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1 Human Performance Laboratory, School of Sport and Exercise Sciences, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK 2 Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, Hassall Road, Alsager, Cheshire ST7 2HL, UK
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Abstract |
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4°C for the 60 min duration (CON, 36.5 ± 0.1°C; FC, 35.7 ± 0.1°C; P < 0.05) but core temperature rose by only 0.25°C with no difference between groups. Circulating prolactin remained stable and showed no increase for the FC group, whereas concentrations increased by 102 ± 34% (P < 0.05) for the CON group. No differences were observed between groups for heart rate, but the sensation of heat was less (P < 0.05) with FC. We suggest that a significant component of the prolactin response to moderate passive heating is mediated by facial skin temperature, and selective cooling of the face is associated with improved perception of thermal comfort. These results indicate that the temperature of only a small part of the total skin area (10%) has a disproportionately large effect on the hormonal and perceptual responses to heat stress.
(Received 1 June 2006;
accepted after revision 15 August 2006; first published online 17 August 2006)
Corresponding author T. Mündel: Human Performance Laboratory, School of Sport and Exercise Sciences, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. Email: t.mundel{at}bham.ac.uk
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Introduction |
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Fatigue and lethargy are common sensations associated with living and working in the heat and are thought to be a reflex response to increasing body temperature (Bruck & Olschewski, 1987). Such activity may arise in the limbic area, hypothalamus or brainstem and involve serotonergic (5-HT) neurones that radiate from the raphe nuclei to higher centres concerned with motivation and motor drive (Hori & Harada, 1976a,b). Central 5-HT and dopaminergic (DA) pathways play an important role in the regulation of body temperature (Cox et al. 1980) but 5-HT and DA activity cannot be assessed directly in humans; instead, many studies have used the release of prolactin (PRL) as an indirect measure, since PRL release from the anterior pituitary is stimulated by 5-HT, and inhibited by DA activity in the hypothalamus (Eison & Temple, 1986; Bridge et al. 2003a). A study using functional brain imaging identified a strong correlation between 5-HT activity in the hypothalamus and the PRL response to a 5-HT2c receptor agonist, m-chlorophenylpiperazine (Anderson et al. 2002).
Whilst a raised core temperature is considered the main stimulus for the autonomic, hormonal and behavioural responses in a hot environment, a common observation is that skin temperature influences the way people feel in the heat (e.g. Frank et al. 1999). Previous observations made during exercise (Bridge et al. 2003b; Armada-da-Silva et al. 2004; Mündel et al. 2004) have indicated that skin temperature is an important and effective mediator of hormonal and perceptual responses to heat stress, independent of possible effects on metabolism. Bridge et al. (2003b) demonstrated that for the same rectal temperature, exercise in a cool environment is associated with a lower PRL response compared to exercise in the heat, suggesting that skin temperature affects the secretion of PRL. The head in particular seems sensitive to cooling and effective in modulating many of the effects of a raised core temperature, probably as a direct consequence of the high concentration of temperature-sensitive nerve endings. The head is also important for determining thermal comfort, and head-cooling has been shown to reduce cognitive performance impairment during heat exposure (Nunneley et al. 1971, 1982). Furthermore, selective face cooling can modulate the neuroendocrine response (PRL) to both passive heating (Brisson et al. 1991) and exercise in the heat (Mündel et al. 2004), as well as reducing the perception of effort associated with exercising at a high core temperature (Armada-da-Silva et al. 2004).
Integration of various temperature signals occurs in the hypothalamus; skin receptors terminate in the preoptic area (POAH), whilst core temperature is sensed in the POAH and brainstem. The work of Brisson et al. (1991) showed that exogenous heat loading induced a significant increase in blood PRL and that face cooling significantly attenuated this effect. It is difficult, however, to distinguish the role that skin and core temperature signals played in the study because both rectal and skin temperatures were high owing to immersion in water at 41°C for 30 min, although data pertaining to skin temperature is not presented; direct contact with water at that temperature would elevate skin temperature by 5–10°C, and the rate of rise for rectal temperature was above 3°C h–1. Furthermore, although no statistical effect was reported, there appears to be an approximate 0.5°C attenuation of rectal temperature rise with the face-cooling treatment, which potentially could have influenced the PRL response in that study. Therefore, by replicating the work of Brisson et al. (1991) but at an ambient (air) temperature and humidity at which heat loss mechanisms can effectively regulate core temperature, it should be possible to identify whether a rise in skin temperature alone can stimulate prolactin secretion.
