Effects of Training Resumption on Conduit Arterial Diameter in Elite Rowers


Medicine & Science in Sports & Exercise: January 2006 - Volume 38 - Issue 1 - pp 86-92
Basic Sciences: Original Investigations

Background: Exercise training is a known stimulus for arteriogenesis, but it is unclear whether elite athletes, who exhibit increased conduit vessel diameter at rest, experience further structural vascular adaptations as a result of intense exercise training.

Methods: Cross-sectional comparisons were performed between elite rowers (N = 17), following a respite from training, and eight untrained age- and gender-matched controls to assess the effects of long-term exercise on vessel structure. To determine the impact of the resumption of intensive exercise training on conduit artery structure, measures were repeated following 3 and 6 months of training in the athletes; the controls remained inactive. Conduit vessel structure was assessed, using high-resolution B-mode ultrasound, as brachial artery diameter at rest (BADr) and in response to 5-min (BAD5) and 10-min (BAD10) periods of forearm cuff ischemia. Shear rate profiles were also analyzed following cuff deflation at all time points.

Results: At entry, all measures of BAD were greater (all P < 0.05) in the athletes relative to controls (athletes vs controls; BADr 4.47 ± 0.10 vs 3.84 ± 0.22 mm; BAD5 4.70 ± 0.10 vs 4.05 ± 0.36 mm, and BAD10 4.93 ± 0.10 vs 4.07 ± 0.25 mm). Resumption of exercise training caused a further increase in brachial artery diameters in the athletes at 3 months (BADr, 4.71 ± 0.10 mm, P < 0.01; BAD5 4.94 ± 0.10 mm, P < 0.05; BAD10 5.12 ± 0.10 mm, P < 0.001), which were maintained, but not further increased, after 6 months of training.

Conclusions: Athletes exhibit enhanced conduit artery diameters at rest and in response to vasodilator stimuli. Despite this long-term training effect on arterial structure, resumption of training further enhances diameter, an effect that occurs within 3 months.

1School of Human Movement and Exercise Science, University of Western Australia, Nedlands, AUSTRALIA; 2Cardiac Transplant Unit, Royal Perth Hospital, Perth, AUSTRALIA; 3Western Australian Institute of Sport and 4School of Medicine and Pharmacology, University of Western Australia, Nedlands, AUSTRALIA

Address for correspondence: Dr. Daniel J. Green, School of Human Movement and Exercise Science, The University of Western Australia, 35 Stirling Highway, Nedlands, 6009, Australia; E-mail: brevis@cyllene.uwa.edu.au.

Submitted for publication May 2005.

Accepted for publication July 2005.

The authors express their gratitude to and thank Chris Reed for his technical assistance throughout the study. We also thank Antonio Maurogiovanni for his involvement in the study.

This study was supported by a grant from the University of Western Australia.

©2006The American College of Sports Medicine