Title

Mediators of Monocyte Migration in Response to Recovery Modalities following Resistance Exercise

Authors

Authors

A. R. Jajtner; M. S. Fragala; J. R. Townsend; A. M. Gonzalez; A. J. Wells; D. H. Fukuda; J. R. Stout;J. R. Hoffman

Comments

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Abbreviated Journal Title

Mediat. Inflamm.

Keywords

INDUCED MUSCLE DAMAGE; ECCENTRIC EXERCISE; STRENUOUS EXERCISE; MAXIMAL; EXERCISE; EXPRESSION; HUMANS; STIMULATION; LEUKOCYTES; INFLAMMATION; CHEMOKINES; Cell Biology; Immunology

Abstract

Mediators of monocyte migration, complement receptor-3 (CR3), and chemokine ligand-4 (CCL4) were measured in response to recovery modalities following resistance exercise. Thirty resistance-trained men (23.1 +/- 2.9 y; 175.2 +/- 7.1 cm; 82.1 +/- 8.4 kg) were given neuromuscular electric stimulation (NMES), cold water immersion (CWI), or control (CON) treatments immediately following resistance exercise. Blood samples were obtained preexercise (PRE), immediately (IP), 30 minutes (30 P), 24 hours (24 H), and 48 hours (48 H) after exercise for measurement of circulating CCL4 and CR3 expression on CD14+ monocytes, by assay and flow cytometry. Circulating CCL4 showed no consistent changes. Inferential analysis indicated that CR3 expression was likely greater in CON at 30 P than NMES (90.0%) or CWI (86.8%). NMES was likely lower than CON at 24H (92.9%) and very likely lower at 48H (98.7%). Expression of CR3 following CWI was very likely greater than CON (96.5%) at 24H. The proportion of CR3+ monocytes was likely greater following CWI than NMES (85.8%) or CON (85.2%) at 24 H. The change in proportion of CR3+ monocytes was likely (86.4%) greater following NMES than CON from IP to 30 P. The increased expression of CR3 and increased proportion of CR3+ monocytes following CWI at 24 H indicate a potentially improved ability for monocyte adhesion to the endothelium, possibly improving phagocytosis of damaged tissues.

Journal Title

Mediators of Inflammation

Publication Date

1-1-2014

Document Type

Article

Language

English

First Page

9

WOS Identifier

WOS:000337434900001

ISSN

0962-9351

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