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1 School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada; Ottawa Health Research Institute, Ottawa, Ontario, Canada
2 School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada
* To whom correspondence should be addressed. E-mail: gkenny{at}uottawa.ca.
The hypothesis that exercise causes an increase in the postexercise esophageal temperature threshold for onset of cutaneous vasodilation through an alteration of active vasodilator activity, was tested in nine subjects. Increases in forearm skin blood flow and arterial blood pressure were measured and used to calculate cutaneous vascular conductance at two superficial forearm sites: one with intact 
-adrenergic vasoconstrictor activity (untreated); and, one infused with bretylium tosylate (bretylium-treated). Subjects remained seated resting for 15 min (no-exercise) or performed 15 min treadmill running at either 55, 70 or 85% VO2peak followed by 20 min seated recovery. A liquid conditioned suit was used to increase mean skin temperature (~4.0°C/hr), while local forearm temperature was clamped at 34°C, until cutaneous vasodilation. No differences in the postexercise threshold for cutaneous vasodilation between untreated and bretylium-treated sites were observed for either the no-exercise or exercise trials. Exercise resulted in an increase in the postexercise threshold for cutaneous vasodilation of 0.19 ± 0.01, 0.39 ± 0.02 and 0.53 ± 0.02°C above those of the no-exercise resting values for the untreated site (P < 0.05). Similarly there was an increase of 0.20 ± 0.01, 0.37 ± 0.02 and 0.54 ± 0.02°C for the treated site for the 55, 70 and 85%VO2peak exercise trials respectively (P < 0.05). It is concluded that reflex activity associated with the postexercise increase in the onset threshold for cutaneous vasodilation is more likely mediated through an alteration of active vasodilator activity rather than through adrenergic vasoconstrictor activity.
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