Submitted on March 5, 2007
Accepted on May 11, 2007
Systemic 
-Adrenergic and Nitric Oxide Inhibition on Basal Limb Blood Flow: Effects of Endurance Training in Middle-aged and Older Adults
Jun Sugawara1*, Hidehiko Komine2, Koichiro Hayashi2, Mutsuko Yoshizawa2, Takeshi Otsuki3, Nobutake Shimojo4, Takashi Miyauchi4, Takashi Yokoi2, Seiji Maeda3, and Hirofumi Tanaka5
1 Department of Kinesiology, University of Texas at Austin, Austin, Texas, United States; Institute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology, Tsukuba, Ibaraki, Japan
2 Institute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology, Tsukuba, Ibaraki, Japan
3 Center for Tsukuba Advanced Research Institute, University of Tsukuba, Tsukuba, Japan
4 Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan
5 Department of Kinesiology, University of Texas at Austin, Austin, Texas, United States
* To whom correspondence should be addressed. E-mail: jun.sugawara{at}mail.utexas.edu.
Endurance training improves endothelium-dependent vasodilation, yet it does not increase basal blood flow in the legs. We determined the effects of a 3-month aerobic exercise intervention on basal leg blood flow, and 
-adrenergic vasoconstriction and nitric oxide (NO) release in seven apparently healthy middle-aged and older adults (60±3 yr). Basal femoral artery blood flow (via Doppler ultrasound) (pre-training: 354±29; post-training: 335±34 ml/min) and vascular conductance did not change significantly with the exercise training. Before the exercise intervention, femoral artery blood flow increased 32±16% with systemic -adrenergic blockade (with phentolamine) (P<0.05), and the addition of nitric oxide synthase (NOS) inhibition using NG-monomethyl-L-arginine (L-NMMA) did not affect femoral artery blood flow. After training, femoral artery blood flow increased 47±7% with -adrenergic blockade (P<0.01) and then decreased 18±7% with the subsequent administration of L-NMMA (P<0.05). Leg vascular conductance showed a greater -adrenergic blockade-induced vasodilation (+1.7±0.5 to +3.0±0.5 U, P<0.05) as well as NOS inhibition-induced vasoconstriction (-0.8±0.4 to -2.7±0.7 U, P<0.05) after the exercise intervention. Resting plasma norepinephrine concentration significantly increased after the training. These results suggest that regular aerobic exercise training enhances NO bioavailability in middle-aged and older adults and that basal limb blood flow does not change with exercise training because of the contrasting influences of sympathetic nervous system activity and endothelium-derived vasodilation on the vasculature.