The purpose of the present study was twofold: first, to determine the extent to which elevated skin temperature is responsible for the hormonal and perceptual responses to passive heating; and second, to determine to what extent face cooling can override the effects of raised skin temperature.
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Methods |
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Subjects underwent two passive heat exposures in a sauna maintained at 58°C and a relative humidity (RH) of 13% to induce heat stress and activate heat loss mechanisms. Visit 1 was an habituation session enabling the subject to become familiar with the protocol. A minimum of 7 days later and having been allocated to one of two experimental groups matched for sex, age, body mass index, body surface area and sweating response, visit 2 involved a 60 min exposure in the sauna, where one of the groups received face cooling (FC) every 5 min and the other control group (CON) received no face cooling. Blood samples were taken prior to and at the end of the heat exposure; heart rate, rectal and skin temperatures were monitored continuously, and subjects were asked to evaluate their subjective thermal discomfort.
Subjects
Sixteen recreationally active, non-heat-acclimated volunteers (4 female, all taking oral hormonal contraception, and 12 male) gave their written informed consent to participate in the study; physical data pertaining to subjects are presented in Table 1. The study was performed according to the Declaration of Helsinki and was approved by the Local Ethics Committee. All subjects had completed a General Health Questionnaire to rule out obvious contra-indications for heat stress. Subjects were kept blind to the purpose of the study.
Experimental protocol
Prior to the two heat exposures, subjects arrived having not consumed more than a light snack in the preceding 4 h and at the same time of day on each occasion. Subjects were instructed to keep well hydrated and to abstain from exercise, alcohol, caffeine and smoking for the 24 h period prior to each visit. Soon after arriving at the laboratory, a cannula (20 gauge; Venflon) was inserted into an antecubital vein and kept patent with saline (Baxter, Norfolk, UK) during the test. Subjects were then asked to insert a rectal thermistor 10 cm beyond the anal sphincter and empty their bladder before being weighed nude. Subjects then rested seated for 40 min under thermoneutral conditions, after which a resting blood sample was taken. Subjects were asked their subjective thermal discomfort and then entered the sauna (58 ± 1°C, 13 ± 3% RH) and remained in an upright seated position for the 60 min duration. Subjects were given 600 ml of water to be consumed within the first 40 min of time in the sauna. Subjects wore shorts and T-shirt, and in the event of a subject needing to urinate during the trial, they did so into a container whilst remaining in the sauna. Following the heat exposure, the subject was weighed nude to estimate sweat loss. Sweat loss was corrected for any urinary loss and quantity of blood drawn. During visit 1, subjects had their underarms wiped dry, and preweighed pads (X-ray gauze pads) were placed in the underarm. Subjects then sat for a further 30 min (remaining in the sauna) before the pads were removed from their underarms and weighed with an accuracy of 0.01 g. Weighing the gauze pads gave a baseline measure of axilla sweat rate.
Face cooling
On entering the sauna and at 5 min intervals thereafter, the faces of the FC group were sprayed with a mist of ice-water (4°C) for 10 s. Care was taken to prevent cooling other body parts, and this was confirmed by skin temperature data.
Blood collection and analysis
Venous blood samples (5 ml) were collected into prechilled EDTA-containing tubes at rest before subjects entered the sauna and at the end of the 60 min sauna exposure. The tubes were then centrifuged at 2300g for 10 min at 4°C, and plasma separated and stored at –70°C until analysed. Prolactin concentrations were measured using a radioimmunoassay technique (Skybio Ltd, Bedford, UK). Average inter- and intra-assay coefficients of variations were 5.9 and 2.7%, respectively. All hormone analyses from a single subject were carried out in the same assay batch.
