肌肉运动能力与神经元型一氧化氮合酶

神经元型一氧化氮合成酶变异型是神经元型一氧化氮合成酶蛋白的一种形式，与骨骼肌的健康密切相关，主要通过一氧化氮合酶变异型信号降低神经肌肉疾病。现在，贾斯汀课题组在西雅图的华盛顿大学实验室已确定神经元型一氧化氮合成酶-β在小鼠骨骼肌，对于运动期间和运动后肌肉力量的产生起着关键作用。

在他们的研究中，鼠肌肉中缺乏nNOS-beta 和 nNOS-mu表现为肌肉质量较小，天生弱小，且易于疲劳。相对于仅缺乏 nNOS-mu的鼠更为明显。该组织nNOS -β特定功能被认为调控骨骼肌结构和功能的完整。相比之下，以前的数据表明，nNOS-mu有助于运动时肌肉代谢加强时的血液供应。关于nNOS -β和nNOS-mu不同的作用，作者发现可能与其在骨骼肌细胞内不同位置有关，前者是定位于高尔基体，而后者定位于肌膜。这些研究表明，一氧化氮合酶蛋白的骨骼肌运动能力方面起着关键的调节作用。

Peak Muscle Performance Requires Two Forms of nNOS Protein

ScienceDaily (Feb. 1, 2010) — The protein nNOS-mu, which is just one form of the nNOS protein, is essential for skeletal muscle health, and signaling via nNOS-mu is commonly reduced in neuromuscular disease. Now, Justin Percival and colleagues, at the University of Washington, Seattle, have identified a crucial role for the nNOS-beta form of nNOS in mouse skeletal muscle, where it enables skeletal muscle to maintain force production during and after exercise.

In the study, mouse muscles lacking both nNOS-beta and nNOS-mu were found to be smaller in mass, to be intrinsically weaker, to be more susceptible to fatigue, and to exhibit more marked postexercise weakness than mouse muscles lacking only nNOS-mu.

The specific function of nNOS-beta was determined to be regulation of skeletal muscle structural and functional integrity. By contrast, previous data have indicated that nNOS-mu helps match blood supply with the metabolic demands of active muscle. These distinct roles for nNOS-beta and nNOS-mu are likely a result of the fact that the authors found the two proteins at distinct locations within skeletal muscle cells; the former was localized to the Golgi apparatus and the latter to the sarcolemma.

These data indicate that nNOS proteins are critical regulators of skeletal muscle exercise performance.