title: Aging alters macrophage properties in human skeletal muscle both at rest and in response to acute resistance exercise.
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 (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.
authors.affiliation: Department of Geriatrics, University of Arkansas for Medical Sciences, 4301 West Markham #807, Little Rock, AR 72205, USA.
authors.forename: Beata
authors.initials: B
authors.lastname: Przybyla
authors.forename: Cathy
authors.initials: C
authors.lastname: Gurley
authors.forename: Jonathan F
authors.initials: JF
authors.lastname: Harvey
authors.forename: Edward
authors.initials: E
authors.lastname: Bearden
authors.forename: Patrick
authors.initials: P
authors.lastname: Kortebein
authors.forename: William J
authors.initials: WJ
authors.lastname: Evans
authors.forename: Dennis H
authors.initials: DH
authors.lastname: Sullivan
authors.forename: Charlotte A
authors.initials: CA
authors.lastname: Peterson
authors.forename: Richard A
authors.initials: RA
authors.lastname: Dennis
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D015415:Biomarkers / Q000032:analysis; D039481:CD11b Antigen / Q000276:immunology; D002452:Cell Count; D019742:Chemokines, CC / Q000032:analysis; D015444:Exercise / Q000502:physiology*; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007375:Interleukin-1 / Q000276:immunology; D016753:Interleukin-10 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D008297:Male; D018482:Muscle, Skeletal / Q000166:cytology / Q000276:immunology / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000276:immunology; D011956:Receptors, Cell Surface / Q000276:immunology; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D000098902:CD163 Antigen; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D039481:CD11b Antigen; D019742:Chemokines, CC; D007375:Interleukin-1; D016753:Interleukin-10; D053583:Interleukin-1beta; D015850:Interleukin-6; D012333:RNA, Messenger; D016186:Receptor, Macrophage Colony-Stimulating Factor; D011956:Receptors, Cell Surface; D017472:Receptors, Interleukin-1; D000098902:CD163 Antigen; C111792:CCL18 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule