Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise

Author:

Coelho Junior Hélio José1,Gambassi Bruno Bavaresco1,Diniz Tiego Aparecido2,Fernandes Isabela Maia da Cruz2,Caperuto Érico Chagas3,Uchida Marco Carlos1,Lira Fabio Santos2,Rodrigues Bruno1ORCID

Affiliation:

1. Faculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, Brazil

2. Exercise and Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, Brazil

3. Human Movement Laboratory, São Judas Tadeu University (USJT), 03166-000 São Paulo, SP, Brazil

Abstract

Inflammatory markers are increased systematically and locally (e.g., skeletal muscle) in stroke patients. Besides being associated with cardiovascular risk factors, proinflammatory cytokines seem to play a key role in muscle atrophy by regulating the pathways involved in this condition. As such, they may cause severe decrease in muscle strength and power, as well as impairment in cardiorespiratory fitness. On the other hand, physical exercise (PE) has been widely suggested as a powerful tool for treating stroke patients, since PE is able to regenerate, even if partially, physical and cognitive functions. However, the mechanisms underlying the beneficial effects of physical exercise in poststroke patients remain poorly understood. Thus, in this study we analyze the candidate mechanisms associated with muscle atrophy in stroke patients, as well as the modulatory effect of inflammation in this condition. Later, we suggest the two strongest anti-inflammatory candidate mechanisms, myokines and the cholinergic anti-inflammatory pathway, which may be activated by physical exercise and may contribute to a decrease in proinflammatory markers of poststroke patients.

Funder

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3