INTRODUCTION

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IN RECENT STUDIES, THE EFFECTS of exercise on the postexercise threshold of cold (i.e., vasoconstriction and shivering) (8, 9) and warm (i.e., cutaneous vasodilation and sweating) (7) thermoregulatory responses have been evaluated during seated upright resting. These studies have indicated that exercise induces a residual effect on thermal control by increasing (~0.3°C) the postexercise resting threshold for cold and warm thermal responses. These data support the previous findings of Thoden et al. (22), who observed that, after 15 min of moderate exercise, skin blood flow and mean skin temperatures (_sk) returned to baseline values within 15-20 min during postexercise resting, despite a sustained prolonged elevation of esophageal temperature (T_es). Furthermore, in a previous effort to address the mechanism for the postexercise increase in thermal response thresholds, subjects were immersed in warm water (42°C) until T_es increased to levels similar to those induced by 15 min of exercise (10). After exit from the warm water, T_es, _sk, and skin blood flow all returned to control values within 10 min. Thus it is likely that the postexercise increase in both T_es and the onset threshold for vasodilation are not a consequence of an increased body heat content (10). Although the actual mechanism of the postexercise thermal response remains unclear, recent evidence may favor a baroreceptor-mediated influence.

It is known that active cutaneous vasodilation is normally under baroreceptor control (5). Acute bouts of exercise have been shown to cause postexercise hypotension (3). A decrease in skin blood flow (i.e., vasoconstriction) would tend to maintain venous return and adequate filling pressure in response to the decrease in systemic arterial resistance. This nonthermal factor may influence the elevated threshold for vasoconstriction (and vasodilation) during exercise recovery.

Therefore, we propose that the nonthermal baroreceptor response may modify the normal thermoregulatory activity in elevating the threshold for vasodilation during exercise recovery. Within this study, we manipulated postexercise venous pooling by means of head-down tilt, in an effort to reverse its impact on baroreceptor unloading. By doing so, we tested the hypothesis that head-down tilt would result in a relative lowering of the resting postexercise elevation in the T_es for forearm cutaneous vasodilation.

	METHODS

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Subjects

Instrumentation

Forearm skin blood flow was assessed with a laser-Doppler flow probe placed on the midanterior forearm (blood perfusion monitor, TSI, St. Paul, MN). Laser-Doppler flowmetry provides a linear index of skin blood flow from ~1 mm² of skin area and is based on the frequency of shift of coherent laser light induced by erythrocytes moving in the cutaneous vessels (20). The laser-Doppler flow sensor was taped to the cleaned skin surface at a location that gave a consistent reading. Only relative values were used, and no attempt was made to evaluate absolute blood flow.

Temperatures were collected and digitized (Hewlett-Packard data acquisition module, model 3497A) at 5-s intervals, displayed graphically on the computer screen, and recorded in spreadsheet format on a hard disk (Hewlett-Packard, model PC-312, 9000).

Experimental Protocol

Each subject performed a total of four experimental trials that were carried out in a random order. The general phases for each of the four experimental trials are presented in Fig. 1. Briefly, the four trials were as follows: 1) Head-up tilt/Exercise/Head-up tilt, 2) Head-up tilt/No-Exercise/Head-up tilt, 3) Head-down tilt/Exercise/Head-down tilt, and 4) Head-down tilt/No-Exercise/Head-down tilt. Each of the four trials involved three distinct phases that were identified as pretreatment period, treatment period, and posttreatment period.

View larger version (15K): [in this window] [in a new window]   Fig. 1.   Protocol time line. O2 max, maximal O2 uptake; HUT, head-up tilt.

Each trial was separated by a minimum of a 24-h period without heavy or prolonged physical activity, the last 12 h of which included abstinence from stimulants and alcohol, 8 h of sleep, and a minimum of 0.25 liter of water during each waking hour. On each study day, care was taken to avoid major thermal stimuli or substantial increase of metabolic rate between awakening and the start of the experiment. All trials were conducted during the winter months from November to February. To ensure that the subjects were euhydrated during each experimental trial, they were encouraged to ingest water ad libitum during the application of the instrumentation on experimental days. The experimental trials were conducted either in the morning (3 subjects) or midafternoon (3 subjects). This allowed us to consider any changes in thermoregulatory thresholds due to circadian rhythms before and after zenith.

