缺乏骨骼肌血清素会损害身体机能。

IF 2.7 Q3 NEUROSCIENCES International Journal of Tryptophan Research Pub Date : 2021-03-22 eCollection Date: 2021-01-01 DOI:10.1177/11786469211003109
Marion Falabrègue, Anne-Claire Boschat, Romain Jouffroy, Marieke Derquennes, Haidar Djemai, Sylvia Sanquer, Robert Barouki, Xavier Coumoul, Jean-François Toussaint, Olivier Hermine, Philippe Noirez, Francine Côté
{"title":"缺乏骨骼肌血清素会损害身体机能。","authors":"Marion Falabrègue,&nbsp;Anne-Claire Boschat,&nbsp;Romain Jouffroy,&nbsp;Marieke Derquennes,&nbsp;Haidar Djemai,&nbsp;Sylvia Sanquer,&nbsp;Robert Barouki,&nbsp;Xavier Coumoul,&nbsp;Jean-François Toussaint,&nbsp;Olivier Hermine,&nbsp;Philippe Noirez,&nbsp;Francine Côté","doi":"10.1177/11786469211003109","DOIUrl":null,"url":null,"abstract":"<p><p>Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle-brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle-brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin-deficient mice, we used a treadmill incremental test. Peripheral serotonin-deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin-deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin-deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.</p>","PeriodicalId":46603,"journal":{"name":"International Journal of Tryptophan Research","volume":"14 ","pages":"11786469211003109"},"PeriodicalIF":2.7000,"publicationDate":"2021-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/11786469211003109","citationCount":"2","resultStr":"{\"title\":\"Lack of Skeletal Muscle Serotonin Impairs Physical Performance.\",\"authors\":\"Marion Falabrègue,&nbsp;Anne-Claire Boschat,&nbsp;Romain Jouffroy,&nbsp;Marieke Derquennes,&nbsp;Haidar Djemai,&nbsp;Sylvia Sanquer,&nbsp;Robert Barouki,&nbsp;Xavier Coumoul,&nbsp;Jean-François Toussaint,&nbsp;Olivier Hermine,&nbsp;Philippe Noirez,&nbsp;Francine Côté\",\"doi\":\"10.1177/11786469211003109\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle-brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle-brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin-deficient mice, we used a treadmill incremental test. Peripheral serotonin-deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin-deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin-deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.</p>\",\"PeriodicalId\":46603,\"journal\":{\"name\":\"International Journal of Tryptophan Research\",\"volume\":\"14 \",\"pages\":\"11786469211003109\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2021-03-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1177/11786469211003109\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Tryptophan Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1177/11786469211003109\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Tryptophan Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/11786469211003109","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 2

摘要

低水平的神经递质血清素与抑郁症的发病有关。虽然传统的治疗方法包括抗抑郁药,但体育锻炼已经成为抑郁症患者的另一种选择。然而,大脑是如何感知运动的这一基本问题仍然存在。肌肉-大脑内分泌循环的存在已经被提出:根据这种情况,运动调节色氨酸在骨骼肌内转化为犬尿氨酸的代谢,这反过来影响大脑,增强对抑郁症的抵抗力。但在运动过程中,色氨酸分解为犬尿氨酸也可能改变血清素的合成,有助于抑制抑郁。在这项研究中,我们调查了外周血清素是否可能在肌肉-大脑沟通中发挥作用,从而适应耐力训练。我们首先量化了4名训练有素的运动员在长距离越野跑前后血液中的色氨酸代谢物,并将色氨酸代谢的变化与身体表现联系起来。同时,为了评估训练对照组和外周血清素缺乏小鼠的运动能力和耐力,我们使用了跑步机增量试验。外周血清素缺乏的小鼠在耐力训练后表现出明显的体能下降。色氨酸代谢产物的脑水平在野生型和外周血清素缺乏的动物中是相似的,在外周血清素缺乏的小鼠的血浆或脑中没有发现肌肉诱导的色氨酸代谢产物。但质谱分析显示,比目鱼肌和跖肌中5-羟吲哚乙酸(5-HIAA)水平显著降低,这表明肌肉中色氨酸代谢为5-羟色胺对耐力训练的适应至关重要。根据这些发现,色氨酸分解为外周血清素,而不是大脑血清素,似乎是肌肉适应耐力训练的限速步骤。数据表明,有一种外围机制负责运动的积极作用,肌肉是具有自分泌-旁分泌作用的分泌器官,其中5 -羟色胺具有局部作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

摘要图片

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Lack of Skeletal Muscle Serotonin Impairs Physical Performance.

Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle-brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle-brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin-deficient mice, we used a treadmill incremental test. Peripheral serotonin-deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin-deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin-deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
7.30
自引率
4.50%
发文量
19
审稿时长
8 weeks
期刊最新文献
Baseline Inflammation but not Exercise Modality Impacts Exercise-induced Kynurenine Pathway Modulation in Persons With Multiple Sclerosis: Secondary Results From a Randomized Controlled Trial. Erratum to 'Dietary Hesperidin Suppresses Lipopolysaccharide-Induced Inflammation in Male Mice'. Investigations Towards Tryptophan Uptake and Transport Across an In Vitro Model of the Oral Mucosa Epithelium. The Tryptophan Metabolite Indole-3-Propionic Acid Raises Kynurenic Acid Levels in the Rat Brain In Vivo. Periconceptional Non-medical Maternal Determinants Influence the Tryptophan Metabolism: The Rotterdam Periconceptional Cohort (Predict Study).
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1