measured at the same time points and renal oxygen delivery was calculated. Results: EPO increased significantly after 6 hr at all altitudes and continued to increase after 24 hr at 2454 m and 2800 m. However, it did not increase further after 24 hr at 1780 m, and 2085 m. The increase in EPO varied markedly among individuals, ranging from -41% to 400% after 24 hr at 2800m. Similar to EPO, urine PO2 decreased after 6 hr at all altitudes and returned to the baseline by 24 hr at the two lowest altitudes, but remained decreased at the two highest altitudes. Urine pO2 was closely related to EPO via a curvilinear relationship (r2=0.99 for grouped data), though this relationship also exhibited prominent individual variability. Mean RBF at sea level was 326 ± 155 ml/min, and it remained unchanged with exposure to all simulated altitudes. SaO2 decreased slightly but significantly after 6 hr at the lowest altitudes, but decreased more prominently at the highest altitudes. There were only modest albeit statistically significant relationships between EPO and measures of SaO2 (r= 0.45, p<0.05), and no significant relationship with renal oxygen delivery. These data suggest: (1) the altitude-induced increase in EPO is "dose" dependent: altitudes 
2100-2,500m appears to be a threshold for stimulating sustained EPO release in the majority of subjects; (2) short-term acclimatization may restore renal tissue oxygenation and restrain the rise in EPO at the lowest altitudes; 3) there is marked individual variability in the erythropoietic response to simulated altitude which is only partially explained by "upstream" physiological factors such as those reflecting oxygen delivery to EPO producing tissues.
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