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

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, the...

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Published inMediators of inflammation Vol. 2016; no. 2016; pp. 1 - 19
Main Authors Rodrigues, Bruno, Uchida, Marco Carlos, Caperuto, Erico Chagas, Fernandes, Isabela Maia da Cruz, Diniz, Tiego Aparecido, Gambassi, Bruno Bavaresco, Coelho Júnior, Hélio José, Lira, Fabio Santos
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 01.01.2016
John Wiley & Sons, Inc
Wiley
Subjects
Analysis
Animals
Anti-Inflammatory Agents - therapeutic use
Cholinergic Agents - chemistry
Chronic illnesses
Cytokines
Disability
Exercise
Growth factors
Heart attacks
Humans
Inflammation
Inflammation - pathology
Insulin
Kinases
Language disorders
Mice
Mortality
Muscle, Skeletal - physiopathology
Muscles
Muscular Atrophy - pathology
Muscular Atrophy - physiopathology
Musculoskeletal system
Nervous system
Physical education
Proteins
Rats
Review
Risk Factors
Stroke
Stroke - physiopathology
Studies
Tumor necrosis factor-TNF
Online AccessGet full text
ISSN0962-9351
1466-1861
1466-1861
DOI10.1155/2016/3957958

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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.
AbstractList 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.
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.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.
Audience Academic
Author Coelho Júnior, Hélio José
Diniz, Tiego Aparecido
Gambassi, Bruno Bavaresco
Lira, Fabio Santos
Uchida, Marco Carlos
Fernandes, Isabela Maia da Cruz
Rodrigues, Bruno
Caperuto, Erico Chagas
AuthorAffiliation 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
1 Faculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, Brazil
AuthorAffiliation_xml – name: 1 Faculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, Brazil
– name: 3 Human Movement Laboratory, São Judas Tadeu University (USJT), 03166-000 São Paulo, SP, Brazil
– name: 2 Exercise and Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, Brazil
Author_xml – sequence: 1
  fullname: Rodrigues, Bruno
– sequence: 2
  fullname: Uchida, Marco Carlos
– sequence: 3
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– sequence: 4
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– sequence: 5
  fullname: Diniz, Tiego Aparecido
– sequence: 6
  fullname: Gambassi, Bruno Bavaresco
– sequence: 7
  fullname: Coelho Júnior, Hélio José
– sequence: 8
  fullname: Lira, Fabio Santos
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27647951$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Copyright © 2016 Hélio José Coelho Junior et al.
COPYRIGHT 2016 John Wiley & Sons, Inc.
Copyright © 2016 Hélio José Coelho Junior et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright © 2016 Hélio José Coelho Junior et al. 2016
Copyright_xml – notice: Copyright © 2016 Hélio José Coelho Junior et al.
– notice: COPYRIGHT 2016 John Wiley & Sons, Inc.
– notice: Copyright © 2016 Hélio José Coelho Junior et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
– notice: Copyright © 2016 Hélio José Coelho Junior et al. 2016
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Issue 2016
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Snippet Inflammatory markers are increased systematically and locally (e.g., skeletal muscle) in stroke patients. Besides being associated with cardiovascular risk...
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StartPage 1
SubjectTerms Analysis
Animals
Anti-Inflammatory Agents - therapeutic use
Cholinergic Agents - chemistry
Chronic illnesses
Cytokines
Disability
Exercise
Growth factors
Heart attacks
Humans
Inflammation
Inflammation - pathology
Insulin
Kinases
Language disorders
Mice
Mortality
Muscle, Skeletal - physiopathology
Muscles
Muscular Atrophy - pathology
Muscular Atrophy - physiopathology
Musculoskeletal system
Nervous system
Physical education
Proteins
Rats
Review
Risk Factors
Stroke
Stroke - physiopathology
Studies
Tumor necrosis factor-TNF
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Title Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise
URI https://search.emarefa.net/detail/BIM-1111043
https://dx.doi.org/10.1155/2016/3957958
https://www.ncbi.nlm.nih.gov/pubmed/27647951
https://www.proquest.com/docview/1820627637
https://www.proquest.com/docview/1822118386
https://pubmed.ncbi.nlm.nih.gov/PMC5018330
https://doaj.org/article/50a053ddd63f4ecb97fdd8003f7505f9
Volume 2016
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