Reduction in α-adrenergic receptor-mediated vascular tone contributes to improved arterial compliance with endurance training☆
Received 2 January 2008; accepted 1 April 2008. published online 08 July 2008.
Abstract
Background
Regular aerobic exercise improves large artery compliance in middle-aged and older humans. However, the underlying mechanisms are unknown. We tested the hypothesis that the improved central arterial compliance with endurance training is mediated by decreased α-adrenergic tone and/or increased endothelial function.
Methods
Seven sedentary healthy adults (60±3 years) underwent systemic α-adrenergic blockade (phentolamine) and nitric oxide synthase (NOS) inhibition using NG-monomethyl-l-arginine in sequence before and after a 3-month moderate endurance training (walk/jog, 4–5 days/week). Phentolamine was given first to isolate the contribution of nitric oxide to arterial compliance by minimizing reflex suppression of sympathetic tone resulting from systemic NOS inhibition as well as to assess the α-adrenergic receptor-mediated modulation of arterial compliance.
Results
Baseline arterial compliance (via simultaneous ultrasound and applanation tonometry on the carotid artery) increased 34±12% after exercise training (P<0.01). When α-adrenergic blockade was performed, arterial compliance increased 37±6% (P<0.01) before the exercise training but did not change significantly after the training. Decreases in arterial compliance from the α-adrenergic blockade to the subsequent additional NOS blockade were not different before and after exercise training.
Conclusion
Our results suggest that the reduction in α-adrenergic receptor-mediated vascular tone contributes to the improved central arterial compliance with endurance training.
aInstitute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology, Ibaraki, Japan
bCardiovascular Aging Research Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas
cCenter for Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki, Japan
dCardiovascular Division, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan
Corresponding author. Department of Kinesiology and Health Education, University of Texas at Austin, 1 University Station, D3700, Austin, TX 78712-1204. Tel.: +1 512 471 8594; fax: +1 512 471 0946.
☆ Grant support: This work was supported by grants-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (18300215, 18650186), JSPS Postdoctoral Fellowship for Research Abroad, and a grant from the National Institutes of Health (AG20966).
ABSTRACT