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Review
. 2020 May 8;9(5):401.
doi: 10.3390/antiox9050401.

Characterization and Modulation of Systemic Inflammatory Response to Exhaustive Exercise in Relation to Oxidative Stress

Affiliations
Review

Characterization and Modulation of Systemic Inflammatory Response to Exhaustive Exercise in Relation to Oxidative Stress

Katsuhiko Suzuki et al. Antioxidants (Basel). .

Abstract

Exhaustive exercise induces systemic inflammatory responses, which are associated with exercise-induced tissue/organ damage, but the sources and triggers are not fully understood. Herein, the basics of inflammatory mediator cytokines and research findings on the effects of exercise on systemic inflammation are introduced. Subsequently, the association between inflammatory responses and tissue damage is examined in exercised and overloaded skeletal muscle and other internal organs. Furthermore, an overview of the interactions between oxidative stress and inflammatory mediator cytokines is provided. Particularly, the transcriptional regulation of redox signaling and pro-inflammatory cytokines is described, as the activation of the master regulatory factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is involved directly or indirectly in controlling pro-inflammatory genes and antioxidant enzymes expression, whilst nuclear factor-kappa B (NF-κB) regulates the pro-inflammatory gene expression. Additionally, preventive countermeasures against the pathogenesis along with the possibility of interventions such as direct and indirect antioxidants and anti-inflammatory agents are described. The aim of this review is to give an overview of studies on the systematic inflammatory responses to exercise, including our own group as well as others. Moreover, the challenges and future directions in understanding the role of exercise and functional foods in relation to inflammation and oxidative stress are discussed.

Keywords: Toll-like receptor (TLR); anti-inflammatory effect of exercise; cytokine; free fatty acids (FFA); immune suppression; lipopolysaccharides (LPS); macrophage; muscle and internal organ injury; neutrophil; reactive oxygen species (ROS).

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Localization of F4/80 (macrophages) (green) and IL-6 (red) of skeletal muscle after exercise detected by immunofluorescence staining [61]. Arrows (yellow) indicate F4/80 and IL-6 double positive cells. The signals of IL-6 were mainly observed in the interstitial space. Exercise increased F4/80 and IL-6 double positive cells but not IL-6 positive myocytes. This result suggests macrophages are one of the sources of IL-6.
Figure 2
Figure 2
The concept of exercise-induced endotoxemia and systemic inflammation. Exercise induces intestinal barrier dysfunction and hyperpermeability. Subsequently, gut-derived bacteria translocate to the circulation and induce systemic inflammation.
Figure 3
Figure 3
A schematic presentation of interactions between nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and nuclear factor-kappa B (NF-κB) transcription factors. Under stressed conditions, Nrf2 translocates to the nucleus and activates the Nrf2/antioxidant responsive element (ARE) signaling pathway, which assists in the downstream regulation of NF-κB activity and expression of inflammatory genes.
Figure 4
Figure 4
Protein from hyperimmunized milk showed protective effects towards exercise-induced inflammation [20].

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