Aging alters macrophage properties in human skeletal muscle both at rest and in response to acute resistance exercise.

Journal Article (Journal Article)

Macrophages are involved in skeletal muscle repair through pro-inflammatory and alternative functions. We tested the hypothesis that aging alters the abundance and properties of skeletal muscle macrophages that will influence their functional response to acute resistance exercise. Total macrophages (CD 68+), as well as pro- (CD 11b+) and anti-inflammatory (CD 163+) subpopulations and associated cytokine mRNAs were quantified in vastus lateralis biopsies from young (N=17) and elderly (N=17) males pre- and 72 h post-exercise. Pre-exercise, young muscle tended to possess a greater number of macrophages, whereas elderly muscle possessed higher levels of IL-1 beta (P=0.001), IL-1 RA (P=0.003), and IL-10 (P=0.028). Post-exercise, total macrophages did not change in either group, however, the number of CD 11b+ (P=0.039) and CD 163+ (P=0.026) cells increased 55 and 29%, respectively, but only in the young. IL-1 beta (P=0.006), IL-10 (P=0.016), and AMAC-1 (P=0.044) also increased, approximately two-fold, and again only in the young. Quantitation of CD 11b+ and CD 163+ cells suggests that the majority of resident macrophages possess alternative functions, and a small subpopulation participates in the inflammatory response. Both subpopulations increased their activity post-exercise, exclusively in the young. These findings suggest that aging results in a defective regulation of muscle macrophage function, both at baseline and in response to resistance exercise, that may limit muscle hypertrophy in older adults.

Full Text

Duke Authors

Cited Authors

  • Przybyla, B; Gurley, C; Harvey, JF; Bearden, E; Kortebein, P; Evans, WJ; Sullivan, DH; Peterson, CA; Dennis, RA

Published Date

  • March 2006

Published In

Volume / Issue

  • 41 / 3

Start / End Page

  • 320 - 327

PubMed ID

  • 16457979

International Standard Serial Number (ISSN)

  • 0531-5565

Digital Object Identifier (DOI)

  • 10.1016/j.exger.2005.12.007


  • eng

Conference Location

  • England