Local sweating and cutaneous blood flow during exercise in hypobaric environments

The effect of acute hypobaric hypoxia on local sweating and cutaneous blood flow was studied in four men and four women (follicular phase of menstrual cycle), who exercised at 60% of their altitude-specific peak aerobic power for 35 min at barometric pressures (PB) of 770 Torr (sea level), 552 Torr (2,596 m), and 428 Torr (4,575 m) at an ambient temperature of 30 degrees C. We measured esophageal temperature (Tes), mean skin temperature (Tsk, 8 sites), and local sweating (ms) from dew-point sensors attached to the skin at the chest, arm, and thigh. Skin blood flow (SkBF) of the forearm was measured once each minute by venous occlusion plethysmography. There were no gender differences in the sensitivity (slope) or the threshold of either ms/Tes or SkBF/Tes at any altitude. No change in the Tes for sweating onset occurred with altitude. The mean slopes of the ms/Tes relationships for the three regional sites decreased with increasing altitude, although these differences were not significant between the two lower PBS. The slope of SkBF/Tes was reduced in five of the eight subjects at 428 Torr. Enhanced body cooling as a response to the higher evaporative capacity of the environment is suggested as a component of these peripheral changes occurring in hypobaric hypoxia.     

Nonthermoregulatory control of human skin blood flow

Although it is well accepted that skin blood flow (SkBF) in humans is controlled by thermoregulatory reflexes, the conclusion that the cutaneous circulation is also controlled by reflexes of nonthermoregulatory origin is not universally held. This review considers the extent to which the cutaneous circulation participates in baroreceptor-mediated reflexes and in the reflexes associated with exercise. Exercise is explored in some detail, because it elicits both thermoregulatory and nonthermoregulatory reflexes. The overall conclusion reached is that thermoregulatory control of SkBF is subject to modification by or competition from several other sources. The fundamental pattern for control of SkBF is described by the threshold and slope of the SkBF-internal temperature relationship. Reflex effects of skin temperature act to shift the threshold of this relationship such that lower levels of skin temperature are associated with higher threshold internal temperatures at which cutaneous vasodilation begins. Similarly, baroreceptor reflexes, reflexes associated with exercise, and effects of some cardiovascular disease also operate against this background. Although modification of the SkBF-internal temperature slope is occasionally seen, the most consistent effect of these nonthermoregulatory factors is to elevate the threshold internal temperature for cutaneous vasodilation. The consequence of this modification of thermoregulatory control of SkBF is that temperature regulation will often suffer when increases in SkBF are delayed or limited. Blood flow to other regions, possibly including active skeletal muscle, may also be compromised when thermoregulatory demands for SkBF are high.     

Heat acclimation increases skin vasodilation and sweating but not cardiac baroreflex responses in heat-stressed humans.

In the present study, to test the hypothesis that exercise-heat acclimation increases orthostatic tolerance via the improvement of cardiac baroreflex control in heated humans, we examined cardiac baroreflex and thermoregulatory responses, including cutaneous vasomotor and sudomotor responses, during whole body heating before and after a 6-day exercise-heat acclimation program [4 bouts of 20-min exercise at 50% peak rate of oxygen uptake separated by 10-min rest in the heat (36 degrees C; 50% relative humidity)]. Ten healthy young volunteers participated in the study. On the test days before and after the heat acclimation program, subjects underwent whole body heat stress produced by a hot water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. The sensitivity of the arterial baroreflex control of heart rate (HR) was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR. The HUT induced a presyncopal sign in seven subjects in the preacclimation test and in six subjects in the postacclimation test, and the tilting time did not differ significantly between the pre- (241 +/- 33 s) and postacclimation (283 +/- 24 s) tests. Heat acclimation did not change the slope in the HR-esophageal temperature (Tes) relation and the cardiac baroreflex sensitivity during heating. Heat acclimation decreased (P < 0.05) the Tes thresholds for cutaneous vasodilation in the forearm and dorsal hand and for sweating in the forearm and chest. These findings suggest that short-term heat acclimation does not alter the spontaneous baroreflex control of HR during heat stress, although it induces adaptive change of the heat dissipation response in nonglabrous skin.     

