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

Beata Przybyla, Cathy Gurley, Jonathan F. Harvey, Edward Bearden, Patrick Kortebein, William J. Evans, Dennis H. Sullivan, Charlotte A. Peterson, Richard A. Dennis

Research output: Contribution to journalArticlepeer-review

129 Scopus citations

Abstract

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 (CD68+), as well as pro- (CD11b+) and anti-inflammatory (CD163+) 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-1β (P=0.001), IL-1RA (P=0.003), and IL-10 (P=0.028). Post-exercise, total macrophages did not change in either group, however, the number of CD11b+ (P=0.039) and CD163+ (P=0.026) cells increased 55 and 29%, respectively, but only in the young. IL-1β (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 CD11b+ and CD163+ 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.

Original languageEnglish
Pages (from-to)320-327
Number of pages8
JournalExperimental Gerontology
Volume41
Issue number3
DOIs
StatePublished - Mar 2006

Bibliographical note

Funding Information:
This research was supported in part by funds provided to the UAMS Microarray Facility through Act 1 of The Arkansas Tobacco Settlement Proceeds Act of 2000; by National Center for Research Resources grants through the BRIN Program (P20 RR-16460) and the General Clinical Research Center at the University of Arkansas for Medical Sciences (M01-RR14288); and by grants from the National Institute on Aging, to CAP (AG012411).

Keywords

  • Aging
  • Inflammation
  • Interleukin
  • Macrophage
  • Resistance exercise
  • Skeletal muscle

ASJC Scopus subject areas

  • Biochemistry
  • Aging
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology

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