Temperature and heart rate measurement
Ambient temperature during each exposure was measured using a wet and dry bulb mercury thermometer (Brannan, Cumbria, UK), and RH was calculated from wet and dry bulb thermometer differential. Deep body temperature (Trec) was measured in all subjects by a rectal probe inserted 10 cm past the anal sphincter and was connected to a Squirrel data logger (Grant Instruments, Cambridge, UK), with values recorded every 10 min. In four subjects within each condition, skin temperature was measured on the forehead, dorsum of hand, calf and lower back, and weighted mean skin temperature (Tmsw) was determined using the four-site formula of Nielsen & Nielsen (1984). Data are also reported for the mean temperature of the three sites excluding the forehead. Heart rate (HR) was recorded continuously throughout by short-range telemetry (Polar Accurex Plus, Polar Electro Oy, Kempele, Finland) in all subjects.
Perceptual measurement
Measurements were taken at rest before subjects entered the sauna and at the end of the 60 min sauna exposure, and a minimum of 1 min after spraying, in the case of the FC group. Subjective thermal discomfort was assessed using a 10-point scale (Frank et al. 1999).
Data and statistical analysis
All statistical analyses were carried out with an SPSS package, version 12.0 (SPSS Inc., Chicago, Illinois, USA). Data were tested for approximation to a normal distribution. Data were analysed using two-way (time x condition) analysis of variance (ANOVA). Values from ANOVA were assessed for sphericity and if necessary corrected using the Huynh-Feldt method. Following a significant F test, pairwise comparisons were identified using Tukey's honestly significant difference (HSD) post hoc procedure. Where appropriate, independent samples t tests were performed. Where data were not normally distributed (PRL and skin temperature data), Friedman and Mann–Whitney U tests were performed to assess for differences between conditions. Data are reported as means ± S.E.M., unless otherwise stated. Statistical significance was accepted at P < 0.05, and analysis was performed on n = 16, unless otherwise stated.
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Results |
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Rectal temperatures before entering the sauna were the same for CON and FC, and there were no differences in the rise in rectal temperature between groups (P > 0.05, Fig. 1). In the CON condition, rectal temperature rose from 37.26 ± 0.08°C at rest to 37.49 ± 0.07°C at 60 min (P < 0.05). In the FC condition, rectal temperature rose from 37.14 ± 0.08°C at rest to 37.39 ± 0.10°C at 60 min (P < 0.05).
There were no differences in baseline skin temperatures between groups (P > 0.05; Fig. 2). In both conditions, mean weighted skin temperature (Fig. 2A) increased rapidly on entering the sauna and continued to rise until 20 (CON) and 40 min (FC) before reaching a plateau, with values significantly lower in the FC condition (CON, 36.5 ± 0.1°C; FC, 35.7 ± 0.1°C; P < 0.05). Face cooling resulted in forehead temperature (Fig. 2B) being on average 2.1 ± 0.3°C lower than in the CON situation (P < 0.001); however, the mean temperature of the three other body sites showed no difference with average temperatures during the sauna of 37.4 ± 0.1°C for CON and 37.6 ± 0.1°C for FC (Fig. 2C; n.s.).
Baseline values of heart rate did not differ between groups (P > 0.05; Fig. 3). In the CON condition, heart rate increased from baseline values upon entering the sauna (from 70 ± 4 to 81 ± 4 beats min–1) and continued to increase steadily until peaking at 60 min (95 ± 5 beats min–1), before returning to 78 ± 5 beats min–1 within 1 min of leaving the sauna. In the FC condition, heart rate increased from baseline values upon entering the sauna (from 68 ± 3 to 84 ± 3 beats min–1) and continued to increase steadily until peaking at 60 min (93 ± 6 beats min–1), before returning to 78 ± 6 beats min–1 within 1 min of leaving the sauna. No significant differences were observed between groups. There was a tendency for sweat loss to be greater in the FC than in the CON group (567 ± 75 versus 446 ± 36 ml), suggesting a higher sweat rate, but this was not significant (P = 0.18).
