Since Bert (1878) and Barcroft (1925), studies on hypoxia are realized by lowering ambient O(2) partial pressure (PO(2)) either by barometric pressure reduction (hypobaric hypoxia HH) or by lowering the O(2) fraction (normobaric hypoxia NH). Today, a question is still debated: "are there any physiological differences between HH and NH for the same ambient PO(2)?" Since published studies are scarce and controversial, we submitted 18 subjects in a random order to a 40-min HH test and to a 40-min NH test at an ambient PO(2) equal to 120 hPa (4500 m). Cardioventilatory variables [breathing frequency (f), tidal volume (V(t)), minute ventilation (V(E)), O(2) and CO(2) end-tidal fractions or pressures (FET(O2) and FET(CO2) or PET(O2) and PET(CO2) respectively), heart rate (HR) and O(2) arterial saturation by pulse oxymetry (SpO(2))] were measured throughout the tests. At the end of the tests, arterial blood samples were taken to measure arterial blood gases [O(2) and CO(2) arterial partial pressures ( Pa(O2) and Pa(CO2)), pH and O(2) arterial saturation (SaO(2))]. Results show that during HH compared to NH, f is greater (P

Assessment of individual susceptibility to altitude illnesses and more particularly to acute mountain sickness (AMS) by means of tests performed in normobaric hypoxia (NH) or in hypobaric hypoxia (HH) is still debated. Eighteen subjects were submitted to HH and NH tests (PIO2=120 hPa, 30 min) before an expedition. Maximal and mean acute mountain sickness scores (AMSmax and mean) were determined using the self-report Lake Louise questionnaire scored daily. Cardio-ventilatory (f, V(T), PetO2 and PetCO2, HR and finger pulse oxymetry SpO2) were measured at times 5 and 30 min of the tests. Arterial (PaO2, PaCO2, pH, SaO2) and capillary haemoglobin (Hb) measurements were performed at times 30 min. Hypoxic ventilatory (HVR) and cardiac (HCR) responses, peripheral O2 blood content (CpO2) were calculated. A significant time effect is found for DeltaSpO2 (P = 0.04). Lower PaCO2 (P = 0.005), SaO2 (P = 0.07) and higher pH (P = 0.02) are observed in HH compared to NH. AMSmax varied from 3 to12 and AMSmean between 0.6 and 3.5. In NH at 30 min, AMSmax is related to PetO2 (R = 0.61, P = 0.03), CpO2 (R = -0.53, P = 0.02) and in HH to CpO2 (R = -0.57, P = 0.01). In NH, AMSmean is related to Deltaf (R = 0.46, P = 0.05), HCR (R = 0.49, P = 0.04), CpO2 (R = -0.51, P = 0.03) and, in HH at 30 min, to V(T) (R = 0.69, P = 0.01) and a tendency for CpO2 (R = -0.43, P = 0.07). We conclude that HH and NH tests are physiologically different and they must last 30 min. CpO2 is an important variable to predict AMS. For practical considerations, NH test is proposed to quantify AMS individual susceptibility using the formulas: AMSmax = 9.47 + 0.104PetO2(hPa)-0.68CpO2 (%), (R = 0.77, P = 0.001); and AMSmean = 3.91 + 0.059Deltaf + 0.438HCR-0.135CpO2 (R = 0.71, P = 0.017).

The aim of this study was first to investigate cardio-ventilatory and haematological responses induced by intermittent acclimation and second to study de-adaptation from high altitude observed after descent. To achieve these objectives nine subjects were submitted to intermittent acclimation in a low barometric chamber (8 h daily for 5 days, day 1 at 4500 m, day 5 at 8500 m) before an expedition to the Himalayas. Cardio-ventilatory changes were measured during a hypobaric poikilocapnic hypoxic test (4500 m, barometric pressure = 589 hPa) and haematological changes were studied at sea level. These measurements were performed before and after acclimation, after return to sea level, but also 1 and 2 months after the expedition. In addition, partial pressures of oxygen and carbon dioxide in arterial blood (PaO2, PaCO2) and arterial erythropoietin concentration [EPO] were measured at rest during the hypoxic test. Results suggested the pre-adaptation protocol was efficient since an increased PaO2 (+12%, P < 0.05), a smaller difference in alveolo-arterial PO2 ( -63%, P < 0.05) and a lower PaCO2 ( -11%, P < 0.05), subsequent to ventilatory changes, were observed after acclimation with a significant increase in reticulocytes and in sea level [EPO] (+44% and +62% respectively, P < 0.05). De-adaptation was characterized by a loss of these cardio-ventilatory changes 1 month after descent, whereas the haematological changes (increased red blood cells and packed cell volume, P < 0.05) persisted for 1 month before disappearing 2 months after descent. This study would also suggest that acute hypoxia performed after a sojourn at high altitude could induce significantly depressed EPO responses (P < 0.05).

Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.