Rat diaphragm mitochondria have lower intrinsic respiratory rates than mitochondria in limb muscles.
Rat diaphragm mitochondria have lower intrinsic respiratory rates than mitochondria in limb muscles.
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DOI：
10.1152/ajpregu.00203.2010
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发表时间：
2011-03
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影响因子：
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通讯作者：
Mary L. García-Cazarín;Jorge L Gamboa;Francisco H Andrade
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文献类型：
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作者：
Mary L. García-Cazarín;Jorge L Gamboa;Francisco H Andrade
骨骼肌的线粒体含量与活动水平成正比，假设所有肌肉的内在线粒体功能都是相同的。这可能不适用于所有肌肉。例如，膈肌是一块持续活跃的肌肉；与其他肌肉相比，它的线粒体可能有本质上的不同。这项研究验证了这样的假设：与小腿三头肌（TS，肢体肌肉）相比，膈肌中的线粒体呼吸速率更高。我们从成年雄性 Sprague Dawley 大鼠的膈肌和 TS 中分离出线粒体。通过极谱法测量线粒体呼吸。通过免疫印迹法测定呼吸复合物、解偶联蛋白 1、2 和 3（UCP1、UCP2 和 UCP3）以及电压依赖性阴离子通道 1 (VDAC1) 的含量。通过分光光度法测量复合物IV活性。线粒体呼吸状态 3（底物和 ADP 驱动）和 5（非耦合）分别为 27 ± 8% 和 24 ± 10%，隔膜中低于 TS（两个比较 P < 0.05）。然而，膈肌线粒体中呼吸复合物 III、IV 和 V、UCP1 和 VDAC1 的含量较高（分别为 23 ± 6、30 ± 8、25 ± 8、36 ± 15 和 18 ± 8%，所有比较 P ≤ 0.04）。隔膜线粒体中复合物 IV 活性高出 64 ± 16% (P ≤ 0.01)。 TS 和膈肌之间线粒体 UCP2 和 UCP3 含量以及复合物 I 活性没有差异。这些数据表明，尽管呼吸复合物的含量较高，但隔膜线粒体的呼吸速率较低。结果推翻了我们最初的假设，并表明线粒体含量并不是横膈膜有氧能力的唯一决定因素。我们认为UCP1和VDAC1在调节膈肌有氧能力方面发挥作用。
The mitochondrial content of skeletal muscles is proportional to activity level, with the assumption that intrinsic mitochondrial function is the same in all muscles. This may not hold true for all muscles. For example, the diaphragm is a constantly active muscle; it is possible that its mitochondria are intrinsically different compared with other muscles. This study tested the hypothesis that mitochondrial respiration rates are greater in the diaphragm compared with triceps surae (TS, a limb muscle). We isolated mitochondria from diaphragm and TS of adult male Sprague Dawley rats. Mitochondrial respiration was measured by polarography. The contents of respiratory complexes, uncoupling proteins 1, 2, and 3 (UCP1, UCP2, and UCP3), and voltage-dependent anion channel 1 (VDAC1) were determined by immunoblotting. Complex IV activity was measured by spectrophotometry. Mitochondrial respiration states 3 (substrate and ADP driven) and 5 (uncoupled) were 27 ± 8% and 24 ± 10%, respectively, lower in diaphragm than in TS (P < 0.05 for both comparisons). However, the contents of respiratory complexes III, IV, and V, UCP1, and VDAC1 were higher in diaphragm mitochondria (23 ± 6, 30 ± 8, 25 ± 8, 36 ± 15, and 18 ± 8% respectively, P ≤ 0.04 for all comparisons). Complex IV activity was 64 ± 16% higher in diaphragm mitochondria (P ≤ 0.01). Mitochondrial UCP2 and UCP3 content and complex I activity were not different between TS and diaphragm. These data indicate that diaphragm mitochondria respire at lower rates, despite a higher content of respiratory complexes. The results invalidate our initial hypothesis and indicate that mitochondrial content is not the only determinant of aerobic capacity in the diaphragm. We propose that UCP1 and VDAC1 play a role in regulating diaphragm aerobic capacity.