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

doi:10.12114/j.issn.1007-9572.2022.0239

中国全科医学 ›› 2022, Vol. 25 ›› Issue (29): 3702-3709.DOI: 10.12114/j.issn.1007-9572.2022.0239

所属专题：肥胖最新文章合辑

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

蔡明¹^,², 王晓军³, 陈晓艳⁴, 胡静芸⁵^,^*()

1．201318　上海市，上海健康医学院康复学院
2．200240　上海市，上海交通大学Bio-X研究院
3．201615　上海市，上海赫尔森康复医院科教科
4．201615　上海市，上海赫尔森康复医院康复治疗管理科
5．201299　上海市浦东新区人民医院中心实验室　病原真菌医学检验中心

收稿日期:2022-01-14 修回日期:2022-04-20 出版日期:2022-10-15 发布日期:2022-05-06
通讯作者: 胡静芸
蔡明，王晓军，陈晓艳，等.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[J].中国全科医学，2022，25（29）：3702-3709. [www.chinagp.net]
作者贡献：蔡明负责文献和资料收集、论文撰写及论文图片制作；王晓军负责文章的质量控制及审校；陈晓艳负责文章的文献/资料整理；胡静芸负责研究命题的提出、设计及负责最终版本修订，对论文负责。所有作者确认论文终稿。
基金资助:
教育部人文社会科学研究青年基金项目（20YJCZH001）——"健康中国2030"战略下老年轻度认知障碍风险因素筛查模式构建及康复干预实证研究; 中国博士后基金面上项目（2021M702128）——间歇性低氧训练激活HIF-1α重塑AD早期海马能量代谢的机制研究; 横向科研项目（HXXM-21-03-005）——虚拟情景互动训练系统对卒中后轻度认知障碍的康复治疗效果验证; 上海市青年科技英才扬帆计划资助项目（22YF1441600）——乳酸在高强度间歇训练调控糖尿病脑病小鼠海马能量代谢中作用及机制探究

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

Ming CAI¹^,², Xiaojun WANG³, Xiaoyan CHEN⁴, Jingyun HU⁵^,^*()

1. College of Rehabilitation Sciences, Shanghai University of Medicine & Health Sciences, Shanghai 201318, China
2. Bio-X Institutes, Shanghai Jiao Tong University, Shanghai 200240, China
3. Department of Science and Education, Shanghai Herson Rehabilitation Hospital, Shanghai 201615, China
4. Department of Rehabilitation Management, Shanghai Herson Rehabilitation Hospital, Shanghai 201615, China
5. Central Lab/Shanghai Key Laboratory of Pathogenic Fungi Medical Testing, Shanghai Pudong New Area People's Hospital, Shanghai 201299, China

Received:2022-01-14 Revised:2022-04-20 Published:2022-10-15 Online:2022-05-06
Contact: Jingyun HU
About author:
CAI M, WANG X J, CHEN X Y, et al. Latest advances in the mitochondrial mechanism of high-intensity interval training improving obesity-induced cognitive impairment[J]. Chinese General Practice, 2022, 25 (29) : 3702-3709.

分享到

摘要/Abstract

摘要： 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。

关键词: 肥胖症, 认知功能障碍, 高强度间歇训练, 线粒体, 综述

Abstract:

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.

Key words: Obesity, Cognitive dysfunction, High-intensity interval training, Mitochondria, Review

蔡明,王晓军,陈晓艳,等. 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[J]. 中国全科医学, 2022, 25(29): 3702-3709. DOI: 10.12114/j.issn.1007-9572.2022.0239.
Ming CAI,Xiaojun WANG,Xiaoyan CHEN, et al. Latest Advances in the Mitochondrial Mechanism of High-intensity Interval Training Improving Obesity-induced Cognitive Impairment[J]. Chinese General Practice, 2022, 25(29): 3702-3709. DOI: 10.12114/j.issn.1007-9572.2022.0239.

