Ma Chunwei, Zhao Yongcai, Ding Xiaoqing, Gao Binghong
School of Kinesiology, Shanghai University of Sport, Shanghai, China.
Department of Physical Education, Yuncheng University, Yuncheng, China.
Front Physiol. 2022 Jul 18;13:921763. doi: 10.3389/fphys.2022.921763. eCollection 2022.
Hypoxic training improves the microcirculation function of human skeletal muscle, but its mechanism is still unclear. Silent information regulator 2 homolog 3 (Sirt3) can improve mitochondrial function and oxidative status. We aimed to examine the role of Sirt3 in the process of hypoxic training, which affects skeletal muscle microcirculation. C57BL/6 mice were assigned to control (C), hypoxic training (HT), Sirt3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP), and 3-TYP + hypoxic training (3-TYP + HT) groups ( = 6/group). Sirt3 inhibition was induced by intraperitoneal injection of Sirt3 inhibitor 3-TYP. After 6 weeks of intervention, microcirculatory capillary formation and vasomotor capacity were evaluated using immunofluorescence, Western blot, biochemical tests, and transmission electron microscopy (TEM). Laser Doppler flowmetry was used to evaluate skeletal muscle microcirculation blood flow characteristics. Six weeks of hypoxic training enhanced skeletal muscle microcirculation function and increased microcirculatory vasodilation capacity and capillary formation. After the pharmacological inhibition of Sirt3, the reserve capacity of skeletal muscle microcirculation was reduced to varying degrees. After the inhibition of Sirt3, mice completed the same hypoxic training, and we failed to observe the microcirculation function adaptation like that observed in hypoxic training alone. The microcirculation vasodilation and the capillaries number did not improve. Hypoxic training improved skeletal muscle microcirculation vasodilation capacity and increased skeletal muscle microcirculation capillary density. Sirt3 is involved in the adaptation of skeletal muscle microcirculation induced by hypoxic training.
低氧训练可改善人体骨骼肌的微循环功能，但其机制尚不清楚。沉默信息调节因子2同源物3（Sirt3）可改善线粒体功能和氧化状态。我们旨在研究Sirt3在影响骨骼肌微循环的低氧训练过程中的作用。将C57BL/6小鼠分为对照组（C）、低氧训练组（HT）、Sirt3抑制剂3-（1H-1,2,3-三唑-4-基）吡啶（3-TYP）组和3-TYP+低氧训练组（3-TYP+HT）（每组n = 6）。通过腹腔注射Sirt3抑制剂3-TYP来抑制Sirt3。干预6周后，采用免疫荧光、蛋白质免疫印迹、生化检测和透射电子显微镜（TEM）评估微循环毛细血管形成和血管舒缩能力。使用激光多普勒血流仪评估骨骼肌微循环血流特征。六周的低氧训练增强了骨骼肌微循环功能，增加了微循环血管舒张能力和毛细血管形成。在对Sirt3进行药物抑制后，骨骼肌微循环的储备能力有不同程度的降低。在抑制Sirt3后，小鼠完成相同的低氧训练，我们未能观察到单独低氧训练时所观察到的微循环功能适应性变化。微循环血管舒张和毛细血管数量均未改善。低氧训练改善了骨骼肌微循环血管舒张能力，增加了骨骼肌微循环毛细血管密度。Sirt3参与了低氧训练诱导的骨骼肌微循环适应性变化。