Exercise thermoregulation after prolonged wakefulness

The effect of 33 h of wakefulness on the control of forearm cutaneous blood flow and forearm sweating during exercise was studied in three men and three women. Subjects exercised for 30 min at 60% peak O2 consumption while seated behind a cycle ergometer (Ta = 35 degrees C, Pw = 1.0 kPa). We measured esophageal temperature (Tes), mean skin temperature, and arm sweating continuously and forearm blood flow (FBF) as an index of skin blood flow, twice each minute by venous occlusion plethysmography. During steady-state exercise, Tes was unchanged by sleep loss. The sensitivity of FBF to Tes was depressed an average of 30% (P less than 0.05) after 33 h of wakefulness with a slight decrease (-0.15 degrees C, P less than 0.05) in the core temperature threshold for vasodilatory onset. Sleep loss did not alter the Tes at which the onset of sweating occurred; however, sensitivity of arm sweating to Tes tended to be lower but was not significant. Arm skin temperature was not different between control and sleep loss experiments. Reflex cutaneous vasodilation during exercise appeared to be reduced by both central and local factors after 33 h of wakefulness.     

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans.

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B(2) receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 microM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 +/- 2% maximal CVC, P < 0.01) and untreated sites (65 +/- 2% maximal CVC, P < 0.01). These responses did not differ between sites (P > 0.05). Because the bradykinin B(2)-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.     

Effects of hypohydration on thermoregulation during exercise before and after 5-day aerobic training in a warm environment in young men

We examined whether enhanced cardiovascular and thermoregulatory responses during exercise after short-term aerobic training in a warm environment were reversed when plasma volume (PV) expansion was reversed by acute isotonic hypohydration. Seven young men performed aerobic training at the 70% peak oxygen consumption rate (Vo(?peak)) at 30°C atmospheric temperature and 50% relative humidity, 30 min/day for 5 days. Before and after training, we performed the thermoregulatory response test while measuring esophageal temperature (T(es)), forearm skin vascular conductance, sweat rate (SR), and PV during 30 min exercise at the metabolic rate equivalent to pretraining 65% Vo(?peak) in euhydration under the same environment as during training in four trials (euhydration and hypohydration, respectively). Hypohydration targeting 3% body mass was attained by combined treatment with low-salt meals to subjects from ~48 h before the test and administration of a diuretic ~4 h before the test. After training, the T(es) thresholds for cutaneous vasodilation and sweating decreased by 0.3 and 0.2°C (P = 0.008 and 0.012, respectively) when PV increased by ~10%. When PV before and after training was reduced to a similar level, ~10% reduction from that in euhydration before training, the training-induced reduction in the threshold for cutaneous vasodilation increased to a level similar to hypohydration before training (P = 0.093) while that for sweating remained significantly lower than that before training (P = 0.004). Thus the enhanced cutaneous vasodilation response after aerobic training in a warm environment was reversed when PV expansion was reversed while the enhanced SR response remained partially.     

Influence of beta-adrenergic blockade on the control of sweating in humans

To evaluate the role of beta-adrenergic receptors in the control of human sweating, we studied six subjects during 40 min of cycle-ergometer exercise (60% maximal O2 consumption) at 22 degrees C 2 h after oral administration of placebo or nonselective beta-blockade (BB, 80 mg propranolol). Internal temperature (esophageal temperature, Tes), mean skin temperature (Tsk), local chest temperature (Tch), and local chest sweat rate (msw) were continuously recorded. The control of sweating was best described by the slope of the linear relationship between msw and Tes and the threshold Tes for the onset of sweating. The slope of the msw-Tes relationship decreased 27% (P less than 0.01), from 1.80 to 1.30 mg X cm-2 X min-1 X degree C-1 during BB. The Tes threshold for sweating (36.8 degrees C) was not altered as the result of BB. These data suggest that BB modified the control of sweating via some peripheral interaction. Since Tsk was significantly (P less than 0.05) reduced during BB exercise, from a control value of 32.8 to 32.2 degrees C, we evaluated the influence of the reduction in local skin temperature (Tsk) in the altered control of sweating. Reductions in Tch accounted for only 45% of the decrease in the slope of the msw-Tes relationship during BB. Since evaporative heat loss requirement during exercise with BB, as estimated from the energy balance equation, was also reduced 18%, compared with control exercise, we concluded that during BB the reduction in sweating at any Tes is the consequence of both a decrease in local Tsk and a direct effect on sweat gland.     

