Degree Name

Doctor of Philosophy


School of Medicine


Humans regulate body temperature across a wide range of environmental conditions. This is achieved through specialised control pathways that enable the body to detect, integrate and respond to variations in internal and external temperatures. Thermoreceptors, located both centrally and peripherally, detect these temperature changes and provide thermoafferent feedback which is integrated by the hypothalamus and results in the modulation of three thermoeffector mechanisms: vasomotion, sudomotion and thermogenesis. Vasomotion primarily regulates body temperature in thermoneutral environments, while sudomotion and thermogenesis are only activated when skin blood flow can no longer defend mean body temperature. Interestingly, the control of each of these thermoeffectors is not only influenced by core temperature, but also by peripheral (skin) temperature. Indeed, it is generally understood that an approximate ratio of 9:1 (core:skin) exists in the heat. However, the interactions of core and local skin temperature, and the determinants of each of these thermoeffectors (vasomotion, sudomotion and thermogenesis) remains to be more clearly elucidated.

Accordingly, the current series of investigations was focussed upon understanding how these thermoeffectors respond and interact during exposure to a range of environmental conditions, but with a particular emphasis upon skin blood flow in the acral and non-acral skin regions. Firstly, we investigated methods for cooling hyperthermic individuals through whole-body water immersion, and the physiological mechanisms associated with this treatment (Chapters 2 and 3). Secondly, we explored the interactions among central and peripheral thermoreceptor feedback, and direct thermal effects on skin blood flow in both acral and non-acral skin regions (Chapter 4 and 5). Finally, we investigated how thermoeffector activation was modified following deliberate modification of the steady-state, pre-exposure mean body temperatures (Chapter 6).

The first phase of these investigations was designed to provide an understanding of the physiological mechanisms associated with cooling hyperthermic individuals using water immersion. In the first experiment (Chapter 2), we explored three different cooling methods to reduce body core temperature of hyperthermic individuals: air (20-22°C); cold-water immersion (14°C); temperate-water immersion (26°C). In the second experiment (Chapter 3), we investigated whether a more powerful vasoconstriction was present during cold-water immersion, as determined by measuring forearm blood flow. It was also hypothesised that a more powerful vasoconstrictor response would occur during cold-water immersion compared to temperate-water immersion, and that this would occur in both normothermic and hyperthermic states.

For experiment one, eight males participated in three trials, and were heated to an oesophageal temperature of 39.5°C by exercising in the heat (36°C, 50% relative humidity) whilst wearing a water-perfusion garment (40°C). Subjects were cooled using each of three methods: air (20-22°C); cold-water immersion (14°C); temperate-water immersion (26°C). The time to reach an oesophageal temperature of 37.5°C averaged 22.81 min (air), 2.16 min (cold) and 2.91 min (temperate). While each of the between-trial comparisons were statistically significant (P0.05), a significantly greater reduction in forearm and cutaneous blood flow occurred during the cold-water immersion (Trial C) at each time point within the first 4 min of immersion following hyperthermia compared to temperate-water immersion. These observations have not previously been described, and have considerable practical significance. It was concluded that, for hyperthermic, but asymptomatic individuals, temperate-water immersion more than adequately facilitated brain cooling, due to the maintenance of a greater peripheral blood flow.

The purpose of phase two of this experimental series was firstly to design, construct and validate water displacement plethysmographs (Part A) for the forearm, hand and foot that could clamp segmental skin temperature whilst simultaneously measuring cutaneous blood flow (Chapter 4), and secondly (Part B) to investigate the interactions of the central (core) drive and peripheral (cutaneous) feedback on the control of skin blood flow in acral and non-acral skin regions (Chapter 5). For this phase, it was hypothesised that forearm vascular conductance, measured with either a mercury-in-silastic strain-gauge plethysmograph or a water-filled (displacement) plethysmograph, would not differ across these measurement techniques and that core temperature would exert the greatest neural influence on skin blood flow within all body regions (forearm, hand, calf and foot), but for a given core temperature, skin blood flow would change in proportion to changes in local skin temperature for each site.

