Park Song-Young, Gifford Jayson R, Andtbacka Robert H I, Trinity Joel D, Hyngstrom John R, Garten Ryan S, Diakos Nikolaos A, Ives Stephen J, Dela Flemming, Larsen Steen, Drakos Stavros, Richardson Russell S
Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah;
Department of Surgery, Huntsman Cancer Hospital, University of Utah, Salt Lake City, Utah;
Am J Physiol Heart Circ Physiol. 2014 Aug 1;307(3):H346-52. doi: 10.1152/ajpheart.00227.2014. Epub 2014 Jun 6.
Unlike cardiac and skeletal muscle, little is known about vascular smooth muscle mitochondrial respiration. Therefore, the present study examined mitochondrial respiratory rates in smooth muscle of healthy human feed arteries and compared with that of healthy cardiac and skeletal muscles. Cardiac, skeletal, and smooth muscles were harvested from a total of 22 subjects (53 ± 6 yr), and mitochondrial respiration was assessed in permeabilized fibers. Complex I + II, state 3 respiration, an index of oxidative phosphorylation capacity, fell progressively from cardiac to skeletal to smooth muscles (54 ± 1, 39 ± 4, and 15 ± 1 pmol·s(-1)·mg(-1), P < 0.05, respectively). Citrate synthase (CS) activity, an index of mitochondrial density, also fell progressively from cardiac to skeletal to smooth muscles (222 ± 13, 115 ± 2, and 48 ± 2 μmol·g(-1)·min(-1), P < 0.05, respectively). Thus, when respiration rates were normalized by CS (respiration per mitochondrial content), oxidative phosphorylation capacity was no longer different between the three muscle types. Interestingly, complex I state 2 normalized for CS activity, an index of nonphosphorylating respiration per mitochondrial content, increased progressively from cardiac to skeletal to smooth muscles, such that the respiratory control ratio, state 3/state 2 respiration, fell progressively from cardiac to skeletal to smooth muscles (5.3 ± 0.7, 3.2 ± 0.4, and 1.6 ± 0.3 pmol·s(-1)·mg(-1), P < 0.05, respectively). Thus, although oxidative phosphorylation capacity per mitochondrial content in cardiac, skeletal, and smooth muscles suggest all mitochondria are created equal, the contrasting respiratory control ratio and nonphosphorylating respiration highlight the existence of intrinsic functional differences between these muscle mitochondria. This likely influences the efficiency of oxidative phosphorylation and could potentially alter ROS production.
与心肌和骨骼肌不同，人们对血管平滑肌线粒体呼吸了解甚少。因此，本研究检测了健康人体足部动脉平滑肌的线粒体呼吸速率，并与健康心肌和骨骼肌的线粒体呼吸速率进行比较。从总共22名受试者（53±6岁）身上获取心肌、骨骼肌和平滑肌，在通透化纤维中评估线粒体呼吸。复合体I+II、状态3呼吸（氧化磷酸化能力的指标）从心肌到骨骼肌再到平滑肌逐渐下降（分别为54±1、39±4和15±1 pmol·s⁻¹·mg⁻¹，P<0.05）。柠檬酸合酶（CS）活性（线粒体密度的指标）也从心肌到骨骼肌再到平滑肌逐渐下降（分别为222±13、115±2和48±2 μmol·g⁻¹·min⁻¹，P<0.05）。因此，当呼吸速率用CS进行标准化（每线粒体含量的呼吸）时，三种肌肉类型之间的氧化磷酸化能力不再有差异。有趣的是，用CS活性标准化的复合体I状态2（每线粒体含量的非磷酸化呼吸指标）从心肌到骨骼肌再到平滑肌逐渐增加，使得呼吸控制率（状态3/状态2呼吸）从心肌到骨骼肌再到平滑肌逐渐下降（分别为5.3±0.7、3.2±0.4和1.6±0.3 pmol·s⁻¹·mg⁻¹，P<0.05）。因此，尽管心肌、骨骼肌和平滑肌中线粒体含量的氧化磷酸化能力表明所有线粒体是相同的，但呼吸控制率和非磷酸化呼吸的差异突出了这些肌肉线粒体之间存在内在功能差异。这可能影响氧化磷酸化的效率，并可能改变活性氧的产生。
