Intermittent hypoxic training: implications for lipid peroxidation induced by acute normoxic exercise in active men
Intermittent hypoxic training: implications for lipid peroxidation induced by acute normoxic exercise in active men
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DOI：
10.1042/cs20010065
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发表时间：
2001-11-01
期刊：
影响因子：
6
通讯作者：
Young, IS
中科院分区：
文献类型：
--
作者：
Bailey, DM;Davies, B;Young, IS
定期体育锻炼期间产生的氧化剂可能会影响适应性反应，这些反应已被证明可以提供针对随后的急性运动引起的氧化应激的保护。为了检验这一点，我们将 32 名男性随机分配到常氧组 (n = 14) 或低氧组 (n = 18)。在急性期，缺氧组的受试者以随机双盲方式进行两次最大循环测试：一次在常氧条件下，另一次在缺氧条件下（O-2 激发分数分别 = 0.21 和 0.16）。间歇期，常氧组和低氧组分别在常氧和缺氧条件下以相同的相对运动强度训练4周。在缺氧条件下的急性运动期间，尽管最大摄氧量（(V)超过点O-2max）相对较低，但脂质氢过氧化物和丙二醛的静脉浓度增加（与常氧相比，P < 0.05）。脂质过氧化氢和丙二醛的增加与运动引起的动脉血红蛋白氧饱和度降低相关（分别为 r = -0.61 和 r = -0.50；P < 0.05），但与点 O-2max 上的 (V) 无关。由于x-生育酚的选择性动员，间歇性低氧训练比常氧训练更有效地减弱急性常氧运动引起的脂质氢过氧化物和丙二醛的增加（P < 0.05）。后者与运动引起的血脂动员/氧化增强有关，因为 (V) 选择性增加超过点 O-2max（与常氧组相比，P < 0.05）。我们得出结论，急性运动诱导的脂质过氧化 (1) 在缺氧期间增加； (2)不完全由(V)对点O-2的质量作用效应调节； (3)通过定期低氧训练选择性减弱。因此，氧化应激可以被认为是人类适应身体应激的生物学先决条件。
Oxidant generation during regular physical exercise training may influence the adaptive responses that have been shown to confer protection against oxidative stress induced by subsequent acute exercise. To examine this, we randomly assigned 32 males to either a normoxic (n = 14) or a hypoxic (n = 18) group. During the acute phase, subjects in the hypoxic group performed two maximal cycling tests in a randomized double-blind fashion :one under conditions of normoxia and the other under hypoxic conditions (inspired fraction of O-2 = 0.21 and 0.16 respectively). During the intermittent phase, the normoxic and hypoxic groups each trained for 4 weeks at the same relative exercise intensity, under conditions of normoxia and hypoxia respectively. During acute exercise under hypoxic conditions, the venous concentrations of lipid hydroperoxides and malondialdehyde were increased, despite a comparatively lower maximal oxygen uptake ((V) over dot O-2max) (P < 0.05 compared with normoxia). The increases in lipid hydroperoxides and malondialdehyde were correlated with the exercise-induced decrease in arterial haemoglobin oxygen saturation (r = -0.61 and r = -0.50 respectively; P < 0.05), but not with (V) over dot O-2max. Intermittent hypoxic training attenuated the increases in lipid hydroperoxides and malondialdehyde induced by acute normoxic exercise more effectively than did normoxic training, due to a selective mobilization of x-tocopherol (P < 0.05). The latter was related to enhanced exercise-induced mobilization/oxidation of blood lipids due to a selective increase in (V) over dot O-2max (P < 0.05 compared with normoxic group). We conclude that lipid peroxidation induced by acute exercise (1) increases during hypoxia; (2) is not regulated exclusively by a mass action effect of (V) over dot O-2; and (3) is selectively attenuated by regular hypoxic training. Oxidative stress may thus be considered as a biological prerequisite for adaptation to physical stress in humans.