图/表 2

图1 引起肥胖患者认知损伤的各因素与线粒体功能障碍间的联系注：High fat food=高脂饮食，Mitochondrial dysfunction=线粒体功能障碍，Mitochondrial swelling=线粒体肿胀，MMP=线粒体膜电位，ATP=三磷酸腺苷，ROS=活性氧，Oxygen consumption=耗氧量，Redox imbalance=氧化还原失衡，Brain=大脑，IR=胰岛素抵抗，Insulin signaling pathway=胰岛素信号通路，Insulin=胰岛素，Insulin receptor=胰岛素受体，IRS-1=胰岛素受体底物1，PI3K/AKT=磷脂酰肌醇激酶/蛋白激酶B，MAPK=丝裂原活化蛋白激酶，Neuroinflammation=神经炎症，NF-κB=核转录因子κB，NLRP3=NOD样受体蛋白3，IL-1β=白介素1β，TNF-α=肿瘤坏死因子α，Inflammatory signaling pathway=炎症信号通路，ERS=内质网应激，GRP78=葡萄糖调节蛋白78，PERK=蛋白激酶R样内质网激酶，IRE1α=肌醇酶1α，eIF2α=真核细胞起始因子2α，Oxidative stress=氧化应激，NRF2=核因子E2相关因子2，Keap1=Kelch样环氧氯丙烷相关蛋白1，Maf=肌肉腱膜纤维肉瘤，ARE=抗氧化反应元件，HO-1=血红素氧合酶1，NQO1=NAD(P)H：醌氧化还原酶1，SOD=超氧化物歧化酶，CAT=过氧化氢酶

Figure 1 The relationship of induction factors of obesity-related cognitive impairment with cerebral mitochondrial dysfunction

图2 HIIT促进认知功能的线粒体机制注：High-intensity interval training=高强度间歇训练，Mitochondrial biogenesis=线粒体生物发生，PGC-1α=过氧化物酶体增殖物激活受体γ共激活因子1α，TFAM=线粒体转录因子，mtDNA=线粒体DNA，Mitochondrial dysfunction=线粒体功能障碍，Cognitive function=认知功能

Figure 2 The possible mechanisms of high-intensity interval training on improving obesity-related cognitive impairment

