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Voluntary Aerobic Exercise Destiffens Arteries of Old Mice Via Inhibition of NADPH Oxidase‐ and Superoxide‐Dependent Oxidative Stress
Author(s) -
Eng Jason Samuel,
Pham Bryant Thanh,
Johnson Lawrence Cody,
GioscaRyan Rachel A,
Seals Douglas R,
Fleenor Bradley S
Publication year - 2013
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.27.1_supplement.lb654
Subject(s) - apocynin , nadph oxidase , superoxide , oxidative stress , chemistry , medicine , nitrotyrosine , endocrinology , superoxide dismutase , reactive oxygen species , aerobic exercise , oxidase test , biochemistry , nitric oxide synthase , nitric oxide , enzyme
We tested the hypothesis that voluntary aerobic exercise (wheel running) reverses age‐related large elastic artery stiffening by inhibiting NADPH oxidase‐ and superoxide‐dependent oxidative stress. Intrinsic mechanical properties were examined in thoracic (TA) and abdominal (AA) aortic segments from young (Y, 8 mo, n=8) and old (O, 26 mo, n=7) cage‐control male C57BL/6 mice, and old animals with access to voluntary running wheels (OVR, 26 mo, n=6) for 10 weeks. Compared with Y, O had greater elastic modulus (EM), an indicator of stiffness, in the TA (5899 ± 731 vs. 3307 ± 324 kPa, p<0.05) and AA (7796 ± 794 vs. 5268 ± 371 kPa, p<0.01), and increased aortic nitrotyrosine abundance (NT, 2.78 ± 0.61 vs. 1.00 ± 0.23 AU, p<0.05), a marker of oxidative stress. Voluntary running decreased EM in the TA (to 3712 ± 878 kPa, p<0.05) and AA (to 5988 ± 507 kPa, p<0.05), and reduced NT abundance (to 0.91 ± 0.25 AU, p<0.05). Additional TA segments were cultured for 72 hr with TEMPOL (100μm), a superoxide scavenger; apocynin (Apo, 1μmol), a NADPH oxidase inhibitor; or vehicle control (C). Treatment with either TEMPOL or Apo normalized EM in O mice to that observed in Y and OVR animals, without affecting EM in the latter groups. Our results demonstrate that voluntary aerobic exercise normalizes age‐associated stiffening of the TA and AA in mice via reversal of NADPH oxidase‐ and superoxide‐dependent oxidative stress. NIH AG013038 , AG000279 , HL007822