Jean-Benoit Martinot

Université Libre de Bruxelles, Brussels, BRU, Belgium

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Publications (15)46.05 Total impact

  • Jean-Benoit Martinot, Hervé Jean-Pierre Guénard
    European Respiratory Journal 05/2014; 43(5):1535-1536. · 7.13 Impact Factor
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    ABSTRACT: Tibetans have been reported to present with a unique phenotypic adaptation to high altitude characterized by higher resting ventilation (VE) and arterial oxygen saturation (SpO2), no excessive polycythemia and lower pulmonary artery pressures (Ppa) compared to other high altitude populations. How this affects exercise capacity is not exactly known. We measured aerobic exercise capacity during an incremental cardiopulmonary exercise test (CPET), lung diffusing capacity for carbon monoxide (DLCO) and nitric oxide (DLNO) at rest, and mean Ppa (mPpa) and cardiac output by echocardiography at rest and at exercise in 13 Sherpas and in 13 acclimatized lowlander controls at the altitude of 5050 m in Nepal. In Sherpas versus lowlanders, SpO2 was 86 ± 1 vs 83 ± 2 %, mean ± SE (P NS), mPpa at rest 19 ± 1 vs 23 ± 1 mmHg (P<0.05), DLCO corrected for hemoglobin 61 ± 4 vs 37 ± 2 ml/min/mmHg (P<0.001), DLNO 226 ± 18 vs 153 ± 9 ml/min/mmHg (P<0.001), maximum oxygen uptake (VO2max) 32 ± 3 vs 28 ± 1 ml/kg/min (P NS) and ventilatory equivalent for carbon dioxide at anaerobic threshold 40 ± 2 vs 48 ± 2 (P<0.001). VO2max was correlated directly to DLCO and inversely to the slope of mPpa-cardiac index relationships in both Sherpas and acclimatized lowlanders. We conclude that Sherpas compared to acclimatized lowlanders have an unremarkable aerobic exercise capacity but with less pronounced pulmonary hypertension, lower ventilatory responses and higher lung diffusing capacity.
    Journal of Applied Physiology 07/2013; · 3.43 Impact Factor
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    ABSTRACT: Acute exposure to high altitude (HA) induces changes in CO membrane conductance (DmCO) and capillary lung volume (Vc). One source of scatter in literature data is exercise, climbing, prior to HA which was avoided in this study. Measurements were performed in 25 lowlanders at Brussels (D0) and at 4300 m after a 2 or 3 days exposure (D2,3), before and after an exercise test, and 5 days later (D7,8) under a trial with two arterial pulmonary vasodilators and a placebo group. The NO/CO transfer method was used applying either an infinite or a finite value to the NO blood conductance (θNO) which could alter sharply the results. A doppler echocardiography provided the haemodynamic data. Compared to sea level, DLCO increased by 24% at D2,3 and returned to control at D7,8. The increase in DLCO resulted from increases in DmCOand Vc whatever the θNO value The alveolar volume (VA) increased by 16% at D2,3 and normalized at D7,8. The mean increase in systolic arterial pulmonary pressure at rest at D2,3 was slight. The increase in Vc in acute condition might be due to the increase in VA and to the increase in capillary pressure. . Compared to the infinite θNO value, the use of a finite θNO value led to about a two-fold increase in DmCO value and to a persistent increase in DmCO at D7,8 compared to D0. After exercise DmCO decreased slightly in subjects treated by the vasodilators suggesting an effect on interstitial oedema.
    Journal of Applied Physiology 04/2013; · 3.43 Impact Factor
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    ABSTRACT: Abstract Pavelescu, Adriana, Vitalie Faoro, Herve Guenard, Claire de Bisschop, Jean-Benoit Martinot, Christian Melot, Robert Naeije. Pulmonary vascular reserve and exercise capacity at sea level and at high altitude. High Alt. Med. Biol. 14:19-26, 2013.-It has been suggested that increased pulmonary vascular reserve, as defined by reduced pulmonary vascular resistance (PVR) and increased pulmonary transit of agitated contrast measured by echocardiography, might be associated with increased exercise capacity. Thus, at altitude, where PVR is increased because of hypoxic vasoconstriction, a reduced pulmonary vascular reserve could contribute to reduced exercise capacity. Furthermore, a lower PVR could be associated with higher capillary blood volume and an increased lung diffusing capacity. We reviewed echocardiographic estimates of PVR and measurements of lung diffusing capacity for nitric oxide (DLNO) and for carbon monoxide (DLCO) at rest, and incremental cardiopulmonary exercise tests in 64 healthy subjects at sea level and during 4 different medical expeditions at altitudes around 5000 m. Altitude exposure was associated with a decrease in maximum oxygen uptake (Vo2max), from 42±10 to 32±8 mL/min/kg and increases in PVR, ventilatory equivalents for CO2 (VE/Vco2), DLNO, and DLCO. By univariate linear regression Vo2max at sea level and at altitude was associated with VE/Vco2 (p<0.001), mean pulmonary artery pressure (mPpa, p<0.05), stroke volume index (SVI, p<0.05), DLNO (p<0.02), and DLCO (p=0.05). By multivariable analysis, Vo2max at sea level and at altitude was associated with VE/Vco2, mPpa, SVI, and DLNO. The multivariable analysis also showed that the altitude-related decrease in Vo2max was associated with increased PVR and VE/Vco2. These results suggest that pulmonary vascular reserve, defined by a combination of decreased PVR and increased DLNO, allows for superior aerobic exercise capacity at a lower ventilatory cost, at sea level and at high altitude.