Exercise throughout 6 degrees head-down tilt bed rest preserves thermoregulatory responses.

Spaceflight and its bed rest analog [6 degrees head-down tilt (HDT)] decrease plasma and blood volume and aerobic capacity. These responses may be associated with impaired thermoregulatory responses observed during exercise and passive heating after HDT exposure. This project tested the hypothesis that dynamic exercise during 13 days of HDT bed rest preserves thermoregulatory responses. Throughout HDT bed rest, 10 subjects exercised for 90 min/day (75% of pre-HDT maximum heart rate; supine). Before and after HDT bed rest, each subject exercised in the supine position at the same workload in a 28 degrees C room. The internal temperature (Tcore) threshold for the onset of sweating and cutaneous vasodilation, as well as the slope of the relationship between the elevation in Tcore relative to the elevation in sweat rate (SR) and cutaneous vascular conductance (CVC; normalized to local heating maximum), were quantified pre- and post-HDT. Tcore thresholds for the onset of cutaneous vasodilation on the chest and forearm (chest: 36.79 +/- 0.12 to 36.94 +/- 0.13 degrees C, P = 0.28; forearm: 36.76 +/- 0.12 to 36.91 +/- 0.11 degrees C, P = 0.16) and slope of the elevation in CVC relative to Tcore (chest: 77.9 +/- 14.2 to 80.6 +/- 17.2%max/ degrees C; P = 0.75; forearm: 76.3 +/- 11.8 to 67.5 +/- 14.3%max/ degrees C, P = 0.39) were preserved post-HDT. Moreover, the Tcore threshold for the onset of SR (36.66 +/- 0.12 to 36.74 +/- 0.10 degrees C; P = 0.36) and the slope of the relationship between the elevation in SR and the elevation in Tcore (1.23 +/- 0.19 to 1.01 +/- 0.14 mg x cm(-2) x min(-1) x degrees C(-1); P = 0.16) were also maintained. Finally, after HDT bed rest, peak oxygen uptake and plasma and blood volumes were not different relative to pre-HDT bed rest values. These data suggest that dynamic exercise during this short period of HDT bed rest preserves thermoregulatory responses.     

Control of internal temperature threshold for active cutaneous vasodilation by dynamic exercise.

Exercise induces shifts in the internal temperature threshold at which cutaneous vasodilation begins. To find whether this shift is accomplished through the vasoconstrictor system or the cutaneous active vasodilator system, two forearm sites (0.64 cm2) in each of 11 subjects were iontophoretically treated with bretylium tosylate to locally block adrenergic vasoconstrictor control. Skin blood flow was monitored by laser-Doppler flowmetry (LDF) at those sites and at two adjacent untreated sites. Mean arterial pressure (MAP) was measured noninvasively. Cutaneous vascular conductance was calculated as LDF/MAP. Forearm sweat rate was also measured in seven of the subjects by dew point hygrometry. Whole body skin temperature was raised to 38 degrees C, and supine bicycle ergometer exercise was then performed for 7-10 min. The internal temperature at which cutaneous vasodilation began was recorded for all sites, as was the temperature at which sweating began. The same subjects also participated in studies of heat stress without exercise to obtain vasodilator and sudomotor thresholds from rest. The internal temperature thresholds for cutaneous vasodilation were higher during exercise at both bretylium-treated (36.95 +/- 0.07 degrees C rest, 37.20 +/- 0.04 degrees C exercise, P less than 0.05) and untreated sites (36.95 +/- 0.06 degrees C rest, 37.23 +/- 0.05 degrees C exercise, P less than 0.05). The thresholds for cutaneous vasodilation during rest or during exercise were not statistically different between untreated and bretylium-treated sites (P greater than 0.05). The threshold for the onset of sweating was not affected by exercise (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cutaneous vasoconstrictor response to whole body skin cooling is altered by time of day.