On arrival at the laboratory, subjects, clothed in shorts and running shoes, were instrumented appropriately. They were then outfitted with a water-perfused suit that covered the entire body except the face, fingers, and feet. It should be noted that the water-perfused suit covered the midanterior forearm that was the site for skin blood flow measurement. Spandex pants, a cotton sweatshirt, and a cotton head cover were worn over the water-perfused suit. To determine the relative treatment effect on the threshold for cutaneous forearm vasodilation (Th_VD), each subject underwent a baseline resting evaluation of Th_VD in all four trials (pretreatment warming). Subjects were positioned in a 65° head-up tilt position on a Hang-Up tilt table in a climatically controlled chamber for a minimum period of 15 min at an ambient temperature of 24°C. Baseline resting was then followed by the respective periods described below.

Pretreatment period. In two of the experimental trials, the pretreatment period was carried out with the subject in the 65° head-up tilt position. In the other two experimental trials, the subject was positioned in a 15° head-down tilt. Once the subject was placed in the respective position, cool water (~20°C) was circulated through the water-perfused suit, and ambient temperature was reduced to 14°C until forearm cutaneous vasoconstriction was noted (cooling, ~25 min). Ambient temperature was then increased to 29°C. _sk was increased at a rate of 7.0°C/h (as the water circulating through the suit was progressively increased to 47°C) until forearm cutaneous vasodilation was noted (warming, ~37 min). T_es and _sk were subsequently decreased to near baseline values by again perfusing the suit with cool water and decreasing ambient temperature to 24°C (cooling, ~30 min).

Treatment period. Immediately after the pretreatment period, subjects either exercised (Exercise) or remained resting (No-Exercise). For the Exercise treatment, the subject performed 15 min of cycle ergometer exercise at 70% of predetermined maximal O₂ uptake. The subject was then moved back to the tilt table to complete 15 min of resting recovery in the 65° head-up tilt position. For the No-Exercise treatment, the subject was instructed to rest in the 65° head-up tilt position for 30 min.

Posttreatment period. To measure the effect of postexercise venous pooling on the resting postexercise Th_VD, posttreatment resting measurements of Th_VD were conducted. Immediately after both the No-Exercise and Exercise treatments, subjects were returned to their original (pretreatment) position on the tilt table. Once the subject was resting in the respective position, the procedure for measuring thermoregulatory thresholds was carried out as that of the pretreatment condition. Specifically, cool water (~20°C) was circulated through the water-perfused suit, and ambient temperature was reduced to 14°C until forearm cutaneous vasoconstriction was noted (cooling, ~32 min). Ambient temperature was then increased to 29°C, _sk was increased at a rate of 7.0°C/h (as the water circulating through the suit was progressively increased to 47°C), and forearm cutaneous vasodilation was noted (warming, ~37 min).

Analysis of Results

	RESULTS

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There were no differences between pre- and postrates of warming for the suit perfusate (~19.5°C/h) in either the No-Exercise and Exercise conditions in the head-up tilt or head-down tilt positions. Thus _sk (~7.0°C/h) and T_es (~0.4°C/h) increased at the same respective rates in both treatment conditions. Baseline resting T_es and _sk were similar for all conditions and remained stable and consistent during the 15-min period before the initial surface cooling.

No-Exercise Treatment: Effect of Time on Forearm Vasodilation

View larger version (19K): [in this window] [in a new window]   Fig. 2.   Mean ( connected by solid line) and individual core corrected thresholds for vasodilation during pre- and posttreatment warming for the No-Exercise condition in both the head-up tilt (top) and head-down tilt (bottom) positions (n = 6). Bars, SD; *significantly different from preresting warming (P < 0.05).

For the pre- and postresting head-up tilt warming, the onset threshold for forearm vasodilation decreased from 36.81 ± 0.12°C to 36.64 ± 0.13°C, respectively (P < 0.05). In contrast, the onset thresholds remained unchanged between pre- and postresting during the head-down tilt warming (36.66 ± 0.16°C and 36.62 ± 0.16°C, respectively).

Exercise Treatment: Effect of Exercise on Forearm Vasodilation

View larger version (18K): [in this window] [in a new window]   Fig. 3.   Mean ( connected by solid line) and individual core corrected thresholds for vasodilation during pre- and posttreatment warming for the Exercise condition in both the head-up tilt (top) and head-down tilt (bottom) positions (n = 6). *Significantly different from preresting warming (P < 0.05).

