Biochemistry Post-graduation Program, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Brazil; Biochemistry Department, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Biochemistry Post-graduation Program, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Brazil; Biochemistry Department, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Exp Neurol. 2021 May;339:113623. doi: 10.1016/j.expneurol.2021.113623. Epub 2021 Jan 30.
Neonatal hypoxia-ischemia (HI) is a major cause of cognitive impairments in infants. Antenatal strategies improving the intrauterine environment can have high impact decreasing pregnancy-derived intercurrences. Physical exercise alters the mother-fetus unity and has been shown to prevent the energetic challenge imposed by HI. This study aimed to reveal neuroprotective mechanisms afforded by pregnancy swimming on early metabolic failure and late cognitive damage, considering animals' sex as a variable. Pregnant Wistar rats were submitted to daily swimming exercise (20' in a tank filled with 32 °C water) during pregnancy. Neonatal HI was performed in male and female pups at postnatal day 7. Electron chain transport, mitochondrial mass and function and ROS formation were assessed in the right brain hemisphere 24 h after HI. From PND45, reference and working spatial memory were tested in the Morris water maze. MicroPET-FDG images were acquired 24 h after injury (PND8) and at PND60, following behavioral analysis. HI induced early energetic failure, decreased enzymatic activity in electron transport chain, increased production of ROS in cortex and hippocampus as well as caused brain glucose metabolism dysfunction and late cognitive impairments. Maternal swimming was able to prevent mitochondrial dysfunction and to improve spatial memory. The intergenerational effects of swimming were sex-specific, since male rats were benefited most. In conclusion, maternal swimming was able to affect the mitochondrial response to HI in the offspring's brains, preserving its function and preventing cognitive damage in a sex-dependent manner, adding relevant information on maternal exercise neuroprotection and highlighting the importance of mitochondria as a therapeutic target for HI neuropathology.
新生儿缺氧缺血性（HI）是婴儿认知障碍的主要原因。改善宫内环境的产前策略可以通过降低妊娠相关并发症产生重大影响。体育锻炼改变了母婴一体性，并已被证明可以预防 HI 带来的能量挑战。本研究旨在揭示妊娠游泳对早期代谢衰竭和晚期认知损伤的神经保护机制，同时考虑动物性别这一变量。妊娠 Wistar 大鼠在妊娠期间每天进行游泳运动（在装满 32°C 水的水箱中游泳 20'）。在出生后第 7 天对雄性和雌性幼仔进行新生儿 HI。HI 后 24 小时评估右侧大脑半球的电子链传递、线粒体质量和功能以及 ROS 形成。从 PND45 开始，在 Morris 水迷宫中测试参考和工作空间记忆。在损伤后 24 小时（PND8）和行为分析后 60 天（PND60）进行 microPET-FDG 图像采集。HI 导致早期能量衰竭，降低电子传递链中的酶活性，增加皮质和海马中的 ROS 产生，并导致脑葡萄糖代谢功能障碍和晚期认知损伤。母体游泳能够预防线粒体功能障碍并改善空间记忆。游泳的代际效应具有性别特异性，因为雄性大鼠受益最大。总之，母体游泳能够影响后代大脑对 HI 的线粒体反应，以依赖于性别的方式保护其功能并预防认知损伤，为母体运动神经保护提供了相关信息，并强调了线粒体作为 HI 神经病理学治疗靶点的重要性。