参考文献 83

[1]	国家国民体质监测中心. 第五次国民体质监测公报[EB/OL]. (2021-12-30)[2022-01-22].
[2]	World Obesity Federation Global Obesity Observatory. Scorecards - Obesity：missing the 2025 targets[EB/OL]. [2022-01-22].
[3]	LIN J D, WU P H, TARR P T，et al. Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1alpha null mice[J]. Cell，2004，119(1):121-135. DOI：10.1016/j.cell.2004.09.013.
[4]	DYE L, BOYLE N B, CHAMP C，et al. The relationship between obesity and cognitive health and decline[J]. Proc Nutr Soc，2017，76(4):443-454. DOI：10.1017/S0029665117002014.
[5]	CRISPINO M, TRINCHESE G, PENNA E，et al. Interplay between peripheral and central inflammation in obesity-promoted disorders：the impact on synaptic mitochondrial functions[J]. Int J Mol Sci，2020，21(17):E5964. DOI：10.3390/ijms21175964.
[6]	SRIPETCHWANDEE J, CHATTIPAKORN N, CHATTIPAKORN S C. Links between obesity-induced brain insulin resistance，brain mitochondrial dysfunction，and dementia[J]. Front Endocrinol （Lausanne），2018，9:496. DOI：10.3389/fendo.2018.00496.
[7]	CAI Q, TAMMINENI P. Alterations in mitochondrial quality control in Alzheimer's disease[J]. Front Cell Neurosci，2016，10:24. DOI：10.3389/fncel.2016.00024.
[8]	RODRIGUEZ A L, WHITEHURST M, FICO B G，et al. Acute high-intensity interval exercise induces greater levels of serum brain-derived neurotrophic factor in obese individuals[J]. Exp Biol Med （Maywood），2018，243(14):1153-1160. DOI：10.1177/1535370218812191.
[9]	DOMÍNGUEZ-SANCHÉZ M A, BUSTOS-CRUZ R H, VELASCO-ORJUELA G P，et al. Acute effects of high intensity，resistance，or combined protocol on the increase of level of neurotrophic factors in physically inactive overweight adults：the BrainFit study[J]. Front Physiol，2018，9:741. DOI：10.3389/fphys.2018.00741.
[10]	KONOPKA A R, ASANTE A, LANZA I R，et al. Defects in mitochondrial efficiency and H₂O₂ emissions in obese women are restored to a lean phenotype with aerobic exercise training[J]. Diabetes，2015，64(6):2104-2115. DOI：10.2337/db14-1701.
[11]	LAHERA V, DE LAS HERAS N, LÓPEZ-FARRÉ A，et al. Role of mitochondrial dysfunction in hypertension and obesity[J]. Curr Hypertens Rep，2017，19(2):11. DOI：10.1007/s11906-017-0710-9.
[12]	DE MELLO A H, COSTA A B, ENGEL J D G，et al. Mitochondrial dysfunction in obesity[J]. Life Sci，2018，192:26-32. DOI：10.1016/j.lfs.2017.11.019.
[13]	CUNARRO J, CASADO S, LUGILDE J，et al. Hypothalamic mitochondrial dysfunction as a target in obesity and metabolic disease[J]. Front Endocrinol （Lausanne），2018，9:283. DOI：10.3389/fendo.2018.00283.
[14]	MARKHAM A, BAINS R, FRANKLIN P，et al. Changes in mitochondrial function are pivotal in neurodegenerative and psychiatric disorders：how important is BDNF?[J]. Br J Pharmacol，2014，171(8):2206-2229. DOI：10.1111/bph.12531.
[15]	WANG D M, YAN J Q, CHEN J，et al. Naringin improves neuronal insulin signaling，brain mitochondrial function，and cognitive function in high-fat diet-induced obese mice[J]. Cell Mol Neurobiol，2015，35(7):1061-1071. DOI：10.1007/s10571-015-0201-y.
[16]	SA-NGUANMOO P, TANAJAK P, KERDPHOO S，et al. FGF21 improves cognition by restored synaptic plasticity，dendritic spine density，brain mitochondrial function and cell apoptosis in obese-insulin resistant male rats[J]. Horm Behav，2016，85:86-95. DOI：10.1016/j.yhbeh.2016.08.006.
[17]	HO L, VARGHESE M, WANG J，et al. Dietary supplementation with decaffeinated green coffee improves diet-induced insulin resistance and brain energy metabolism in mice[J]. Nutr Neurosci，2012，15(1):37-45. DOI：10.1179/1476830511Y.0000000027.
[18]	PATTI M E, CORVERA S. The role of mitochondria in the pathogenesis of type 2 diabetes[J]. Endocr Rev，2010，31(3):364-395. DOI：10.1210/er.2009-0027.
