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Senescence of human skeletal muscle impairs the local inflammatory cytokine response to acute eccentric exercise
Author(s) -
Hamada Koichiro,
Vannier Edouard,
Sacheck Jennifer M.,
Witsell Alice L.,
Roubenoff Rnenn
Publication year - 2005
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.03-1286fje
Subject(s) - skeletal muscle , eccentric , medicine , cytokine , inflammation , endocrinology , senescence , interleukin 6 , eccentric exercise , tumor necrosis factor alpha , muscle damage , physics , quantum mechanics
The impact of aging on the cytokine response of human skeletal muscle to exercise‐induced injury remains poorly understood. We enrolled physically active, young (23–35 years old, n =15) and old (66–78 years old, n =15) men to perform 45 min of downhill running (16% descent) at 75% VO 2max . Biopsies of vastus lateralis were obtained 24 h before and 72 h after acute eccentric exercise. Transcripts for inflammatory (TNF‐α, IL‐1β) and anti‐inflammatory cytokines (IL‐6, TGF‐β 1 ) were quantified by real‐time PCR. Before exercise, cytokine transcripts did not differ with age. At old age, exercise induced a blunted accumulation of transcripts encoding the pan‐leukocyte surface marker CD18 (young: 10.1‐fold increase, P <0.005; old: 4.7‐fold increase, P =0.02; young vs. old: P <0.05). In both age groups, CD18 transcript accumulation strongly correlated with TNF‐α (young, r =0.87, P <0.001; old, r =0.72, P =0.002) and TGF‐β 1 transcript accumulation (young, r =0.80, P <0.001; old, r =0.64, P =0.008). At old age, there was no correlation between IL‐1 β and CD18 transcript accumulation. Furthermore, exercise induced IL‐6 transcript accumulation in young (3.6‐fold, P =0.057) but not in old men. Our results suggest that aging impairs the adaptive response of human skeletal muscle to eccentric exercise by differential modulation of a discrete set of inflammatory and anti‐inflammatory cytokine genes.