Commentaries on Viewpoint: Managing the power grid: How myoglobin can regulate Po2 and energy distribution in skeletal muscle.
Commentaries on Viewpoint: Managing the power grid: How myoglobin can regulate Po2 and energy distribution in skeletal muscle.
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观点评论：管理电网：肌红蛋白如何调节骨骼肌中的 Po2 和能量分布。
DOI：
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发表时间：
2019
影响因子：
3.3
通讯作者：
H. Gunga
中科院分区：
文献类型：
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作者：
J. Bock;N. Kruse;C. Donnelly;D. Hirai;J. Craig;Trenton D. Colburn;T. Musch;D. Poole;R. Rosenberry;Fenghua Tian;Hanli Liu;M. Nelson;B. Piknova;W. Willis;L. Zuo;Tingyang Zhou;A. Riveros;E. Cristancho;H. Gunga
致编辑：克兰顿（1）最近发表的一篇文章强调了一个有见地的观点，即肌红蛋白（Mb）在运动过程中通过从一氧化氮（NO）消耗者转变为NO生产者而作为间质性PO2（PiO2）调节剂的新作用。我们提出了一个争论点，现在众所周知的作用，NO在运动过程中调节PiO2可能包括独立的线粒体“电网”的机制。在过去的十年中，在无机硝酸盐补充的背景下，脱氧肌红蛋白在低PiO2期间将亚硝酸盐还原为NO已被越来越多地讨论。事实上，无机硝酸盐的膳食补充剂（例如，甜菜根汁）通过脱氧Mb促进的连续还原增加循环NO生物利用度（4）。在这里，NO促进小动脉血管平滑肌内的cGMP，增加局部PiO2。最近支持这一观点的研究表明，8周的无机硝酸盐补充改善了血流和血管舒张（即，外周动脉疾病患者运动期间的O2输送）（3）。无机硝酸盐补充增加PiO2的第二种机制可能包括在运动期间抑制介导的血管收缩（功能性交感神经溶解）（2）。纳尔逊及其同事（5）先前的研究表明，单剂量无机硝酸盐可以通过减弱交感神经血管收缩来改善缺血患者的功能性肌肉氧合。总的来说，运动期间调节PiO2可能不仅仅依赖于线粒体的肩膀，特别是在临床人群中。因此，Mb在运动过程中通过NO调节PiO2的作用可能不仅仅限于骨骼肌线粒体，现在可能是时候超越“网格”进行思考了。
TO THE EDITOR: A recent article by Clanton (1) highlights an insightful Viewpoint regarding the emerging role of myoglobin (Mb) as an interstitial PO2 (PiO2) regulator during exercise by switching from a nitric oxide (NO) consumer to an NO producer. We propose a point of contention that the now well-known role of NO in regulating PiO2 during exercise may include mechanisms independent of the mitochondrial “power grid.” The reduction of nitrite to NO during periods of low-PiO2 by deoxyMb has been increasingly discussed over the past decade in the context of inorganic nitrate supplementation. Indeed, dietary supplementation of inorganic nitrate (e.g., beetroot juice) increases circulating NO bioavailability through serial reduction facilitated by deoxyMb (4). Here, NO boosts cGMP within arteriolar vascular smooth muscle increasing local PiO2. Recent works supporting this notion demonstrated that 8 weeks of inorganic nitrate supplementation improved blood flow and vasodilation (i.e., O2 delivery) during exercise in patients with peripheral artery disease (3). A second mechanism by which inorganic nitrate supplementation increases PiO2 may include suppressing -mediated vasoconstriction during exercise (functional sympatholysis) (2). Previous works by Nelson and colleagues (5) demonstrated a single dose of inorganic nitrate can improve functional muscle oxygenation in patients with ischemia by blunting sympathetic vasoconstriction. Collectively, regulating PiO2 during exercise may not rest solely on the shoulders of mitochondria, especially in clinical populations. Thus, the role of Mb in regulating PiO2 via NO during exercise may not be exclusive to skeletal muscle mitochondria and it could be time to think beyond the “grid.”
影响因子：
15.9
作者：
RICHARDSON, RS;NOYSZEWSKI, EA;WAGNER, PD
通讯作者：
WAGNER, PD