Melanocortin Receptor Expression Is Associated with Reduced CRP in Response to Resistance Training
2012

Abstract
The existing paradigm of exercise-induced decreases in chronic inflammation focuses on the expression of inflammatory receptors on systemic monocytes in response to exercise training, with the role of anti-inflammatory receptors largely ignored. Our recent preliminary studies indicate that the anti-inflammatory melanocortin receptors (MCRs) play a role in modulating exercise-induced decreases in chronic inflammation. Here we present a study designed to determine the effect of intense, resistance exercise training on systemic monocyte MCR expression. Because low-grade chronic inflammation is associated with elevated cardiometabolic risk in healthy populations and exercise decreases chronic inflammation, we investigated the associations between systemic monocyte cell surface expression of MCRs and inflammatory markers as a possible mechanism for the beneficial anti-inflammatory effects of resistance training. To this end, the present study includes 40 adults (aged 19-27 years) and implements a 12wk periodized, intensive resistance training intervention. Melanocortin 1 (MC1R) and 3 (MC3R) receptor expression on systemic monocytes and inflammatory markers, including C-reactive protein (CRP), interleukin 6 (IL-6), 1 beta (IL-1?) and 10 (IL-10), were measured before (PRE) and after (POST) the intervention. Resistance training significantly altered MCR systemic monocyte cell surface expression, had no chronic effects on IL-6, IL-1? or IL-10 expression but significantly decreased CRP levels from a moderate to a low cardiovascular disease (CVD) risk category. More specifically, decreased MC3R expression significantly correlated with decreased CRP, independent of changes in adipose tissue. These data suggest that the observed responses in MCR expression and decreases in CVD risk in response to resistance training represent an important anti-inflammatory mechanism in regulating exercise-induced decreases in chronic inflammation that occur independent of chronic changes in systemic cytokines.