Cutaneous active vasodilation in humans during passive heating postexercise

Abstract

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 alpha-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 ( approximately 4.0 degrees C/h), while local forearm temperature was clamped at 34 degrees 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 degrees 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 degrees 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.

The Postexercise Increase in the Threshold for Cutaneous Vasodilation and Sweating is Not Observed With Extended Recovery

“…Our observations of a postexercise increase in Th VD and Th SW measured during whole-body warming following a short recovery (<20 min) are similar to previous findings (Kenny et al, 2000a;2003a;2003b). However, no comparable increase in Th VD and Th SW was observed when exercise recovery was extended to 60 minutes prior to threshold determination.…”

“…Specifically, exercise induces a residual effect on thermal control, resulting in an increase of ~0.3-0.4 °C in the postexercise esophageal temperature at which cutaneous vasodilation and sweating (Kenny et al, 2000a) occurs. Furthermore, an increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was shown to result in a relative increase in the onset thresholds for cutaneous vasodilation (Kenny et al, 2003a) and ecrrine sweating (Kenny et al, 2003b), an overall decrease in the rate of heat loss, and a concomitant increase in the postexercise core temperature recovery time (Kenny and Neidre, 2002). These observations suggest a possible physiological link between the observed postexercise cardiovascular changes and the altered thermal response thresholds for cutaneous vasodilation and sweating.…”

Menstrual cycle and oral contraceptive use do not modify postexercise heat loss responses

“…Our findings confirm an elevation in Th VD and Th SW following exercise as previously demonstrated in men (31,32,33) and in women during the FP (28,31). A novel finding of this study is that the postexercise elevation in Th VD and Th SW is similar in both menstrual cycle phases.…”

Non-thermal modification of heat-loss responses during exercise in humans

“…This discrepancy in responses at rest might be due to different levels of baroreceptor loading and heat stress used in each study. Kenny and Journeay (2010) have reviewed postexercise thermoregulation from a standpoint of separating thermal and non-thermal effects, and indicated that a greater level of postexercise hypotension, induced by exercise of increasing intensity, causes a relative increase in onset threshold of sweating (Kenny et al 2003b) and skin vasodilation (Kenny et al 2003a) during passive heating. These findings suggest that unloading of cardiopulmonary and arterial baroreceptors attenuates heat-loss responses after exercise.…”