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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Format: | Article |
Language: | English |
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Wiley
2016-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2016/3957958 |
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author | Hélio José Coelho Junior Bruno Bavaresco Gambassi Tiego Aparecido Diniz Isabela Maia da Cruz Fernandes Érico Chagas Caperuto Marco Carlos Uchida Fabio Santos Lira Bruno Rodrigues |
author_facet | Hélio José Coelho Junior Bruno Bavaresco Gambassi Tiego Aparecido Diniz Isabela Maia da Cruz Fernandes Érico Chagas Caperuto Marco Carlos Uchida Fabio Santos Lira Bruno Rodrigues |
author_sort | Hélio José Coelho Junior |
collection | DOAJ |
description | 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. |
format | Article |
id | doaj-art-50a053ddd63f4ecb97fdd8003f7505f9 |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2016-01-01 |
publisher | Wiley |
record_format | Article |
series | Mediators of Inflammation |
spelling | doaj-art-50a053ddd63f4ecb97fdd8003f7505f92025-02-03T01:24:27ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/39579583957958Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical ExerciseHélio José Coelho Junior0Bruno Bavaresco Gambassi1Tiego Aparecido Diniz2Isabela Maia da Cruz Fernandes3Érico Chagas Caperuto4Marco Carlos Uchida5Fabio Santos Lira6Bruno Rodrigues7Faculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, BrazilFaculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, BrazilExercise and Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, BrazilExercise and Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, BrazilHuman Movement Laboratory, São Judas Tadeu University (USJT), 03166-000 São Paulo, SP, BrazilFaculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, BrazilExercise and Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, BrazilFaculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, BrazilInflammatory 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.http://dx.doi.org/10.1155/2016/3957958 |
spellingShingle | Hélio José Coelho Junior Bruno Bavaresco Gambassi Tiego Aparecido Diniz Isabela Maia da Cruz Fernandes Érico Chagas Caperuto Marco Carlos Uchida Fabio Santos Lira Bruno Rodrigues Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise Mediators of Inflammation |
title | Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise |
title_full | Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise |
title_fullStr | Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise |
title_full_unstemmed | Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise |
title_short | Inflammatory Mechanisms Associated with Skeletal Muscle Sequelae after Stroke: Role of Physical Exercise |
title_sort | inflammatory mechanisms associated with skeletal muscle sequelae after stroke role of physical exercise |
url | http://dx.doi.org/10.1155/2016/3957958 |
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