[19]	YAMASHIMA T, OTA T, MIZUKOSHI E，et al. Intake of ω-6 polyunsaturated fatty acid-rich vegetable oils and risk of lifestyle diseases[J]. Adv Nutr，2020，11(6):1489-1509. DOI：10.1093/advances/nmaa072.
[20]	LEE S, KIM J Y, KIM E，et al. Assessment of cognitive impairment in a mouse model of high-fat diet-induced metabolic stress with touchscreen-based automated battery system[J]. Exp Neurobiol，2018，27(4):277-286. DOI：10.5607/en.2018.27.4.277.
[21]	XU L, XU S, LIN L F，et al. High-fat diet mediates anxiolytic-like behaviors in a time-dependent manner through the regulation of SIRT1 in the brain[J]. Neuroscience，2018，372:237-245. DOI：10.1016/j.neuroscience.2018.01.001.
[22]	YANG J L, LIU D X, JIANG H，et al. The effects of high-fat-diet combined with chronic unpredictable mild stress on depression-like behavior and leptin/LepRb in male rats[J]. Sci Rep，2016，6:35239. DOI：10.1038/srep35239.
[23]	CHOI J M, LEE S I, CHO E J. Effect of Vigna angularis on high-fat diet-induced memory and cognitive impairments[J]. J Med Food，2020，23(11):1155-1162. DOI：10.1089/jmf.2019.4644.
[24]	TUCSEK Z, TOTH P, TARANTINI S，et al. Aging exacerbates obesity-induced cerebromicrovascular rarefaction，neurovascular uncoupling，and cognitive decline in mice[J]. J Gerontol Ser A Biol Sci Med Sci，2014，69(11):1339-1352. DOI：10.1093/gerona/glu080.
[25]	MARQUES NETO S R, CASTIGLIONE R C, DA SILVA T C B，et al. Effects of high intensity interval training on neuro-cardiovascular dynamic changes and mitochondrial dysfunction induced by high-fat diet in rats[J]. PLoS One，2020，15(10):e0240060. DOI：10.1371/journal.pone.0240060.
[26]	PLUM L, SCHUBERT M, BRÜNING J C. The role of insulin receptor signaling in the brain[J]. Trends Endocrinol Metab，2005，16(2):59-65. DOI：10.1016/j.tem.2005.01.008.
[27]	KULLMANN S, KLEINRIDDERS A, SMALL D M，et al. Central nervous pathways of insulin action in the control of metabolism and food intake[J]. Lancet Diabetes Endocrinol，2020，8(6):524-534. DOI：10.1016/S2213-8587(20)30113-3.
[28]	KOTHARI V, LUO Y W, TORNABENE T，et al. High fat diet induces brain insulin resistance and cognitive impairment in mice[J]. Biochim Biophys Acta BBA Mol Basis Dis，2017，1863(2):499-508. DOI：10.1016/j.bbadis.2016.10.006.
[29]	MACIEJCZYK M, ZEBROWSKA E, CHABOWSKI A. Insulin resistance and oxidative stress in the brain：what's new?[J]. Int J Mol Sci，2019，20(4):E874. DOI：10.3390/ijms20040874.
[30]	POMYTKIN I, PINELIS V. Brain insulin resistance：focus on insulin receptor-mitochondria interactions[J]. Life （Basel），2021，11(3):262. DOI：10.3390/life11030262.
[31]	PIPATPIBOON N, PRATCHAYASAKUL W, CHATTIPAKORN N，et al. PPARγ agonist improves neuronal insulin receptor function in Hippocampus and brain mitochondria function in rats with insulin resistance induced by long term high-fat diets[J]. Endocrinology，2012，153(1):329-338. DOI：10.1210/en.2011-1502.
[32]	BEIRAMI E, ORYAN S, SEYEDHOSSEINI TAMIJANI S M，et al. Intranasal insulin treatment restores cognitive deficits and insulin signaling impairment induced by repeated methamphetamine exposure[J]. J Cell Biochem，2018，119(2):2345-2355. DOI：10.1002/jcb.26398.
[33]	NEHA, KUMAR A, JAGGI A S，et al. Silymarin ameliorates memory deficits and neuropathological changes in mouse model of high-fat-diet-induced experimental dementia[J]. Naunyn Schmiedebergs Arch Pharmacol，2014，387(8):777-787. DOI：10.1007/s00210-014-0990-4.
[34]	KIM J D, YOON N A, JIN S，et al. Microglial UCP2 mediates inflammation and obesity induced by high-fat feeding[J]. Cell Metab，2019，30(5):952-962.e5. DOI：10.1016/j.cmet.2019.08.010.
