Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise
Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise
复制标题
DOI：
10.1152/japplphysiol.01173.2006
复制
发表时间：
2007-05-01
影响因子：
3.3
通讯作者：
Sahlin, Kent
中科院分区：
文献类型：
--
作者：
Fernstrom, Maria;Bakkman, Linda;Sahlin, Kent
超耐力运动影响肌肉线粒体功能的假说已被研究。超长耐力运动员在24小时内以其峰值O-2消耗的60%进行跑步、皮划艇和骑自行车。在运动前（Pre-Ex）、运动后（Post-Ex）和恢复28小时后（Rec）进行肌肉活检。在状态3（偶联ATP合成）和状态4（非偶联呼吸）下，分别用脂肪酸[棕榈酰肉碱（PC）]或与丙酮酸（Pyr）一起对分离的线粒体进行呼吸分析。用NADH测定透性线粒体的电子传递链活性。与线粒体蛋白和电子传递链活性相关的状态3呼吸增加了39%和41% （P < 0.05）。状态3呼吸随Pyr无明显变化（P < 0.05）。在Rec时，PC组的状态4呼吸增加，但低于前ex组（P < 0.05）。线粒体效率[ADP添加量除以状态3耗氧量（P/O比）]分别在PC和PC + Pyr组降低了9%和6% （P < 0.05）。肌解偶联蛋白3 (Muscle uncoupling protein 3)，用Western blotting测定，在ex后没有改变，但在ex前有降低的趋势（P = 0.07）。总之，极限耐力运动降低了线粒体的效率。这将增加需氧量，并可能部分解释在标准化运动中观察到的全身耗氧量升高（+13%）。线粒体PC氧化能力的增加表明线粒体水平上底物氧化的可塑性，这在长时间运动中可能是有利的。
The hypothesis that ultraendurance exercise influences muscle mitochondrial function has been investigated. Athletes in ultraendurance performance performed running, kayaking, and cycling at 60% of their peak O-2 consumption for 24 h. Muscle biopsies were taken preexercise (Pre-Ex), postexercise (Post-Ex), and after 28 h of recovery (Rec). Respiration was analyzed in isolated mitochondria during state 3 (coupled to ATP synthesis) and state 4 (noncoupled respiration), with fatty acids alone [palmitoyl carnitine (PC)] or together with pyruvate (Pyr). Electron transport chain activity was measured with NADH in permeabilized mitochondria. State 3 respiration with PC increased Post-Ex by 39 and 41% (P < 0.05) when related to mitochondrial protein and to electron transport chain activity, respectively. State 3 respiration with Pyr was not changed (P > 0.05). State 4 respiration with PC increased Post-Ex but was lower than Pre-Ex at Rec (P < 0.05 vs. Pre-Ex). Mitochondrial efficiency [amount of added ADP divided by oxygen consumed during state 3 (P/O ratio)] decreased Post-Ex by 9 and 6% (P < 0.05) with PC and PC + Pyr, respectively. P/O ratio remained reduced at Rec. Muscle uncoupling protein 3, measured with Western blotting, was not changed Post-Ex but tended to decrease at Rec (P = 0.07 vs. Pre-Ex). In conclusion, extreme endurance exercise decreases mitochondrial efficiency. This will increase oxygen demand and may partly explain the observed elevation in whole body oxygen consumption during standardized exercise (+13%). The increased mitochondrial capacity for PC oxidation indicates plasticity in substrate oxidation at the mitochondrial level, which may be of advantage during prolonged exercise.