Hormonal responses
There were no differences in baseline concentrations of PRL between groups (Fig. 4). In the CON condition, PRL increased from 158 ± 21 miU l–1 at baseline to 340 ± 78 miU l–1 at 60 min, an increase of 102 ± 34% (P < 0.05). By contrast, in the FC condition, PRL remained stable with concentrations of 219 ± 53 and 209 ± 19 miU l–1 at baseline and 60 min, respectively (n.s.). No effects of condition were observed (n.s.).
Perceptual responses
There were no differences in baseline subjective thermal discomfort between groups (n.s.), and main effects of time were observed for both groups (Fig. 5; P < 0.05). By 60 min, ratings had increased to a greater magnitude in the CON condition, so that ratings in the FC condition were significantly lower (8.4 ± 0.3 and 7.7 ± 0.2, respectively; P < 0.05).
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Discussion |
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Influence of core and skin temperatures
External heat loading has previously been shown to be a potent prolactinotrophic stimulus (Mills & Robertshaw, 1981; Christensen et al. 1985; Leppaluoto et al. 1986; Brisson et al. 1991); however, there have also been reports of heat exposure having no effect on plasma prolactin (Follenius et al. 1979; Brandenberger et al. 1979). An explanation for this might be the differing degrees to which core temperature had risen from baseline, and Brisson et al. (1991) argued that a certain body temperature threshold must be reached for heat loads to induce significant changes in blood prolactin. Prolactin release from the anterior pituitary is primarily stimulated by 5-HT receptor activation (Eison & Temple, 1986), and an increased deep body temperature has been shown to increase brain 5-HT concentration in animals (Mohamed & Rahman, 1982; Dey et al. 1993), with similar effects likely in man. In the present study, passive warming in the CON condition resulted in a significant rise in circulating prolactin, despite a rise in rectal temperature of only 0.23 ± 0.03°C after 60 min at an ambient temperature of 58°C. It seems unlikely that such a small rise in core temperature would stimulate this response, since Follenius et al. (1979) observed no effect on plasma prolactin during 90 min of heat exposure during which rectal temperature increased by nearly three times the level we observed (0.65°C). However, just as Brisson et al. (1991) concluded that there may be a threshold for core temperature to initiate the release of prolactin, it is possible that there is also a threshold for skin temperature. Skin temperature responds much more quickly than core temperature, and in the absence of a rise in core temperature, it is possible that an increase in skin temperature of 4°C from baseline or skin temperature approaching that of core temperature may be sufficient to stimulate the release of prolactin. In the present study, mean skin temperatures rose to 37°C, an increase of 4°C from baseline. An increase in skin temperature to this level would have the detrimental effect of reducing the body core to skin temperature gradient, potentially attenuating heat loss but augmenting heat gain mechanisms.
Afferent information from skin and spinal thermoreceptors is known to stimulate a change in firing rates of temperature-sensitive neurones within the POAH, the thermoregulatory control centre (Boulant, 1981, 2000), and in rodents a change in POAH temperature initiates thermoregulatory and behavioural responses such as saliva grooming, body extension and panting (Spector et al. 1968; Roberts & Mooney, 1974). There is also good evidence that some of these temperature-sensitive neurones are dopaminergic (Cox et al. 1980), and others that project into the POAH from the dorsal raphe nuclei are serotonergic (Dickenson, 1977; Cox et al. 1980). It is therefore possible that skin afferents directly activate these temperature-sensitive neurones, altering the activity of dopaminergic and/or serotonergic pathways, this being reflected in changing levels of prolactin. An alternative explanation might be that it is the greater thermal discomfort during CON, resulting from a higher skin temperature, which stimulates the prolactin release rather than a direct effect of skin afferents within the POAH.