    High altitude medicine & biology 03/2013; 14(1):19-26. · 1.58 Impact Factor
  • American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012
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    ABSTRACT: Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (Vo(2 max)). The diffusing capacities for nitric oxide (DL(NO)) and carbon monoxide (DL(CO)) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DL(CO) (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DL(CO), DL(NO), and Dm but a slight decrease in Vc. Exercise at altitude decreased DL(NO) and Dm. Sitaxsentan intake improved Vo(2 max) together with an increase in resting and postexercise DL(NO) and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DL(NO). Both DL(CO) and DL(NO) were correlated to Vo(2 max) at sea level (r = 0.41-0.42, P < 0.1) and more so at altitude (r = 0.56-0.59, P < 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity.
    Journal of Applied Physiology 01/2012; 112(1):20-5. · 3.43 Impact Factor
  • American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado; 05/2011
  • American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado; 05/2011
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    ABSTRACT: Lung carbon monoxide (CO) transfer and pulmonary capillary blood volume (Vc) at high altitudes have been reported as being higher in native highlanders compared to acclimatised lowlanders but large discrepancies appears between the studies. This finding raises the question of whether hypoxia induces pulmonary angiogenesis. Eighteen highlanders living in Bolivia and 16 European lowlander volunteers were studied. The latter were studied both at sea level and after acclimatisation to high altitude. Membrane conductance (Dm(CO)) and Vc, corrected for the haemoglobin concentration (Vc(cor)), were calculated using the NO/CO transfer technique. Pulmonary arterial pressure and left atrial pressures were estimated using echocardiography. Highlanders exhibited significantly higher NO and CO transfer than acclimatised lowlanders, with Vc(cor)/VA and Dm(CO)/VA being 49 and 17% greater (VA: alveolar volume) in highlanders, respectively. In acclimatised lowlanders, Dm(CO) and Dm(CO)/VA values were lower at high altitudes than at sea level. Echocardiographic estimates of cardiac output and pulmonary arterial pressure were significantly elevated at high altitudes as compared to sea level. The decrease in Dm(CO) in lowlanders might be due to altered gas transport in the airways due to the low density of air at high altitudes. The disproportionate increase in Vc in Andeans compared to the change in Dm(CO) suggests that the recruitment of capillaries is associated with a thickening of the blood capillary sheet. Since there was no correlation between the increase in Vc and the slight alterations in haemodynamics, this data suggests that chronic hypoxia might stimulate pulmonary angiogenesis in Andeans who live at high altitudes.
    Nitric Oxide 11/2010; 23(3):187-93. · 3.27 Impact Factor
  • American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans; 05/2010
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    ABSTRACT: High-altitude exposure is a cause of pulmonary hypertension and decreased exercise capacity, but associated changes in cardiac function remain incompletely understood. The aim of this study was to investigate right ventricular (RV) and left ventricular function in acclimatized Caucasian lowlanders compared with native Bolivian highlanders at high altitudes. Standard echocardiography and tissue Doppler imaging studies were performed in 15 healthy lowlanders at sea level; <24 hours after arrival in La Paz, Bolivia, at 3,750 m; and after 10 days of acclimatization and ascent to Huayna Potosi, at 4,850 m, and the results were compared with those obtained in 15 age- and body size-matched inhabitants of Oruro, Bolivia, at 4,000 m. Acute exposure to high altitude in lowlanders caused an increase in mean pulmonary arterial pressure, to 20 to 25 mm Hg, and altered RV and left ventricular diastolic function, with prolonged