Caractéristiques physiologiques des alpinistes de haute altitude

Richalet, J.-P.; Keromes, A; Dersch, B.; Corizzi, F.; Mehdioui, H.; Pophillat, B.; Chardonnet, H.; Tassery, F.; Herry, J.-P.; Rathat, C; Chaduteau, Carine; Darnaud, B.

doi:10.1016/s0765-1597(88)80002-9

Cited by 54 publications

(46 citation statements)

References 36 publications

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“…Individual values showed a slightly greater overlap compared to resting values. In contrast to a previous study, we found no significant differences between groups in the decrease of Sa,O 2 and the increase of ventilation during a steady-state exercise over 15 min [32]. The discrepancy may be due to a lower level of exercise intensity (35 vs, 50%V 'O 2 ,max) and hypoxia (14 vs 11.5%) which were chosen for reasons of safety.…”

Section: Discussioncontrasting

confidence: 99%

Ventilatory and pulmonary vascular response to hypoxia and susceptibility to high altitude pulmonary oedema

Hohenhaus¹,

Paul²,

McCullough³

et al. 1995

Eur Respir J

144

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Reduced tolerance to high altitude may be associated with a low ventilatory and an increased pulmonary vascular response to hypoxia. We therefore, examined whether individuals susceptible to acute mountain sickness (AMS) or high altitude pulmonary oedema (HAPE) could be identified by noninvasive measurements of these parameters at low altitude. Ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) at rest and during exercise, as well as hypoxic pulmonary vascular response (HPVR) at rest, were examined in 30 mountaineers whose susceptibility was known from previous identical exposures to high altitude. Isocapnic HVR expressed as difference in minute ventilation related to difference in arterial oxygen saturation (delta V'E/ delta Sa,O2) (L.min-1/%) was significantly lower in subjects susceptible to HAPE (mean +/- SEM 0.8 +/- 0.1; n = 10) compared to nonsusceptible controls (1.5 +/- 0.2; n = 10), but was not significantly different from subjects susceptible to AMS (1.2 +/- 0.2; n = 10). Hypercapnic ventilatory response was not significantly different between the three groups. Discrimination between groups could not be improved by measurements of HVR during exercise (50% maximum oxygen consumption (V'O2,max)), or by assessing ventilation and oxygen saturation during a 15 min steady-state exercise (35% V'O2,max) at fractional inspiratory oxygen (FI,O2) of 0.14. Pulmonary artery pressure (Ppa) estimated by Doppler measurements of tricuspid valve pressure at an FI,O2 of 0.21 and 0.12 (10 min) did not lead to a further discrimination between subjects susceptible to HAPE and AMS with the exception of three subjects susceptible to HAPE who showed an exaggerated HPVR. It is concluded that a low ventilatory response to hypoxia is associated with an increased risk for high altitude pulmonary oedema, whilst susceptibility to acute mountain sickness may be associated with a high or low ventilatory response to hypoxia. A reliable discrimination between subjects susceptible to high altitude pulmonary oedema and acute mountain sickness with a low ventilatory response to hypoxia is not possible by Doppler echocardiographic estimations of hypoxic pulmonary vascular response.

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Section: Discussioncontrasting

confidence: 99%

Ventilatory and pulmonary vascular response to hypoxia and susceptibility to high altitude pulmonary oedema

Hohenhaus¹,

Paul²,

McCullough³

et al. 1995

Eur Respir J

144

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“…This test is a submaximal exercise test performed at a power output corresponding to 30% of the normoxic _ V O 2 max measured before the training session. We used a slightly modified test previously described by Richalet et al (1988) which is composed of four phases of 5 min each: rest in normoxia, rest in hypoxia (corresponding to 11.5% of oxygen in gas mixture, i.e. 4,800 m), exercise in hypoxia (11.5% of oxygen in gas mixture), exercise in normoxia.…”

Section: Performance and Hematologymentioning

confidence: 99%

“…Pulmonary ventilation was recorded breath by breath and averaged every 30 seconds (CPX/D cardiopulmonary exercise system; Medical Graphics, Minneapolis, MN, USA). Calculated parameters were: Hypoxic Ventilatory Response at exercise (HVRe), Hypoxic Cardiac Response at exercise (HCRe) and desaturation at exercise (DSaO 2 e) (Richalet et al 1988) (see below for the calculation formulas of DSaO 2 e, HVRe and HCRe).…”

Section: Performance and Hematologymentioning

confidence: 99%

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Living high-training low: tolerance and acclimatization in elite endurance athletes

Brugniaux

Schmitt

Robach³

et al. 2005

Eur J Appl Physiol

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The "living high-training low" (LHTL) model is frequently used to enhance aerobic performance. However, the clinical tolerance and acclimatization process to this intermittent exposure needs to be examined. Forty one athletes from three federations (cross-country skiers, n=11; swimmers, n=18; runners, n=12) separately performed a 13 to 18-day training at the altitude of 1,200 m, by sleeping either at 1,200 m (CON) or in hypoxic rooms (HYP), with an O2 fraction corresponding to 2,500 m (5 nights for swimmers and 6 for skiers and runners), 3,000 m (6 nights for skiers, 8 for swimmers and 12 for runners) and 3,500 m (6 nights for skiers). Measurements performed before, 1 or 15 days after training were ventilatory response (HVRe) and desaturation (deltaSaO2e) during hypoxic exercise, an evaluation of cardiac function by echocardiography, and leukocyte count. Lake Louise AMS score and arterial O2 saturation during sleep were measured daily for HYP. Subjects did not develop symptoms of AMS. Mean nocturnal SaO2 decreased with altitude down to 90% at 3,500 m and increased with acclimatization (except at 3,500 m). Leukocyte count was not affected except at 3,500 m. The heart function was not affected by LHTL. Signs of ventilatory acclimatization were present immediately after training (increased HVRe and decreased deltaSaO2e) and had disappeared 15 days later. In conclusion, LHTL was well tolerated and compatible with aerobic training. Comparison of the three patterns of training suggests that a LHTL session should not exceed 3,000 m, for at least 18 days, with a minimum of 12 h day(-1) of exposure.

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“…These measurements were performed either in hypoxia or in normoxia. The main results reported from normoxic tests show that maximal oxygen uptake (Richalet et al 1988;Milledge et al 1991;Savourey et al 1995a), pulmonary functional measurements such as forced vital capacity and forced expiratory volume by second (Savourey et al 1995a), percentage of body fat content (Savourey et al 1995a) were not related to AMS. Body mass index (BMI) has been inversely related to AMS susceptibility by Hirata et al (1989) and Kayser (1991) but not by Savourey et al (1995a).…”

Section: Introductionmentioning

confidence: 97%

Normo or hypobaric hypoxic tests: propositions for the determination of the individual susceptibility to altitude illnesses

et al. 2007

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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).

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Caractéristiques physiologiques des alpinistes de haute altitude

Cited by 54 publications

References 36 publications

Ventilatory and pulmonary vascular response to hypoxia and susceptibility to high altitude pulmonary oedema

Ventilatory and pulmonary vascular response to hypoxia and susceptibility to high altitude pulmonary oedema

Living high-training low: tolerance and acclimatization in elite endurance athletes

Normo or hypobaric hypoxic tests: propositions for the determination of the individual susceptibility to altitude illnesses

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