[35]	DE LUCA C, OLEFSKY J M. Inflammation and insulin resistance[J]. FEBS Lett，2008，582(1):97-105. DOI：10.1016/j.febslet.2007.11.057.
[36]	ACTIS G C. The gut microbiome[J]. Inflamm Allergy Drug Targets，2014，13(4):217-223. DOI：10.2174/1871528113666140623113221.
[37]	KIM M J, YOON J H, RYU J H. Mitophagy：a balance regulator of NLRP3 inflammasome activation[J]. BMB Rep，2016，49(10):529-535. DOI：10.5483/bmbrep.2016.49.10.115.
[38]	PRIETO G A, SNIGDHA S, BAGLIETTO-VARGAS D，et al. Synapse-specific IL-1 receptor subunit reconfiguration augments vulnerability to IL-1β in the aged Hippocampus[J]. PNAS，2015，112(36):E5078-5087. DOI：10.1073/pnas.1514486112.
[39]	TAN B L, NORHAIZAN M E. Effect of high-fat diets on oxidative stress，cellular inflammatory response and cognitive function[J]. Nutrients，2019，11(11):E2579. DOI：10.3390/nu11112579.
[40]	JASSIM A H, INMAN D M, MITCHELL C H. Crosstalk between dysfunctional mitochondria and inflammation in glaucomatous neurodegeneration[J]. Front Pharmacol，2021，12:699623. DOI：10.3389/fphar.2021.699623.
[41]	WILKINS H M, CARL S M, GREENLIEF A C S，et al. Bioenergetic dysfunction and inflammation in Alzheimer's disease：a possible connection[J]. Front Aging Neurosci，2014，6:311. DOI：10.3389/fnagi.2014.00311.
[42]	DAVIS C H O, KIM K Y, BUSHONG E A，et al. Transcellular degradation of axonal mitochondria[J]. Proc Natl Acad Sci U S A，2014，111(26):9633-9638. DOI：10.1073/pnas.1404651111.
[43]	LI F, LIU B B, CAI M，et al. Excessive endoplasmic Reticulum stress and decreased neuroplasticity-associated proteins in prefrontal cortex of obese rats and the regulatory effects of aerobic exercise[J]. Brain Res Bull，2018，140:52-59. DOI：10.1016/j.brainresbull.2018.04.003.
[44]	CAI M, WANG H, LI J J，et al. The signaling mechanisms of hippocampal endoplasmic Reticulum stress affecting neuronal plasticity-related protein levels in high fat diet-induced obese rats and the regulation of aerobic exercise[J]. Brain Behav Immun，2016，57:347-359. DOI：10.1016/j.bbi.2016.05.010.
[45]	CAI M, HU J Y, LIU B B，et al. The molecular mechanisms of excessive hippocampal endoplasmic Reticulum stress depressing cognition-related proteins expression and the regulatory effects of Nrf2[J]. Neuroscience，2020，431:152-165. DOI：10.1016/j.neuroscience.2020.02.001.
[46]	BHANDARY B, MARAHATTA A, KIM H R，et al. An involvement of oxidative stress in endoplasmic Reticulum stress and its associated diseases[J]. Int J Mol Sci，2012，14(1):434-456. DOI：10.3390/ijms14010434.
[47]	ARRUDA A P, PERS B M, PARLAKGÜL G，et al. Chronic enrichment of hepatic endoplasmic Reticulum-mitochondria contact leads to mitochondrial dysfunction in obesity[J]. Nat Med，2014，20(12):1427-1435. DOI：10.1038/nm.3735.
[48]	BORYS J, MACIEJCZYK M, ANTONOWICZ B，et al. Glutathione metabolism，mitochondria activity，and nitrosative stress in patients treated for mandible fractures[J]. J Clin Med，2019，8(1):E127. DOI：10.3390/jcm8010127.
[49]	FREEMAN L R, ZHANG L, NAIR A，et al. Obesity increases cerebrocortical reactive oxygen species and impairs brain function[J]. Free Radic Biol Med，2013，56:226-233. DOI：10.1016/j.freeradbiomed.2012.08.577.
[50]	MORRISON C D, PISTELL P J, INGRAM D K，et al. High fat diet increases hippocampal oxidative stress and cognitive impairment in aged mice：implications for decreased Nrf2 signaling[J]. J Neurochem，2010，114(6):1581-1589. DOI：10.1111/j.1471-4159.2010.06865.x.
[51]	MA W W, DING B J, WANG L J，et al. Involvement of nuclear related factor 2 signaling pathway in the brain of obese rats and obesity-resistant rats induced by high-fat diet[J]. J Med Food，2016，19(4):404-409. DOI：10.1089/jmf.2015.3500.
