Vascular pathologies represent the leading causes of mortality worldwide. The nervous system has evolved mechanisms to compensate for the cerebral hypoxia caused by many of these conditions. Vessel dilation and growth of new vessels are two prominent responses to hypoxia, both of which play a critical role in maintaining cerebral homeostasis. One way to facilitate cerebrovascular plasticity, and develop neuroprotection against vascular pathologies, is through aerobic exercise. The present study explored the long-term consequences of aerobic exercise on vascular structure and function in the motor cortex. Rats were assigned to a sedentary condition or were provided access to running wheels for 26 weeks. Rats were then anesthetized, and angiograms were captured using spectral domain optical coherence tomography (SD-OCT) to explore cerebrovascular reactivity in response to altered oxygen and carbon dioxide status. Following this procedure, all rats were euthanized, and unbiased stereological quantification of blood vessel density was collected from sections of the primary motor cortex infused with India ink. Results demonstrated that chronic exercise increased capillary and arteriole surface area densities and enhanced arteriole reactivity in response to hypercapnia-hypoxia, as displayed by increased vasodilation within the motor cortex of exercised animals.

中文翻译：

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连续跑26周与大鼠运动皮层中持续的血管可塑性有关。

血管病理学是世界范围内导致死亡的主要原因。神经系统已经进化出可以补偿由许多这些状况引起的脑缺氧的机制。血管扩张和新血管的生长是对缺氧的两个重要反应，两者在维持脑稳态中都起着至关重要的作用。促进脑血管可塑性和发展针对血管病变的神经保护作用的一种方法是通过有氧运动。本研究探讨了有氧运动对运动皮层血管结构和功能的长期影响。将大鼠分配到久坐的状态，或者让他们使用行走轮26周。然后将大鼠麻醉，并使用光谱域光学相干断层扫描（SD-OCT）捕获血管造影照片，以探索响应于氧气和二氧化碳状态变化的脑血管反应性。按照此程序，对所有大鼠实施安乐死，并从注入印度墨水的初级运动皮层切片中收集血管密度的无偏立体学量化。结果表明，慢性运动增加了对高碳酸血症-低氧的反应，毛细血管和小动脉的表面积密度，并增强了小动脉的反应性，表现为运动动物运动皮层内血管舒张的增加。并从注入印度墨水的主要运动皮层切片中收集血管密度的无偏立体学量化。结果表明，慢性运动增加了对高碳酸血症-低氧的反应，毛细血管和小动脉的表面积密度，并增强了小动脉的反应性，表现为运动动物运动皮层内血管舒张的增加。并从注入印度墨水的主要运动皮层切片中收集血管密度的无偏立体学量化。结果表明，慢性运动增加了对高碳酸血症-低氧的反应，毛细血管和小动脉的表面积密度，并增强了小动脉的反应性，表现为运动动物运动皮层内血管舒张的增加。