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1 Human Performance and Environmental Medicine
Research Laboratory, School of Human Kinetics, Faculty of Health Sciences,
University of Ottawa, Ottawa, Ontario K1N 6N5; and
2 Ottawa Health Research Institute, Ottawa, Ontario,
Canada K1Y 4E9
Submitted 10 April 2003
; accepted in final form 27 May 2003
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
of treadmill running at either 55, 70, or 85% of peak oxygen consumption
followed by 20 min of seated recovery. A liquid-conditioned suit was used to
increase mean skin temperature ( 4.0°C/h), 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 0.53 ±
0.02°C for the treated site for the 55, 70, and 85% 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.
postexercise hypotension; skin blood flow; exercise intensity; baroreceptor; thermoregulation
Address for reprint requests and other correspondence: G. P. Kenny, University
of Ottawa, Faculty of Health Sciences, Human Performance and Environmental
Physiology Research Laboratory, Montpetit Hall, Rm. 376, 125 University Ave.,
Ottawa, ON, Canada K1N 6N5 (E-mail:
gkenny{at}uottawa.ca ).