To test for a diurnal difference in the vasoconstrictor control of the cutaneous circulation, we performed whole body skin cooling (water-perfused suits) at 0600 (AM) and 1600 (PM). After whole body skin temperature (T(sk)) was controlled at 35 degrees C for 10 min, it was progressively lowered to 32 degrees C over 18-20 min. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry at three control sites and at a site that had been pretreated with bretylium by iontophoresis to block noradrenergic vasoconstriction. After whole body skin cooling, maximal cutaneous vascular conductance (CVC) was measured by locally warming the sites of SkBF measurement to 42 degrees C for 30 min. Before whole body skin cooling, sublingual temperature (T(or)) in the PM was significantly higher than that in the AM (P < 0.05), but CVC, expressed as a percentage of maximal CVC (%CVC(max)), was not statistically different between AM and PM. During whole body skin cooling, %CVC(max) levels at bretylium-treated sites in AM or PM were not significantly reduced from baseline. In the PM, %CVC(max) at control sites fell significantly at T(sk) of 34.3 +/- 0.01 degrees C and lower (P < 0.05). In contrast, in the AM %CVC(max) at control sites was not significantly reduced from baseline until T(sk) reached 32.3 +/- 0.01 degrees C and lower (P < 0.05). Furthermore, the decrease in %CVC(max) in the PM was significantly greater than that in AM at T(sk) of 33.3 +/- 0.01 degrees C and lower (P < 0.05). Integrative analysis of the CVC response with respect to both T(or) and T(sk) showed that the cutaneous vasoconstrictor response was shifted to higher internal temperatures in the PM. These findings suggest that during whole body skin cooling the reflex control of the cutaneous vasoconstrictor system is shifted to a higher internal temperature in the PM. Furthermore, the slope of the relationship between CVC and T(sk) is steeper in the PM compared with that in the AM.     

Effect of exercise hemoconcentration and hyperosmolality on exercise responses

We investigated the effects of a decrease in plasma volume (PV) and an increase in plasma osmolality during exercise on circulatory and thermoregulatory responses. Six subjects cycled at approximately 65% of their maximum O2 uptake in a warm environment (30 degrees C, 40% relative humidity). After 30 min of control (C) exercise (no infusion), PV decreased 13.0%, or 419 +/- 106 (SD) ml, heart rate (HR) increased to 167 +/- 3 beats/min, and esophageal temperature (Tes) rose to 38.19 +/- 0.09 degrees C (SE). During infusion studies (INF), infusates were started after 10 min of exercise. The infusates contained 5% albumin suspended in 0.45, 0.9, or 3.0% saline. The volume of each infusate was adjusted so that during the last 10 min of exercise PV was maintained at the preexercise level and osmolality was allowed to differ. HR was significantly lower (10-16 beats/min) during INF than during C. Tes was reduced significantly during INF, with trends for increased skin blood flow and decreased sweating rates. No significant differences in HR, Tes, or sweating rate occurred between the three infusion conditions. We conclude that the decrease in PV, which normally accompanies moderate cycle exercise, compromises circulatory and thermal regulations. Increases in osmolality appear to have small if any effects during such short-term exercise.     

Attenuated thermoregulatory sweating and cutaneous vasodilation after 14-day bed rest in humans.

We investigated the effect of head-down bed rest (HDBR) for 14 days on thermoregulatory sweating and cutaneous vasodilation in humans. Fluid intake was ad libitum during HDBR. We induced whole body heating by increasing skin temperature for 1 h with a water-perfused blanket through which hot water (42 degrees C) was circulated. The experimental room was air-conditioned (27 degrees C, 30-40% relative humidity). We measured skin blood flow (chest and forearm), skin temperatures (chest, upper arm, forearm, thigh, and calf), and tympanic temperature. We also measured sweat rate by the ventilated capsule method in which the skin area for measurement was drained by dry air conditioned at 27 degrees C under similar skin temperatures in both trials. We calculated cutaneous vascular conductance (CVC) from the ratio of skin blood flow to mean blood pressure. From tympanic temperature-sweat rate and -CVC relationships, we assessed the threshold temperature and sensitivity as the slope response of variables to a given change in tympanic temperature. HDBR increased the threshold temperature for sweating by 0.31 degrees C at the chest and 0.32 degrees C at the forearm, whereas it reduced sensitivity by 40% at the chest and 31% at the forearm. HDBR increased the threshold temperature for cutaneous vasodilation, whereas it decreased sensitivity. HDBR reduced plasma volume by 11%, whereas it did not change plasma osmolarity. The increase in the threshold temperature for sweating correlated with that for cutaneous vasodilation. In conclusion, HDBR attenuated thermoregulatory sweating and cutaneous vasodilation by increasing the threshold temperature and decreasing sensitivity. HDBR increased the threshold temperature for sweating and cutaneous vasodilation by similar magnitudes, whereas it decreased their sensitivity by different magnitudes.     

