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1 School of Physical and Health Education and Department of Physiology, Queen's University, Kingston, Ontario, Canada
* To whom correspondence should be addressed. E-mail: mt29{at}post.queensu.ca.
We tested the hypothesis that nitric oxide (NO) and prostaglandins (PGs) contribute to the rapid vasodilation that accompanies a transition from mild to moderate exercise. Nine healthy volunteers (2 women, 7 men) lay supine with their forearm at heart level. Subjects were instrumented for continuous brachial artery infusion of saline (control condition), or combined infusion of L-NAME and Ketorolac (drug condition) to inhibit NO synthase and cyclooxygenase, respectively. A step increase from 5 min steady state mild (5.4 kg) rhythmic, dynamic forearm handgrip exercise (1-s contraction/2-s relaxation duty cycle) to moderate (10.9 kg) exercise for 30 s was performed. Steady state forearm blood flow (FBF; Doppler ultrasound) and forearm vascular conductance (FVC) were attenuated in drug (D) condition compared with saline (S) (FBF: D 196.8 ± 30.8 vs. S 281.4 ± 34.3 ml.min-1; FVC: D 179.3 ± 29.4 vs. S 277.8 ± 34.8 ml.min-1 100 mmHg-1, both P < 0.01). FBF and FVC increased from steady state following release of the initial contraction at the higher workload in both saline and drug conditions (
FBF: S 72.4 ± 8.7 ml.min-1; D 52.9 ± 7.8 ml.min-1; FVC: S 66.3 ± 7.3 ml.min-1. 100 mmHg-1; D 44.1 ± 7.0 ml.min-1.100 mmHg-1, all P < 0.05). Importantly, the % FBF and % FVC were not different during saline infusion or combined inhibition of NO and PG's (% FBF: S 27.2 ± 3.1 vs. D 28.1 ± 3.8%, P = 0.78; % FVC: S 25.7 ± 3.2 vs. D 26.0 ± 4.0%, P = 0.94). These data suggest that NO and vasodilatory PGs are not obligatory for rapid vasodilation at the onset of a step increase from mild to moderate intensity forearm exercise. Additional vasodilatory mechanisms not dependent on NO and PG release contribute to the immediate and early increase in blood flow in an exercise-exercise transition.
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