	DISCUSSION

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The purpose of this study was to evaluate the influence of venous pooling on postexercise thermoregulatory thresholds. More specifically, we evaluated the effect of a reduction in postexercise venous pooling by means of head-down tilt on the postexercise Th_VD. The most important observation of this study was the absence of an elevated postexercise Th_VD in the head-down tilt condition. It was noted that 1) at rest, the esophageal Th_VD was higher in the head-up position (36.81 ± 0.12°C) compared with the head-down position (36.66 ± 0.16°C) (P < 0.05); 2) exercise produced an expected increase in the T_es Th_VD in the head-up tilt position (0.24°C) (P < 0.05); and 3) the increase in the postexercise T_es Th_VD was attenuated in the head-down tilt position. The increase in the postexercise resting threshold for cutaneous vasodilation confirms a similar increase of warm (i.e., sweating) (7) and cold (i.e., vasoconstriction and shivering) thermal responses (8, 9) measured during upright seating.

The postexercise increase in the threshold for cutaneous vasodilation during head-up tilting was not caused by differences in rate of change of either T_es or _sk because warming rates were not significantly different for the pre- and postexercise warming period.

Brengelmann et al. (2) have demonstrated a time-dependent decrease in sweating threshold in experiments of >2-h duration. Thus it is thought that the prolonged protocol used in this study in and of itself probably did not contribute to the observed postexercise elevated threshold for cutaneous vasodilation (in the head-up tilt position). The observed time-dependent decrease in the threshold for cutaneous vasodilation under resting conditions [i.e., 0.17 and 0.04°C for head-up tilt (P < 0.05) and head-down tilt (not significant), respectively] is most likely and at best an underestimation of the exercise-induced increase in the threshold for cutaneous vasodilation. The circadian effect on set-point shift and therefore the time of day at which the tests were conducted may have had some bearing on the observed results. However, the results of those experimental trials conducted at zenith in early afternoon were comparable to those conducted in early morning.

It has been demonstrated that baroreceptor unloading increases the threshold for cutaneous vasodilation. Specifically, Mosley (15) showed that there is cutaneous vasoconstrictor activity in response to head-up tilting. Similar results have been demonstrated during lower body negative pressure (1, 13, 18, 23). This modification has been demonstrated during passive heating at rest (4) and by exercise (11). Our data are consistent with these findings in that we showed a lower pretreatment threshold for vasodilation during head-down tilting for both No-Exercise (0.15°C) and Exercise (0.12°C) conditions, respectively, compared with head-up tilting (Figs. 2 and 3). Thus it is clear that, with the lack of peripheral pooling after exercise in the head-down tilt position, the exercise effect on the T_es Th_VD is attenuated. These data suggest that baroreceptor unloading due to peripheral blood pooling in the postexercise period contributes to the postexercise increase in the T_es Th_VD.

Although the mechanism(s) for thermoregulatory control of skin blood flow before and during exercise have been described (4, 6, 19, 21), postexercise regulation remains unclear. It is known, however, that the cutaneous vasodilator system is under baroreceptor control (6). Cutaneous vascular tone is a determinant of blood flow and blood pressure regulation during both exercise and upright posture (17). Acute bouts of exercise have been shown to cause postexercise hypotension. This is likely due to the persisting blood pooling in the previously active musculature. The resultant baroreceptor unloading elicits peripheral vasoconstriction in an attempt to maintain blood pressure. If peripheral vasoconstriction is not adequate to overcome the hypotension caused by blood pooling, then the hypotensive condition persists. It can be noted, however, that, in an attempt to preserve blood pressure (via peripheral vasoconstriction), the body's ability to dissipate accumulated heat is diminished. It is plausible, therefore, that the increase in the postexercise threshold for cutaneous vasodilation is the result of a strong nonthermoregulatory drive (i.e., baroreceptor reflex) to maintain normal postexercise blood pressure.

Thus it would seem that skin blood flow control after exercise is subject to significant modifications by nonthermoregulatory baroreceptor reflexes. Because acute reductions in central venous pressure have been shown to delay or decrease the rise in cutaneous blood flow during heat stress (11, 14, 16), a reasonable postulate is that cardiopulmonary baroreceptors are involved in the postexercise cutaneous vasoconstriction during postexercise resting. Modification of baroreceptor response on cutaneous vascular tone would be manifested either as an activation of sympathetic adrenergic vasoconstrictor nerves or as a withdrawal of active vasodilator activity (5).

We have shown that manipulating postexercise venous pooling, by means of head-down tilt, in an effort to reverse its impact on baroreceptor unloading, resulted in a relative lowering of the resting postexercise elevation in the T_es for forearm cutaneous vasodilation. Thus it would seem that the nonthermal factor of baroreceptor control significantly influences cutaneous vasomotor control during exercise recovery. Further studies are required to examine the mechanism of control and to determine how nonthermoregulatory reflexes, such as baroreceptor control, may possibly modify postexercise warm and cold thermal responses.