[52]	PINTANA H, SRIPETCHWANDEE J, SUPAKUL L，et al. Garlic extract attenuates brain mitochondrial dysfunction and cognitive deficit in obese-insulin resistant rats[J]. Appl Physiol Nutr Metab，2014，39(12):1373-1379. DOI：10.1139/apnm-2014-0255.
[53]	CAMPBELL W W, KRAUS W E, POWELL K E，et al. High-intensity interval training for cardiometabolic disease prevention[J]. Med Sci Sports Exerc，2019，51(6):1220-1226. DOI：10.1249/MSS.0000000000001934.
[54]	DA SILVA M A R, BAPTISTA L C, NEVES R S，et al. The effects of concurrent training combining both resistance exercise and high-intensity interval training or moderate-intensity continuous training on metabolic syndrome[J]. Front Physiol，2020，11:572. DOI：10.3389/fphys.2020.00572.
[55]	VIANA R B, NAVES J P A, COSWIG V S，et al. Is interval training the magic bullet for fat loss? A systematic review and meta-analysis comparing moderate-intensity continuous training with high-intensity interval training （HIIT）[J]. Br J Sports Med，2019，53(10):655-664. DOI：10.1136/bjsports-2018-099928.
[56]	WEWEGE M, VAN DEN BERG R, WARD R E，et al. The effects of high-intensity interval training vs. moderate-intensity continuous training on body composition in overweight and obese adults：a systematic review and meta-analysis[J]. Obes Rev，2017，18(6):635-646. DOI：10.1111/obr.12532.
[57]	ROBINSON M M, LOWE V J, NAIR K S. Increased brain glucose uptake after 12 weeks of aerobic high-intensity interval training in young and older adults[J]. J Clin Endocrinol Metab，2018，103(1):221-227. DOI：10.1210/jc.2017-01571.
[58]	DRIGNY J, GREMEAUX V, DUPUY O，et al. Effect of interval training on cognitive functioning and cerebral oxygenation in obese patients：a pilot study[J]. J Rehabil Med，2014，46(10):1050-1054. DOI：10.2340/16501977-1905.
[59]	BERNARDO T C, MARQUES-ALEIXO I, BELEZA J，et al. Physical exercise and brain mitochondrial fitness：the possible role against Alzheimer's disease[J]. Brain Pathol，2016，26(5):648-663. DOI：10.1111/bpa.12403.
[60]	GAN Z J, FU T T, KELLY D P，et al. Skeletal muscle mitochondrial remodeling in exercise and diseases[J]. Cell Res，2018，28(10):969-980. DOI：10.1038/s41422-018-0078-7.
[61]	LUCAS S J, COTTER J D, BRASSARD P，et al. High-intensity interval exercise and cerebrovascular health：curiosity，cause，and consequence[J]. J Cereb Blood Flow Metab，2015，35(6):902-911. DOI：10.1038/jcbfm.2015.49.
[62]	TAKIMOTO M, HAMADA T. Acute exercise increases brain region-specific expression of MCT1，MCT2，MCT4，GLUT1，and COX IV proteins[J]. J Appl Physiol （1985），2014，116(9):1238-1250. DOI：10.1152/japplphysiol.01288.2013.
[63]	GUSDON A M, CALLIO J, DISTEFANO G，et al. Exercise increases mitochondrial complex I activity and DRP1 expression in the brains of aged mice[J]. Exp Gerontol，2017，90:1-13. DOI：10.1016/j.exger.2017.01.013.
[64]	RAI S, CHOWDHURY A, RENIERS R L E P，et al. A pilot study to assess the effect of acute exercise on brain glutathione[J]. Free Radic Res，2018，52(1):57-69. DOI：10.1080/10715762.2017.1411594.
[65]	FREITAS D A, ROCHA-VIEIRA E, SOARES B A，et al. High intensity interval training modulates hippocampal oxidative stress，BDNF and inflammatory mediators in rats[J]. Physiol Behav，2018，184:6-11. DOI：10.1016/j.physbeh.2017.10.027.
[66]	MELO C S, ROCHA-VIEIRA E, FREITAS D A，et al. A single session of high-intensity interval exercise increases antioxidants defenses in the hippocampus of Wistar rats[J]. Physiol Behav，2019，211:112675. DOI：10.1016/j.physbeh.2019.112675.
