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Reduction in mononuclear cell mRNA expression of pro‐inflammatory and pro‐oxidant genes with habitual aerobic exercise in older humans
Author(s) -
Gano Lindsey Brooke,
Seals Douglas R.,
Roeca Cassandra,
Hamza Muhammad,
Pierce Gary L.,
Donato Anthony J.
Publication year - 2009
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/fasebj.23.1_supplement.776.8
Subject(s) - aerobic exercise , peripheral blood mononuclear cell , medicine , endocrinology , tumor necrosis factor alpha , monocyte , endothelium , glycation , receptor , immunology , chemistry , biochemistry , in vitro
The biological properties of circulating mononuclear cells (MC) interact with and influence the vascular endothelium. Recently we reported that impaired vascular endothelial function (endothelium‐dependent dilation, EDD) with age in healthy adults is associated with a pro‐inflammatory/pro‐oxidant gene expression profile in circulating mononuclear cells (MC). To determine if habitual aerobic exercise can reverse this profile, 11 sedentary older adults (62±1yr) walked 6 days/week for ~45 min/day at a moderate intensity (70‐75% of max heart rate) for 8 weeks. Walking increased measures of maximal aerobic exercise capacity (P<0.05) and improved EDD (brachial artery flow‐mediated dilation) by 28% (P<0.05). Walking reduced MC mRNA expression (real time RT‐PCR) of nuclear factor κB (‐0.8±0.4 fold change (FC), P=0.05), monocyte chemoattractant protein‐1 (‐2.7±0.9 FC, P=0.01), tumor necrosis factor‐α (‐0.9±0.6 FC, P=0.07), NADPH oxidase p47 (‐0.5±0.2 FC, P<0.05) and receptor for advanced glycation end products (‐1.7±0.6 FC, P<0.01), but did not affect interleukin‐6 (P=0.49) or inducible nitric oxide synthase (P=0.21). These preliminary results indicate that regular aerobic exercise may exert anti‐inflammatory and antioxidant influences on gene expression in circulating MC of older healthy adults. Such effects may represent a novel mechanism by which habitual exercise preserves vascular endothelial function in settings of aging and cardiovascular disease. NIH AG013038 , AG022241 , AG006537 , AG029337 , AG000279 , RR00051