Influence of isometric exercise on blood flow and sweating in glabrous and nonglabrous human skin.

The distribution of the reflex effects of isometric exercise on cutaneous vasomotor and sudomotor function is not clear. We examined the effects of isometric exercise by different muscle masses on skin blood flow (SkBF) and sweat rate (SR) in nonglabrous skin and in glabrous skin. The latter contains arteriovenous anastomoses (AVAs), which cause large fluctuations in SkBF. SkBF was measured by laser-Doppler flowmetry (LDF) and reported as cutaneous vascular conductance (CVC; LDF/mean arterial pressure). SR was measured by capacitance hygrometry. LDF and SR were measured at the sole, palm, forearm, and ventral leg during separate bouts of isometric handgrip (IHG) and isometric leg extension (ILE). CVC and its standard deviation decreased significantly during IHG and ILE in the palm and sole (P < 0.05) but not in the forearm or leg (P > 0.05). Only palmar SR increased significantly during IHG and ILE (P < 0.05). We conclude that the major reflex influences of isometric exercise on the skin include AVAs and palmar sweat glands and that this is true for both arm and leg exercise.     

Graded cutaneous vascular responses to dynamic leg exercise

The cutaneous vascular conductance-esophageal temperature (CVC-Tes) relationship was examined at five work loads (75-200 W) in each of four men to find whether there is a role for exercise intensity in the control of skin blood flow (SkBF). Several factors contributed to our evaluation of the CVC-Tes relationship during work. Laser-Doppler velocimetry (LDF) provided a continuous measure of SkBF that is not influenced by underlying muscle blood flow. Local warming to 39 degrees C at the site of measurement of SkBF provided a consistent skin temperature and facilitated observation of changes in LDF. Mean arterial pressure was measured noninvasively once per minute to calculate CVC. Supine exercise minimized baroreceptor-induced cutaneous vasoconstriction. Our major finding was that the internal temperature at which CVC began to rise during exercise (CVC threshold) was graded with work load beyond 125 W (P less than 0.05). In that range the CVC threshold increased by 0.16 degrees C for every increment of 25 W. The CVC threshold was never reached at the highest work load in three of the four subjects. There was no consistent effect of work load on the slope of the CVC-Tes relationship or on the internal temperature at which sweating began during exercise (sweat rate threshold). We conclude that the level of work beyond 125 W affects the CVC-Tes relationship in a graded fashion, principally through shifts in threshold.     

Sweat rate vs. forearm blood flow during lower body negative pressure

Skin blood flow is inhibited when hyperthermia and added hypovolemic stresses are superimposed. We tested the hypothesis that part of this inhibition is a reduced drive for cutaneous active vasodilatation (AVD) with sweat rate (SR) taken as an indirect measure of the efferent drive for cutaneous AVD. We also inquired whether SR itself changes with redistribution of blood volume. Six healthy supine men were subjected to lower body negative pressure (LBNP) after heating in water-perfused suits increased esophageal temperatures (Tes) to a mean of 37.2 degrees C and at least doubled SR and forearm vascular conductance (FVC). Heating continued throughout LBNP and recovery. Sweat rate did not decrease with LBNP onset, although SR-Tes slopes during LBNP were reduced 28% from control. In four subjects the SR-Tes slope did not recover when LBNP was discontinued. These observations suggest that SR is not an effector of the low-pressure baroreflex. In contrast to SR, FVC abruptly fell 22% at the onset of LBNP. Thereafter, FVC-Tes slopes near zero or less occurred. The major effector for FVC inhibition with LBNP appears to be the neural vasoconstrictor system. A minor component due to reduced drive for cutaneous AVD probably occurs as well.     

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women.

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.     

Interactions between local and reflex influences on human forearm skin blood flow.

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.     

Cholinergic mechanisms of cutaneous active vasodilation during heat stress in cystic fibrosis.

