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Mediators of Inflammation
Volume 2014 (2014), Article ID 145817, 9 pages
http://dx.doi.org/10.1155/2014/145817
Research Article

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

Institute of Exercise Physiology and Wellness, University of Central Florida, Orlando, FL, USA

Received 6 February 2014; Revised 14 April 2014; Accepted 5 May 2014; Published 2 June 2014

Academic Editor: Sandra Helena Penha Oliveira

Copyright © 2014 Adam R. Jajtner 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

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 (  y;  cm;  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 24 H (92.9%) and very likely lower at 48 H (98.7%). Expression of CR3 following CWI was very likely greater than CON (96.5%) at 24 H. 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.