Lactate during exercise at extreme altitude.
Lactate during exercise at extreme altitude.
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发表时间：
1986-12
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通讯作者：
J. West
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作者：
J. West
在极端海拔高度进行最大限度的运动会导致严重的动脉低氧血症，并可能导致严重的组织缺氧。现有的最佳证据表明，珠峰峰峰顶的静息动脉PO2约为28 mmHg，在运动期间甚至会进一步下降。尽管如此，大约有10名登山者在没有补充氧气的情况下到达了山顶。奇怪的是，在高海拔地区，对于一个给定的工作速率，在适应的受试者的血乳酸基本上是相同的，在海平面。因为工作能力随着海拔高度的增加而明显下降，最大血乳酸也会下降福尔斯。外推现有的数据高达6300米表明，登山者谁达到珠峰首脑会议将没有增加血乳酸。在极高海拔地区运动时低血乳酸的原因尚不完全清楚。一种可能性是在适应的受试者中血浆碳酸氢盐的耗尽，这减少了缓冲并导致对于给定的乳酸盐释放的H+浓度的大幅增加。随之而来的pH的局部下降可能抑制酶，例如，磷酸果糖激酶（EC 2.7.1.56），在糖酵解途径中。
Maximal exercise at extreme altitude results in profound arterial hypoxemia and, presumably, extreme tissue hypoxia. The best evidence available indicates that the resting arterial PO2 on the summit of Mount Everest is about 28 torr and that it falls even further during exercise. Nevertheless, some 10 climbers have now reached the summit without supplementary oxygen. Paradoxically, blood lactate for a given work rate at high altitude in acclimatized subjects is essentially the same as at sea level. Because work capacity decreases markedly with increasing altitude, maximal blood lactate also falls. Extrapolation of available data up to 6300 m indicates that a climber who reaches the Everest summit will have no increase in blood lactate. The cause of the low blood lactate during exercise at extreme altitude is not fully understood. One possibility is depletion of plasma bicarbonate in acclimatized subjects, which reduces buffering and results in large increases in H+ concentration for a given release of lactate. The consequent local fall in pH may inhibit enzymes, e.g., phosphofructokinase (EC 2.7.1.56), in the glycolytic pathway.