Galbès O, Goret L, Caillaud C, Mercier J, Obert P, Candau R, Py G
UMR 866, Différenciation Cellulaire et Croissance, INRA, Université Montpellier 1, Montpellier, France.
Acta Physiol (Oxf). 2008 Jun;193(2):163-73. doi: 10.1111/j.1748-1716.2007.01794.x. Epub 2007 Dec 14.
To determine whether endurance training can counterbalance the negative effects of hypoxia on mitochondrial phosphorylation and expression of the long chain mitochondrial fatty acid transporter muscle carnitine palmitoyl transferase 1 (mCPT-1).
Male Wistar rats were exposed either to hypobaric hypoxia (at a simulated altitude of approximately 4000 m, PIO(2) approximately 90 mmHg) or to normoxia (sea level) for 5 weeks. In each environment, rats were randomly assigned to two groups. The trained group went through a 5-week endurance training programme. The control group remained sedentary for the same time period. Muscle fatty acid oxidation capacity was evaluated after the 5-week period on isolated mitochondria prepared from quadriceps muscles with the use of palmitoylcarnitine or pamitoylCoA + carnitine.
Chronic hypoxia decreased basal (V(0), -31% with pamitoylCoA + carnitine and -21% with palmitoylcarnitine, P < 0.05) and maximal (V(max), -31% with pamitoylCoA + carnitine, P < 0.05) respiration rates, hydroxyacylCoA dehydrogenase activity (-48%, P < 0.05), mCPT-1 activity index (-34%, P < 0.05) and mCPT-1 protein content (-34%, P < 0.05). Five weeks of endurance training in hypoxia brought V(0), mCPT-1 activity index and mCPT-1 protein content values back to sedentary normoxic levels. Moreover, in the group trained in hypoxia, V(max) reached a higher level than in the group that maintained a sedentary lifestyle in normoxia (24.2 nmol O(2). min(-1) . mg(-1) for hypoxic training vs. 19.9 nmol O(2) . min(-1) . mg(-1) for normoxic sedentarity, P < 0.05).
Endurance training can attenuate chronic hypoxia-induced impairments in mitochondrial fatty acid oxidation. This training effect seems mostly mediated by mCPT-1 activity rather than by mCPT-1 content.
确定耐力训练是否能抵消缺氧对线粒体磷酸化以及长链线粒体脂肪酸转运蛋白肌肉肉碱棕榈酰转移酶1（mCPT - 1）表达的负面影响。
将雄性Wistar大鼠置于低压缺氧环境（模拟海拔约4000米，吸入氧分压约90 mmHg）或常氧环境（海平面）5周。在每个环境中，大鼠被随机分为两组。训练组进行为期5周的耐力训练计划。对照组在同一时间段保持 sedentary 状态。5周后，使用棕榈酰肉碱或棕榈酰辅酶A + 肉碱，对从股四头肌制备的分离线粒体评估肌肉脂肪酸氧化能力。
慢性缺氧降低了基础（V(0)，使用棕榈酰辅酶A + 肉碱时降低31%，使用棕榈酰肉碱时降低21%，P < 0.05）和最大（V(max)，使用棕榈酰辅酶A + 肉碱时降低31%，P < 0.05）呼吸速率、羟酰辅酶A脱氢酶活性（-48%，P < 0.05）、mCPT - 1活性指数（-34%，P < 0.05）和mCPT - 1蛋白含量（-34%，P < 0.05）。在缺氧环境中进行5周耐力训练使V(0)、mCPT - 1活性指数和mCPT - 1蛋白含量值恢复到常氧久坐水平。此外，在缺氧训练组中，V(max)达到的水平高于常氧环境中久坐生活方式组（缺氧训练组为24.2 nmol O(2).min(-1).mg(-1)，常氧久坐组为19.9 nmol O(2).min(-1).mg(-1)，P < 0.05）。
耐力训练可减轻慢性缺氧诱导的线粒体脂肪酸氧化损伤。这种训练效果似乎主要由mCPT - 1活性介导，而非mCPT - 1含量。