[67]	FETER N, SPANEVELLO R M, SOARES M S P，et al. How does physical activity and different models of exercise training affect oxidative parameters and memory?[J]. Physiol Behav，2019，201:42-52. DOI：10.1016/j.physbeh.2018.12.002.
[68]	LI B X, LIANG F, DING X Y，et al. Interval and continuous exercise overcome memory deficits related to β-Amyloid accumulation through modulating mitochondrial dynamics[J]. Behav Brain Res，2019，376:112171. DOI：10.1016/j.bbr.2019.112171.
[69]	HU J Y, CAI M, SHANG Q H，et al. Elevated lactate by high-intensity interval training regulates the hippocampal BDNF expression and the mitochondrial quality control system[J]. Front Physiol，2021，12:629914. DOI：10.3389/fphys.2021.629914.
[70]	RAEFSKY S M, MATTSON M P. Adaptive responses of neuronal mitochondria to bioenergetic challenges：roles in neuroplasticity and disease resistance[J]. Free Radic Biol Med，2017，102:203-216. DOI：10.1016/j.freeradbiomed.2016.11.045.
[71]	ZHANG F, ZHANG L, QI Y，et al. Mitochondrial cAMP signaling[J]. Cell Mol Life Sci，2016，73(24):4577-4590. DOI：10.1007/s00018-016-2282-2.
[72]	MEYER J N, LEUTHNER T C, LUZ A L. Mitochondrial fusion，fission，and mitochondrial toxicity[J]. Toxicology，2017，391:42-53. DOI：10.1016/j.tox.2017.07.019.
[73]	POPOV L D. Mitochondrial biogenesis：an update[J]. J Cell Mol Med，2020，24(9):4892-4899. DOI：10.1111/jcmm.15194.
[74]	E L, BURNS J M, SWERDLOW R H. Effect of high-intensity exercise on aged mouse brain mitochondria，neurogenesis，and inflammation[J]. Neurobiol Aging，2014，35(11):2574-2583. DOI：10.1016/j.neurobiolaging.2014.05.033.
[75]	ETTCHETO M, PETROV D, PEDRÓS I，et al. Evaluation of neuropathological effects of a high-fat diet in a presymptomatic Alzheimer's disease stage in APP/PS1 mice[J]. J Alzheimers Dis，2016，54(1):233-251. DOI：10.3233/JAD-160150.
[76]	FANIBUNDA S E, DEB S, MANIYADATH B，et al. Serotonin regulates mitochondrial biogenesis and function in rodent cortical neurons via the 5-HT2A receptor and SIRT1-PGC-1α axis[J]. Proc Natl Acad Sci U S A，2019，116(22):11028-11037. DOI：10.1073/pnas.1821332116.
[77]	SONG K, ZHANG Y F, GA Q，et al. Increased insulin sensitivity by high-altitude hypoxia in mice with high-fat diet-induced obesity is associated with activated AMPK signaling and subsequently enhanced mitochondrial biogenesis in skeletal muscles[J]. Obes Facts，2020，13(5):455-472. DOI：10.1159/000508112.
[78]	WANG S W, SHENG H, BAI Y F，et al. Neohesperidin enhances PGC-1α-mediated mitochondrial biogenesis and alleviates hepatic steatosis in high fat diet fed mice[J]. Nutr Diabetes，2020，10(1):27. DOI：10.1038/s41387-020-00130-3.
[79]	HEINONEN S, JOKINEN R, RISSANEN A，et al. White adipose tissue mitochondrial metabolism in health and in obesity[J]. Obes Rev，2020，21(2):e12958. DOI：10.1111/obr.12958.
[80]	E L, LU J H, SELFRIDGE J E，et al. Lactate administration reproduces specific brain and liver exercise-related changes[J]. J Neurochem，2013，127(1):91-100. DOI：10.1111/jnc.12394.
[81]	MARQUES-ALEIXO I, SANTOS-ALVES E, BALÇA M M，et al. Physical exercise improves brain cortex and cerebellum mitochondrial bioenergetics and alters apoptotic，dynamic and auto（mito）phagy markers[J]. Neuroscience，2015，301:480-495. DOI：10.1016/j.neuroscience.2015.06.027.
[82]	STEINER J L, MURPHY E A, MCCLELLAN J L，et al. Exercise training increases mitochondrial biogenesis in the brain[J]. J Appl Physiol （1985），2011，111(4):1066-1071. DOI：10.1152/japplphysiol.00343.2011.
[83]	GIBALA M J, LITTLE J P, MACDONALD M J，et al. Physiological adaptations to low-volume，high-intensity interval training in health and disease[J]. J Physiol，2012，590(5):1077-1084. DOI：10.1113/jphysiol.2011.224725.

