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Articles in PresS, published online ahead of print May 23, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00049.2002
Submitted on January 22, 2002
Accepted on May 3, 2002
1 Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia; Cardiac Transplant & Unit, Royal Perth Hospital, Perth, WA, Australia; Cardiology, Royal Perth Hospital, Perth, WA, Australia
2 Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia; Cardiac Transplant & Unit, Royal Perth Hospital, Perth, WA, Australia
3 Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia
4 Cardiac Transplant & Unit, Royal Perth Hospital, Perth, WA, Australia; Cardiology, Royal Perth Hospital, Perth, WA, Australia
5 Cardiology, Royal Perth Hospital, Perth, WA, Australia
6 Cardiac Transplant & Unit, Royal Perth Hospital, Perth, WA, Australia; Cardiology, Royal Perth Hospital, Perth, WA, Australia; Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia
* To whom correspondence should be addressed. E-mail: brevis{at}cyllene.uwa.edu.au.
We examined vascular function in an inactive muscle bed, the forearm, during lower limb exercise, and determined the contribution of endothelium-derived nitric oxide (NO) to the hyperemic response. Eight young males were randomized to participate in two studies, each consisting of two bouts of lower limb exercise, separated by a 30 min recovery. Peak forearm blood flow (PFBF) and mean blood flow (MFBF) were continuously recorded at baseline and during exercise using continuous high resolution vascular ultrasound and Doppler flow velocity (v) measurement. During one session, the brachial artery was cannulated to allow continuous infusion of saline or L-NMMA, an inhibitor of NO synthase. The alternate session was performed to control for possible effects of repeated exercise. At 60, 100 and 160W, L-NMMA significantly decreased both PFBF and MFBF, compared to the saline infusion. These results suggest that systemic production of NO occurs during exercise in resting vessel beds which do not feed metabolically active tissue. This finding provides a plausible explanation for the anti-atherogenic benefits of exercise.
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