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单羧酸转运蛋白依赖性机制赋予了在高海拔低氧环境中抵抗运动性疲劳的能力。

A monocarboxylate transporter-dependent mechanism confers resistance to exercise-induced fatigue in a high-altitude hypoxic environment.

机构信息

Department of General Practice, The 940Th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, BinHe South Road, No.333, Lanzhou, 730050, Gansu, China.

出版信息

Sci Rep. 2023 Feb 20;13(1):2949. doi: 10.1038/s41598-023-30093-1.

DOI:10.1038/s41598-023-30093-1
PMID:36807596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9941081/
Abstract

The body is more prone to fatigue in a high-altitude hypoxic environment, in which fatigue occurs in both peripheral muscles and the central nervous system (CNS). The key factor determining the latter is the imbalance in brain energy metabolism. During strenuous exercise, lactate released from astrocytes is taken up by neurons via monocarboxylate transporters (MCTs) as a substrate for energy metabolism. The present study investigated the correlations among the adaptability to exercise-induced fatigue, brain lactate metabolism and neuronal hypoxia injury in a high-altitude hypoxic environment. Rats were subjected to exhaustive incremental load treadmill exercise under either normal pressure and normoxic conditions or simulated high-altitude, low-pressure and hypoxic conditions, with subsequent evaluation of the average exhaustive time as well as the expression of MCT2 and MCT4 in the cerebral motor cortex, the average neuronal density in the hippocampus, and the brain lactate content. The results illustrate that the average exhaustive time, neuronal density, MCT expression and brain lactate content were positively correlated with the altitude acclimatization time. These findings demonstrate that an MCT-dependent mechanism is involved in the adaptability of the body to central fatigue and provide a potential basis for medical intervention for exercise-induced fatigue in a high-altitude hypoxic environment.

摘要

在高原缺氧环境中,身体更容易疲劳,外周肌肉和中枢神经系统(CNS)都会出现疲劳。后者的关键因素是大脑能量代谢失衡。在剧烈运动中,星形胶质细胞释放的乳酸通过单羧酸转运蛋白(MCTs)被神经元摄取,作为能量代谢的底物。本研究探讨了高原缺氧环境下运动性疲劳适应、脑乳酸代谢和神经元缺氧损伤之间的相关性。在常压常氧或模拟高原低压缺氧条件下,对大鼠进行递增负荷跑台运动至力竭,随后评估平均力竭时间以及大脑运动皮层 MCT2 和 MCT4 的表达、海马神经元平均密度和脑乳酸含量。结果表明,平均力竭时间、神经元密度、MCT 表达和脑乳酸含量与高原适应时间呈正相关。这些发现表明,MCT 依赖性机制参与了身体对中枢疲劳的适应,为高原缺氧环境下运动性疲劳的医学干预提供了潜在依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/6e0b8102a27f/41598_2023_30093_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/6f2cec9affbc/41598_2023_30093_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/7fc98e5b7f1e/41598_2023_30093_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/75b00e88f48f/41598_2023_30093_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/f8bdf9ede868/41598_2023_30093_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/6e0b8102a27f/41598_2023_30093_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/6f2cec9affbc/41598_2023_30093_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/7fc98e5b7f1e/41598_2023_30093_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/75b00e88f48f/41598_2023_30093_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/f8bdf9ede868/41598_2023_30093_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/9941081/6e0b8102a27f/41598_2023_30093_Fig5_HTML.jpg

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