It has been shown that in animals, increases in prolactin can be mediated by stress, either by exposure to ether or by physical restraint (Freeman et al. 2000). Although prolactin was not measured during the habituation visit in this study, subjects in the study of Brisson et al. (1991) sat resting in a control condition (i.e. immersed in water at 37°C) for the same duration (30 min) without any rise in prolactin, suggesting that the laboratory procedures involved do not per se cause changes in prolactin.
In the present study, rectal temperature was used as a measure of core body temperature; however, although it is a common measure used to assess core temperature, it is likely that it is not a true representation of the blood perfusing the brain. Oesophageal temperature is measured close to the heart and aorta and is therefore seen as a closer, yet still indirect, measure of blood entering the brain (for review see Moran & Mendal, 2002). Nevertheless, owing to insertion difficulties, irritation to nasal/throat passages, general discomfort to the subject and the potential for temperature anomalies caused by the ingestion of a beverage, the present study employed the use of a rectal thermistor. Furthermore, although differences in lag time and absolute values have been demonstrated during exercise (see Moran & Mendal, 2002), these differences are attenuated during resting conditions (e.g. O'Brien et al. 1998), suggesting sufficient agreement between rectal and oesophageal temperatures.
Responses to face cooling
Face cooling has previously been shown to attenuate the prolactin response to heat stress at rest (Brisson et al. 1991) and during exercise (Mündel et al. 2004) without affecting the rise in core temperature. In the present study, the rise of rectal temperature was the same in both conditions (0.25°C), suggesting that face cooling had no effect on core temperature. In contrast to the CON group, in which there was a significant doubling in levels of prolactin, face cooling inhibited the prolactin response so that there was no significant increase from baseline values to 60 min. Mean weighted skin temperature was significantly lower in the FC condition, and it may be postulated that this difference alone was enough to inhibit the prolactin response. It is important to note, however, that although mean weighted skin temperature was lower during FC, this was probably an artefact of a significantly lower forehead temperature, since mean temperature for other body sites was not affected (Fig. 2). The face is served by a high concentration of temperature- and touch-sensitive nerve endings (trigeminal), and the inhibition of the prolactin response in the FC condition may have been a direct consequence of facial skin afferent stimulation or a consequence of greater subjective comfort (see below).
Perceptual responses
It has previously been demonstrated that manipulating skin temperature (30, 34 and 36°C) whilst maintaining core temperature at 37°C significantly affected subjective thermal discomfort (Frank et al. 1999). In the present study, ratings of thermal discomfort increased significantly for both groups (i.e. subjects felt warmer). It is unlikely that a rise in core temperature of only 0.25°C is responsible for these changes, whereas an increase in skin temperature of 4°C would be a strong stimulus. Furthermore, since face cooling attenuated this response so that by 60 min subjective thermal discomfort was significantly lower when compared with the CON group, it seems plausible that not all areas of the skin are equal in determining thermal discomfort, and this has been demonstrated previously (Nunneley et al. 1971, 1982). A recent study by Arens et al. (2006) concluded that in a warm environment: (1) the head feels warmer than the rest of the body; and (2) overall (dis)comfort follows the warmest local (head) sensation, which may explain why this part of the body is most responsive to cooling. Taken together, the above data suggest that an elevated skin temperature has a significant effect on the perception of the thermal environment, independent of core temperature, and that cooling the face can positively affect subjective discomfort during moderate heating.
The original hypothesis was that levels of circulating prolactin would increase under conditions of passive heating in which heat loss mechanisms are effective in limiting the rise in core temperature, and that face cooling would attenuate this response. The results showed that in the absence of a large rise in core temperature, an elevated skin temperature can induce a significant increase in prolactin secretion, indicating the importance of skin temperature in modulating the hormonal response to passive heating. Face cooling inhibited this response so that no significant increase in plasma prolactin was observed, indicating that during moderate passive heating, the entire prolactin response can be controlled by the temperature of the face. This supports the suggestion of the face/head as a significant determinant of thermal discomfort.
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)
Significant difference between trials. * Significant difference from presauna rest period in both trials. n
= 8.