isovolumic relaxation time, an increased RV Tei index, and maintained RV systolic function as estimated by tricuspid annular plane excursion and the tricuspid annular S wave. This profile was essentially unchanged after acclimatization and ascent to 4,850 m, except for higher pulmonary arterial pressure. The native highlanders presented with relatively lower pulmonary arterial pressures but more pronounced alterations in diastolic function, decreased tricuspid annular plane excursion and tricuspid annular S waves, and increased RV Tei indexes. In conclusion, cardiac adaptation to high altitude was qualitatively similar in acclimatized Caucasian lowlanders and in Bolivian native highlanders. However, lifelong exposure to high altitude may be associated with different cardiac adaptation to milder hypoxic pulmonary hypertension.
    The American journal of cardiology 06/2009; 103(11):1605-9. · 3.58 Impact Factor
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    ABSTRACT: Aerobic exercise capacity is decreased at altitude because of combined decreases in arterial oxygenation and in cardiac output. Hypoxic pulmonary vasoconstriction could limit cardiac output in hypoxia. We tested the hypothesis that acetazolamide could improve exercise capacity at altitude by an increased arterial oxygenation and an inhibition of hypoxic pulmonary vasoconstriction. Resting and exercise pulmonary artery pressure (Ppa) and flow (Q) (Doppler echocardiography) and exercise capacity (cardiopulmonary exercise test) were determined at sea level, 10 days after arrival on the Bolivian altiplano, at Huayna Potosi (4,700 m), and again after the intake of 250 mg acetazolamide vs. a placebo three times a day for 24 h. Acetazolamide and placebo were administered double-blind and in a random sequence. Altitude shifted Ppa/Q plots to higher pressures and decreased maximum O(2) consumption ((.)Vo(2max)). Acetazolamide had no effect on Ppa/Q plots but increased arterial O(2) saturation at rest from 84 +/- 5 to 90 +/- 3% (P < 0.05) and at exercise from 79 +/- 6 to 83 +/- 4% (P < 0.05), and O(2) consumption at the anaerobic threshold (V-slope method) from 21 +/- 5 to 25 +/- 5 ml.min(-1).kg(-1) (P < 0.01). However, acetazolamide did not affect (.)Vo(2max) (from 31 +/- 6 to 29 +/- 7, and the maximum respiratory exchange ratio decreased from 1.2 +/- 0.06 to 1.05 +/- 0.03 (P < 0.001). We conclude that acetazolamide does not affect maximum exercise capacity or pulmonary hemodynamics at high altitudes. Associated changes in the respiratory exchange ratio may be due to altered CO(2) production kinetics.
    Journal of Applied Physiology 11/2007; 103(4):1161-5. · 3.43 Impact Factor
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    Circulation 04/2007; 115(9):e308-9. · 14.95 Impact Factor
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    ABSTRACT: The phosphodiesterase-5 inhibitor sildenafil has been reported to improve hypoxic exercise capacity, but the mechanisms accounting for this observation remain incompletely understood. Sixteen healthy subjects were included in a randomized, double-blind, placebo-controlled, cross-over study on the effects of 50-mg sildenafil on echocardiographic indexes of the pulmonary circulation and on cardiopulmonary cycle exercise in normoxia, in acute normobaric hypoxia (fraction of inspired O2, 0.1), and then again after 2 weeks of acclimatization at 5000 m on Mount Chimborazo (Ecuador). In normoxia, sildenafil had no effect on maximum VO2 or O2 saturation. In acute hypoxia, sildenafil increased maximum VO2 from 27 +/- 5 to 32 +/- 6 mL/min/kg and O2 saturation from 62% +/- 6% to 68% +/- 9%. In chronic hypoxia, sildenafil did not affect maximum VO2 or O2 saturation. Resting mean pulmonary artery pressure increased from 16 +/- 3 mmHg in normoxia to 28 +/- 5 mmHg in normobaric hypoxia and 32 +/- 6 mmHg in hypobaric hypoxia. Sildenafil decreased pulmonary vascular resistance by 30% to 50% in these different conditions. We conclude that sildenafil increases exercise capacity in acute normobaric hypoxia and that this is explained by improved arterial oxygenation, rather than by a decrease in right ventricular afterload.
    High Altitude Medicine & Biology 02/2007; 8(2):155-63. · 1.82 Impact Factor
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Publication Stats

111 Citations
46.05 Total Impact Points


  • 2009–2013
    • Université Libre de Bruxelles
      • • Laboratory of Physiology and Physiopathology (PHYSIO)
      • • Faculty of Medicine
      Brussels, BRU, Belgium
    • Sankt Elisabeth Hospital
      Bielefeld, North Rhine-Westphalia, Germany
  • 2012
    • Université de Poitiers
      Poitiers, Poitou-Charentes, France
  • 2007
    • Vrije Universiteit Brussel
      Bruxelles, Brussels Capital Region, Belgium