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Aging, Exercise Training, and eNOS Uncoupling
Author(s) -
MullerDelp Judy M
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.420.4
Subject(s) - enos , endocrinology , medicine , nitric oxide , tetrahydrobiopterin , endurance training , skeletal muscle , chemistry , aerobic exercise , nitric oxide synthase
We sought to determine the effects of age and exercise training on coupling of endothelial nitric oxide synthase (eNOS) and flow‐mediated dilation in skeletal muscle arterioles. Young (4 mos) and old (22 mos) rats underwent exercise training or remained sedentary for 10 weeks. Flow‐induced increases in NO and O 2 − were assessed in arterioles from soleus muscle. Levels of the co‐factor, tetrahydrobiopterin (BH 4 ) were also determined. Flow‐induced increases in NO were reduced in arterioles from old rats as compared to those from old rats. L‐NAME eliminated flow‐induced increases in NO. Flow increased O 2 − , which was inhibited by L‐NAME, in arterioles from old but not young rats. Exercise training augmented flow‐induced increases in NO in arterioles from old but not young rats. Exercise training increased flow‐induced O 2 − production (which was inhbiited by L‐NAME) in arterioles from young but not old rats. Arteriolar BH 4 levels were reduced with age, and restored by exercise training. Thus, reduced BH 4 and uncoupling of eNOS contributes to the age‐induced reduction of NO signaling in skeletal muscle arterioles. In arterioles from old rats, exercise training restores BH 4 and increases flow‐induced production of NO, whereas, in arterioles from young rats, eNOS‐derived production of O 2 − is increased by exercise training.