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• W2053485485 abstract "Un séjour prolongé (>8 semaines) en haute altitude produit des modifications importantes du métabolisme aérobie et anaérobie. La puissance maximale aérobie subit une réduction progressive provoquée 1) par la baisse de la pression partielle d'O2 dans l'air ambiant et, par conséquent, du pourcentage d'oxyhémoglobine, seulement en partie compensée par la hausse du taux d'hématocrite; 2) par une détérioration du muscle, dont la masse ainsi que l'activité de nombreuses enzymes de la glycolyse et du cycle de Krebs, apparaissent considérablement réduites. Le sujet acclimaté à l'altitude subit aussi une baisse de sa capacité lactique maximale (dette maximum d'oxygène) suite à une réduction du pouvoir tampon de l'organisme provoquée par l'hypocapnie. La puissance maximale développée par les muscles des membres inférieurs, expression de la cinétique de l'hydrolyse de l'ATP, n'est pas réduit par l'hypoxie comme telle. Toutefois, il subit une diminution suite à la réduction de la masse musculaire, provoquée par l'hypoxie chronique. High-altitude exposure impairs the maximal anaerobic (lactic and alactic) performance of man. The maximal aerobic power (VO2max) of man drops with decreasing barometric pressure (PB) at constant FIO2 and/or with decreasing O2 partial pressure in the inspired air (PIO2). For a given decrease of PIO2, the reduction of VO2max found is approximately the same in acute hypoxic subjects, in acclimated lowlanders, and in altitude natives. A sudden rise of PIO2 to 380 Torr was found to raise the VO2max of lowlanders acclimated to 5,350 m from 70% to only 92% of the control sea level VO2max value despite a 37% increase of blood Hb concentration. Since maximal cardiac output (Qmax) at 5,350 m was only 10–20% lower than at sea level, the observed persisting limitation of VO2max upon restoration of normoxia (or even in hyperoxia) can be attributed to a peripheral reduction in O2 transport due to impaired muscle perfusion and/or utilization by the tissue. Consistent with the above hypothesis are the following experimental findings, obtained on subjects acclimated for 5–8 weeks to altitudes of 5,200 m and above in the course of the 1981 Swiss Expedition of Mt Lhotse Shar (8,398 m): (1) a 30–40% reduction of muscle blood flow during two standardized submaximal cycloergometric efforts; (2) a 10–15% decrease of muscle mass as assessed by computer tomography of the thigh; (3) a reduction of the activity of some enzymes of the glycolytic pathway and of the TCA cycle. In lowlanders acclimated to ∼5,500 m, while the resting blood lactate concentrations were found to be unchanged, the maximal lactate concentrations observed after exhausting exercise were reduced to about half the sea level control values, along with a similar decrease of the «apparent buffer value of the body which parallels the drop of bicarbonates in plasma and in extracellular space. The rate of lactate removal from blood after a supramaximal exercise in acclimated lowlanders was found to be the same as at sea level. However, lactate diffusion from the muscle into blood appears to be initially slower, likely because of the decrease of muscle perfusion. The maximal muscular power (Qmax), assessed during a standing high jump off both feet on a force platform, is not affected by chronic hypoxia up to 3 weeks exposure to 5,200 m. Longer exposures, however, lead to a ∼25% drop of wmax, presumably due to a reduction of muscle proteins, itself being dependent on chronic hypoxic exposure. It is concluded that (1) whereas in acute hypoxia maximal aerobic performance is primarily reduced by the drop of blood O2 saturation, the primary factor limiting aerobic exercise in chronic hypoxia is located in the muscle, and (2) prolonged exposure to hypoxia (>5 weeks) has a substantial negative effect on maximal anaerobic muscle power." @default.
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• W2053485485 date "1988-08-01" @default.
• W2053485485 modified "2023-09-25" @default.
• W2053485485 title "Métabolismes aérobie et anaérobie en altitude" @default.
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• W2053485485 doi "https://doi.org/10.1016/s0765-1597(88)80003-0" @default.
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