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Mol Cell Biochem. 2016 Oct;421(1-2):111-25. doi: 10.1007/s11010-016-2791-1. Epub 2016 Aug 13.

Modulation of rat monocyte/macrophage innate functions by increasing intensities of swimming exercise is associated with heat shock protein status.

Author information

1
Laboratory of Cellular Physiology (FisCel), Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite 500, 2° andar, Porto Alegre, RS, 90050-170, Brazil.
2
Physiology Research Group (GPeF), Department of Life Sciences (DCVida), Regional University of Northwestern Rio Grande do Sul State (UNIJUÍ), Ijuí, RS, 98700-000, Brazil.
3
Laboratory of Cellular Physiology (FisCel), Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite 500, 2° andar, Porto Alegre, RS, 90050-170, Brazil. pauloivo@ufrgs.br.

Abstract

Moderate exercise positively impacts innate immune functions, bringing about a better resistance against infections and general immunosurveillance. Exercise of high workloads (i.e., high intensity and/or duration) such as elite marathon, on the other hand, may have detrimental effects over immune function, but neither how long nor how intense should be the exercise sessions to be deleterious is known, this being a matter of intense dispute. Exercise is, at the same time, one of the most powerful inducers of the 70 kDa family of heat shock proteins (HSPAs, formerly known as HSP70s), which are protein chaperones characterized by a marked anti-inflammatory potency, when located intracellularly (iHSPA), but may act as pro-inflammatory cytokines if in the extracellular space (eHSPA). The above observations led us to suppose that short-term exercise could impose long-lasting effects on macrophage function that should be related to the eHSPA-to-iHSPA ratio, viz. H-index. Sedentary adult male Wistar rats were then submitted to 20 min swimming sessions with an overload (as a percentage of body weight attached to the tail base) of either 2, 4, 6, or 8 %. Control animals were maintained at rest in shallow water. Monocyte/macrophage functions (phagocytic capacity, nitric oxide [NO], and hydrogen peroxide [H2O2]) were assessed just after and 12 h after exercise and compared with HSPA status and oxidative stress markers. The results showed that exercise increased phagocytosis and H2O2 immediately after the bouts in a workload-dependent way. This was accompanied by increased H-index but no alteration in the redox status. Enhanced phagocytic capacity persisted for up to 12 h, when a marked rise in NO production was also observed, but H-index resumes its control values, suggesting that immune alertness returned to basal levels. Of note was the detection of the cognate form of eHSPA (encoded by hspa8 gene and formerly known as HSP73) in the rat sera. In total, acute exercise may evoke 12 h long workload-dependent effects associated with HSPA status.

KEYWORDS:

Exercise; Heat shock protein; Hydrogen peroxide; Monocyte/macrophage; Nitric oxide; Phagocytosis

PMID:
27522667
DOI:
10.1007/s11010-016-2791-1
[Indexed for MEDLINE]

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