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Exercise training increases extracellular superoxide dismutase protein content in soleus muscle feed arteries of aged rats.
Author(s) -
Trott Daniel Wayne,
Woodman Christopher R
Publication year - 2008
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.22.1_supplement.1235.2
Subject(s) - enos , superoxide dismutase , medicine , endocrinology , sed , nitric oxide synthase , chemistry , aerobic exercise , antioxidant , nitric oxide , endothelium , superoxide , enzyme , biochemistry , oxidative stress
Exercise training attenuates or reverses age‐induced endothelial dysfunction in skeletal muscle vascular beds. The purpose of this study was to test the hypothesis that exercise training improves endothelium‐dependent dilation through alterations in vascular antioxidant enzyme protein content and phosphorylation of endothelial nitric oxide synthase (eNOS) on ser1177 (Ser 1177 phospho‐eNOS). Young (2 mo) and Old (22 mo) male Fischer 344 rats were exercise trained (Ex) or remained sedentary (Sed) for 10–12 weeks resulting in four groups of rats: Young Sed (4 mo; n = 7), Young Ex (4 mo; n = 8), Old Sed (24 mo; n = 8), Old Ex (24mo; n = 8). At the end of the exercise training program, immunoblotting was performed on soleus muscle feed arteries (SFA) to assess eNOS, Ser 1177 phospho‐eNOS, Cu/Zn cytosolic superoxide dismutase (Cu/ZnSOD) and extracelluar superoxide dismutase (ecSOD) protein content. Results indicate that eNOS and Ser 1177 phospho‐eNOS content was greater in Old rats compared to Young regardless of training status. Exercise training induced increases in ecSOD protein content in both Young and Old rats. There were no differences in Cu/ZnSOD protein content between groups. These data suggest that exercise training improves endothelium‐dependent dilation in senescent SFA in part due to increases in ecSOD protein content, resulting in an improvement in vascular antioxidant capacity. Supported by NIH AG‐00988, AHA Texas Affiliate Grant 0765043Y and an ACSM Foundation Research Grant (FRG)