Endurance training improves endothelium-dependent vasodilation, yet it does not increase basal blood flow in the legs. We determined the effects of a 3-mo aerobic exercise intervention on basal leg blood flow and α-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) (pretraining: 354 ± 29; posttraining: 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 α-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 was completed, femoral artery blood flow increased 47 ± 7% with α-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 α-adrenergic blockade-induced vasodilation (+1.7 ± 0.5 to +3.0 ± 0.5 units, P < 0.05) as well as NOS inhibition-induced vasoconstriction (-0.8 ± 0.4 to -2.7 ± 0.7 units, 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.
|ジャーナル||American Journal of Physiology - Heart and Circulatory Physiology|
|出版ステータス||Published - 2007 9|
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