Title

Ccl2 And Ccr2 Variants Are Associated With Skeletal Muscle Strength And Change In Strength With Resistance Training

Keywords

Genetics; Muscle size; Muscle strength; Single-Nucleotide Polymorphism

Abstract

Baseline muscle size and muscle adaptation to exercise are traits with high variability across individuals. Recent research has implicated several chemokines and their receptors in the pathogenesis of many conditions that are influenced by inflammatory processes, including muscle damage and repair. One specific chemokine, chemokine (C-C motif) ligand 2 (CCL2), is expressed by macrophages and muscle satellite cells, increases expression dramatically following muscle damage, and increases expression further with repeated bouts of exercise, suggesting that CCL2 plays a key role in muscle adaptation. The present study hypothesizes that genetic variations in CCL2 and its receptor (CCR2) may help explain muscle trait variability. College-aged subjects [n = 874, Functional Single-Nucleotide Polymorphisms Associated With Muscle Size and Strength (FAMUSS) cohort] underwent a 12-wk supervised strength-training program for the upper arm muscles. Muscle size (via MR imaging) and elbow flexion strength (1 repetition maximum and isometric) measurements were taken before and after training. The study participants were then genotyped for 11 genetic variants in CCL2 and five variants in CCR2. Variants in the CCL2 and CCR2 genes show strong associations with several pretraining muscle strength traits, indicating that inflammatory genes in skeletal muscle contribute to the polygenic system that determines muscle phenotypes. These associations extend across both sexes, and several of these genetic variants have been shown to influence gene regulation. Copyright © 2010 the American Physiological Society.

Publication Date

12-1-2010

Publication Title

Journal of Applied Physiology

Volume

109

Issue

6

Number of Pages

1779-1785

Document Type

Article

Personal Identifier

scopus

DOI Link

https://doi.org/10.1152/japplphysiol.00633.2010

Socpus ID

78651265601 (Scopus)

Source API URL

https://api.elsevier.com/content/abstract/scopus_id/78651265601

This document is currently not available here.

Share

COinS