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Updated: Aug 10, 2026

Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures
Published on: November 2, 2015
Oxygen transport system before and after exposure to chronic hypoxia
G Ferretti1, U Boutellier, D R Pendergast
1Department of Physiology, University of Geneva Medical School, Switzerland.
Abstract:
Maximal VO2 on the treadmill (VO2max) and on the bicycle ergometer (VO2peak), maximal cardiac output (Qmax), by a CO2 rebreathing method, maximal heart rate (HRmax), blood hemoglobin concentration (Hb), and hematocrit (Hct) were measured on six subjects before (B) and 3 weeks after (A) prolonged exposure to chronic hypoxia. It was observed that after high-altitude exposure VO2max, VO2peak, and Qmax were lower (P less than 005) than before [A: 4.13 +/- 0.67; 3.28 +/- 0.41 and 16.89 +/- 2.49 (l/min +/- SD); B: 4.39 +/- 0.39; 3.53 +/- 0.34 and 21.81 +/- 1.27, respectively], whereas Hb and Hct were larger (A: 162 +/- 8 g/l and 0.46 +/- 0.02; B: 142 +/- 7 and 0.41 +/- 0.02) and HRmax was unchanged (178 +/- 7 vs 175 +/- 9 bts/min). Thus, the calculated stroke volume of the heart and the Hb flow at VO2 peak were lower in A than in B (95 +/- 15 vs 124 +/- 7 ml and 2,723 +/- 307 vs 3,129 +/- 196 g/min) (P less than 0.05, respectively), whereas the arteriovenous O2 difference was greater in A than in B (195 +/- 16 vs 162 +/- 19 ml O2/l; P less than 0.05). At any given submaximal work load, VO2 and HR were the same in B and in A, whereas Q was lower in A by approximately 2-3 l/min. However, because of the increased Hb, leading to a higher arterial O2 content, at any work load the O2 flow remained unchanged.
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