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Mediators of Inflammation
Volume 2016, Article ID 3957958, 19 pages
http://dx.doi.org/10.1155/2016/3957958
Review Article

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

1Faculty of Physical Education, University of Campinas (UNICAMP), 13083-851 Campinas, SP, Brazil
2Exercise and Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, Brazil
3Human Movement Laboratory, São Judas Tadeu University (USJT), 03166-000 São Paulo, SP, Brazil

Received 3 June 2016; Accepted 26 July 2016

Academic Editor: Vera L. Petricevich

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.

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.