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

RichHTML

PDF

可视化

摘要/Abstract

引用本文

使用本文

图/表 2

参考文献 83

相关文章 15

编辑推荐

Metrics

留言

[1]	王婷婷, 唐勇, 张文轲, 李志刚. 高尿酸血症运动干预的研究进展[J]. 中国全科医学, 2025, 28(30): 3841-3846.
[2]	周晟, 邓长生, 邹冠炀, 宋健平. 疟疾心血管疾病并发症发病机制的研究进展[J]. 中国全科医学, 2025, 28(27): 3466-3472.
[3]	黄雨琳, 王浩云, 李燕梅, 萧雪英. 胃癌患者化疗期间症状群的范围综述[J]. 中国全科医学, 2025, 28(26): 3338-3344.
[4]	向心月, 张冰青, 欧阳煜钦, 汤文娟, 冯文焕. 短期内科门诊减重对肥胖患者动脉粥样硬化性心血管疾病风险的影响研究[J]. 中国全科医学, 2025, 28(26): 3229-3239.
[5]	刘银银, 隋鸿平, 李婷婷, 姜桐桐, 史铁英, 夏云龙. 乳腺癌治疗相关心脏毒性风险预测模型的研究进展[J]. 中国全科医学, 2025, 28(24): 3072-3078.
[6]	李苗秀, 朱博文, 孔令军, 房敏. 青少年脊柱侧弯保守治疗临床评估工具研究进展[J]. 中国全科医学, 2025, 28(24): 3079-3088.
[7]	魏云鸿, 杨莉, 王玉路, 叶秋芳, 代安妮, 何燕. 肥胖相关性高血压患者不同运动阶段心肺功能的研究[J]. 中国全科医学, 2025, 28(24): 2972-2978.
[8]	肖瑶, 万钧. 直接口服抗凝药在静脉血栓栓塞特殊人群中的临床应用[J]. 中国全科医学, 2025, 28(24): 3066-3071.
[9]	阮万百, 李俊峰, 尹艳梅, 彭磊, 朱克祥. 胰腺癌靶向治疗及免疫治疗的研究新进展[J]. 中国全科医学, 2025, 28(23): 2950-2960.
[10]	周连鹏, 李伟峰, 董新刚, 王晓元. 铜稳态调节机制在认知障碍中的作用探析[J]. 中国全科医学, 2025, 28(23): 2941-2949.
[11]	石小天, 王珊, 杨华昱, 杨一帆, 李旭, 马清. 中国老年人体重指数和死亡的相关性：一项队列研究[J]. 中国全科医学, 2025, 28(22): 2791-2797.
[12]	刘美霞, 尹金念, 吴玫, 杨星, 周全湘, 杨敬源. 体重指数对三酰甘油葡萄糖指数与认知功能关联的影响：一项贵州农村老年人群的现况研究[J]. 中国全科医学, 2025, 28(22): 2806-2812.
[13]	王爽, 吴树法, 令垚, 谭茜蔚, 曹汝岱, 曾慧婷, 孔丹莉, 丁元林, 于海兵. 基于代谢组学探究非脂质代谢物在肥胖与糖尿病视网膜病变间的中介作用：孟德尔随机化研究[J]. 中国全科医学, 2025, 28(21): 2625-2634.
[14]	董浩铖, 郝潇, 安东, 李浩翰, 李树仁. 射血分数超常的心力衰竭的研究进展[J]. 中国全科医学, 2025, 28(21): 2692-2696.
[15]	杜琼靓, 林白浪, 郭洪花. 群组育儿保健模式的研究进展及启示[J]. 中国全科医学, 2025, 28(21): 2672-2678.