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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.
Controversy exists regarding the contribution of a rapid vasodilatory mechanism(s) to immediate exercise hyperemia. Previous in vivo investigations have exclusively examined rest-to-exercise (R-E) transitions where both the muscle pump and early vasodilator mechanisms may be activated. To isolate vasodilatory onset, the current study investigated the onset of exercise hyperemia in an exercise-to-exercise (E-E) transition where no further increase in muscle pump contribution would occur. Eleven subjects lay supine and performed a step increase from rest to 3 min of mild (10% maximal voluntary contraction; MVC), rhythmic dynamic forearm handgrip exercise, followed by a further step to moderate exercise (20% MVC) in each of arm above (A) or below (B) heart level. Beat-by-beat measures of brachial artery blood flow (Doppler ultrasound) and blood pressure (arterial tonometry) were performed. We observed an immediate increase in forearm vascular conductance in E-E transitions, and the magnitude of this increase matched that of the R-E transitions within each of the arm positions (A, E-E 52.8 ±10.7 vs. R-E 60.3 ±11.7 ml.min-1.100 mmHg-1, P = 0.66; B, E-E 43.2 ±12.8 vs. R-E 33.9 ±8.2 ml.min-1.100 mmHg-1, P = 0.52). Furthermore, changes in forearm vascular conductance were identical between R-E and E-E transitions over the first 9 contraction/relaxation cycles in condition A. The immediate and identical increase in forearm vascular conductance in rest-to-exercise and exercise-to-exercise transitions within arm positions provides strong evidence that rapid vasodilation contributes to immediate exercise hyperemia in humans. Specific vasodilatory mechanisms responsible remain to be determined.
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