高强度间歇训练改善肥胖患者认知功能的线粒体机制研究进展

Latest Advances in the Mitochondrial Mechanism of High-intensity Interval Training Improving Obesity-induced Cognitive Impairment

肥胖和相关的代谢变化已被证明是认知功能下降的重要危险因素并能损害认知功能,但潜在的神经生物学机制还未完全阐明。大量研究表明,肥胖个体脑内线粒体形态和功能出现异常改变。因此,脑线粒体功能障碍很可能是肥胖患者认知受损的潜在机制之一,而提高线粒体功能将是防治肥胖患者认知损伤的突破口。近年来高强度间歇训练(HIIT)被证明在肥胖健康管理、改善认知障碍方面卓有成效,可作为临床改善肥胖认知损伤的有效方法。HIIT对认知功能产生的有益效应常伴随脑内线粒体功能的提高。本文全面总结和讨论了线粒体功能和肥胖、HIIT之间的内在联系,以及HIIT改善肥胖个体认知损伤的线粒体机制,可为临床上应用HIIT治疗肥胖患者认知损伤提供理论基础。

Obesity and its related metabolic changes have proved to be important risk factors and causes for cognitive decline,but the potential neurobiological mechanisms remain incompletely clear.Numerous studies have shown that there are abnormal alterations in cerebral mitochondrial morphology and function in obese individuals.So cerebral mitochondrial dysfunction may be a probable mechanism for cognitive impairment in obesity,and improving which will be a breakthrough in the prevention and treatment of obesity-related cognitive impairment.High-intensity interval training(HIIT)has recently been proved to be effective in improving obesity-related health management and cognitive impairment,which may be used clinically as an efficient approach to improving obesity-related cognitive impairment.The cognitive benefits from HIIT are often manifested by improved cerebral mitochondrial function.We reviewed the latest advances in the internal relationship of cerebral mitochondrial function with obesity and HIIT,and the mitochondrial mechanism of HIIT improving obesity-related cognitive impairment,which may be evidence for clinical application of HIIT in the treatment of obesity-related cognitive impairment.