To test the hypothesis that cutaneous active vasodilation in heat stress is mediated by a redundant cholinergic cotransmitter system, we examined the effects of atropine on skin blood flow (SkBF) increases during heat stress in persons with (CF) and without cystic fibrosis (non-CF). Vasoactive intestinal peptide (VIP) has been implicated as a mediator of cutaneous vasodilation in heat stress. VIP-containing cutaneous neurons are sparse in CF, yet SkBF increases during heat stress are normal. In CF, augmented ACh release or muscarinic receptor sensitivity could compensate for decreased VIP; if so, active vasodilation would be attenuated by atropine in CF relative to non-CF. Atropine was administered into skin by iontophoresis in seven CF and seven matched non-CF subjects. SkBF was monitored by laser-Doppler flowmetry (LDF) at atropine treated and untreated sites. Blood pressure [mean arterial pressure (MAP)] was monitored (Finapres), and cutaneous vascular conductance was calculated (CVC = LDF/MAP). The protocol began with a normothermic period followed by a 3-min cold stress and 30-45 min of heat stress. Finally, LDF sites were warmed to 42 degrees C to effect maximal vasodilation. CVC was normalized to its site-specific maximum. During heat stress, CVC increased in both CF and non-CF (P < 0.01). CVC increases were attenuated by atropine in both groups (P < 0.01); however, the responses did not differ between groups (P = 0.99). We conclude that in CF there is not greater dependence on redundant cholinergic mechanisms for cutaneous active vasodilation than in non-CF.     

Cardiovascular responses to apneic facial immersion during altered cardiac filling.

The hypothesis that reduced cardiac filling, as a result of lower body negative pressure (LBNP) and postexercise hypotension (PEH), would attenuate the reflex changes to heart rate (HR), skin blood flow (SkBF), and mean arterial pressure (MAP) normally induced by facial immersion was tested. The purpose of this study was to investigate the cardiovascular control mechanisms associated with apneic facial immersion during different cardiovascular challenges. Six subjects randomly performed 30-s apneic facial immersions in 6.0 +/- 1.2 degrees C water under the following conditions: 1) -20 mmHg LBNP, 2) +40 mmHg lower body positive pressure (LBPP), 3) during a period of PEH, and 4) normal resting (control). Measurements included SkBF at one acral (distal phalanx of the thumb) and one nonacral region of skin (ventral forearm), HR, and MAP. Facial immersion reduced HR and SkBF at both sites and increased MAP under all conditions (P < 0.05). Reduced cardiac filling during LBNP and PEH significantly attenuated the absolute HR nadir observed during the control immersion (P < 0.05). The LBPP condition did not result in a lower HR nadir than control but did result in a nadir significantly lower than that of the LBNP and PEH conditions (P < 0.05). No differences were observed in either SkBF or MAP between conditions; however, the magnitude of SkBF reduction was greater at the acral site than at the nonacral site for all conditions (P < 0.05). These results suggest that the cardiac parasympathetic response during facial immersion can be attenuated when cardiac filling is compromised.     

Relationship between mean body temperature calculated by two- or three-compartment models and active cutaneous vasodilation in humans: a comparison between cool and warm environments during leg exercise

The aim of this study was to assess whether the three-compartment model of mean body temperature (Tb3) calculated from the esophageal temperature (Tes), temperature in deep tissue of exercising muscle (Tdt), and mean skin temperature (Tsk) has the potential to provide a better match with the thermoregulatory responses than the two-component model of mean body temperature (Tb2) calculated from Tes and Tsk. Seven male subjects performed 40 min of a prolonged cycling exercise at 30% maximal oxygen uptake at 21°C or 31°C (50% relative humidity). Throughout the experiment, Tsk, Tb2, Tb3, and Tdt were significantly (P < 0.01) lower at 21°C than at 31°C temperature conditions, while Tes was similar under both conditions. During exercise, an increase in cutaneous vascular conductance (skin blood flow / mean arterial pressure) over the chest (%CVCc) was observed at both 21°C and 31°C, while no increase was observed at the forearm at 21°C. Furthermore, the Tb3 and Tdt threshold for the onset of the increase in %CVCc was similar, but the Tes and Tb2 threshold differed significantly (P < 0.05) between the conditions tested. These results suggest that active cutaneous vasodilation at the chest is related more closely to Tb3 or Tdt than that measured by Tes or Tb2 calculated by Tes and Tsk during exercise at both 21°C and 31°C.