Oxygen transport system before and after exposure to
chronic hypoxia.
Ferretti G, Boutellier U, Pendergast DR, Moia C, Minetti AE, Howald H, di Prampero PE
Department of Physiology, University of Geneva Medical School, Switzerland.
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.