For part A, two experiments were performed. In the first, the forearm plethysmograph was validated against a mercury-in-silastic plethysmograph under thermoneutral conditions, with and without forearm heating. Cutaneous vascular conductance was elevated almost three-fold by this treatment, however, there were no significant differences between the two forms of plethysmography in either state (P>0.05). In study two, hand and foot blood flows were measured under clamped thermoneutral conditions, but with three local skin temperature treatments (5°, 25°, 40°C). The hand had significantly higher blood flows than the foot at both 25°C (4.07 versus 2.20 mL.100 mL-1.min-1; P-1.min-1; P

For Part B of this research phase, subjects completed three trials where segmental blood flow was measured using four water-filled plethysmographs (forearm, hand, calf and foot) under three separate thermal states, induced using whole-body water immersion and five local skin temperatures. Core temperature for each state was either hypothermic (36.07°C ±0.37), normothermic (37.04°C ±0.27 ) or hyperthermic (38.47°C ±0.34). During each trial, five local skin temperatures (5°, 15°, 25°, 33° and 40°C) were induced at each of four treatment sites (forearm, hand, calf and foot). The lowest recorded skin blood flow, during whole-body hypothermia and local cooling (5°C), was 0.27 mL.100 mL-1.min-1 in the foot, and the highest recorded skin blood flow, during whole-body hyperthermia and local heating (40°C), was in the hand (27.6 mL.100 mL-1.min-1). For each of the four measurement sites (forearm, hand, calf and foot) local skin temperature had little to no effect on skin blood flow during the cold exposure. Indeed, the thermosensitivity remained close to zero for each site: forearm (0.04 mL.100 mL-1.min-1.°C ±0.02); hand (0.04 mL.100mL-1.min-1.°C ±0.02); calf (0.02 mL.100 mL-1.min-1.°C ±0.01); and foot (0.05 mL.100mL-1.min-1.°C ±0.05). However, the rate of increase in skin blood flow with increased local skin temperature (sensitivity) was more than double that observed during the cold exposure at each site. This study provided further supporting evidence that local skin temperature has minimal influence on skin blood flow across either acral or non-acral skin regions within hypothermic individuals, due to the presence of very powerful, centrally driven, vasoconstriction under these conditions. In contrast, the influence of local skin temperature became more pronounced in normothermic individuals. When individuals were hyperthermic, the graded changes in local skin temperature augmented skin blood flow to a greater extent than during both the hypothermic and normothermic conditions across all sites.

Finally, to understand how each of the thermoeffectors respond to changes in mean body temperature, an investigation of the effects of slight deviations in the steady-state, pre-exposure mean body temperature upon the vasomotor, sweating and shivering thresholds was completed. This was achieved by altering the pre-exposure mean body temperature through either whole-body heating or cooling, and then by driving body temperature in the opposite direction whilst measuring the thermoeffector thresholds. It was hypothesised that pre-cooling and pre-heating would shift the mean body temperature thermoeffector thresholds for sweating and shivering by a magnitude equal to that of the pre-exposure displacement of mean body temperature, and that the mean body temperature for vasodilatation and sweating thresholds would occur simultaneously during heating, while the vasoconstrictor threshold would always precede the shivering thresholds during cooling. Each trial consisted of a pre-experimental whole-body water immersion (28-2°C, 35°C or 39°C) phase followed by an experimental phase of either passive heating or passive cooling. During the experimental phase, subjects were passively warmed or cooled, with the use of a water-perfusion garment in the opposite direction to the pre-treatment exposure temperature.

Following whole-body cooling, the threshold for precursor forearm sweating was elevated by 0.18°C (±0.03; P=0.07), whilst that for discharged sweat was raised by 0.19°C (±0.04; P0.05). Conversely, the thresholds for shivering and forearm skin blood flow (vasoconstriction) were 32.9°C (±0.1) and 33.0°C (±0.2), respectively (P>0.05) following whole-body heating. The change in pre-cooling temperature was 0.82oC (±0.2) and was not significantly different from the change in temperature for the shivering threshold, which was increased by 0.67 (±0.2; P>0.05). The vasomotor zone between vasoconstriction and vasodilatation was 3.7°C and 3.2°C for the control and treatment trials, respectively. The most significant finding from this study was that, following pre-treatment, the threshold for vasodilatation and shivering were shifted in equal proportions to the change in mean body temperature induced by each of the two pre-treatments, and this supported our hypotheses. Interestingly, the sudomotor threshold was shifted to a higher mean body temperature following whole-body pre-cooling, and this outcome could indicate that the two thermoeffectors might work independently in response to heat loss requirements, with sudomotor activation being initiated only when vasodilatation fails to dissipate sufficient heat from the skin to the surrounding environment.

In summary, the present series of investigations provided a comprehensive examination on the interactions of vasomotion, sudomotion and thermogenesis, both separately and inter-dependently, across a wide range of environmental conditions with emphases on the physiological mechanisms associated with the treatment of exertional heat illness, the mapping of skin blood flow across a range of core and local skin temperatures, the regional differences in skin blood flow and on the interactions between mean body temperature displacement and the thermoeffector thresholds. The resulting observations have significantly increased our understanding of thermoeffector activation across a range of thermal states.