scholarly journals Two isothermal challenges yield comparable physiological and subjective responses

2020 ◽  
Vol 120 (12) ◽  
pp. 2761-2772
Author(s):  
L. Klous ◽  
A. Psikuta ◽  
K. Gijsbertse ◽  
D. Mol ◽  
M. van Schaik ◽  
...  

Abstract Purpose Ventilated vests are developed to reduce thermal stress by enhancing convective and evaporative cooling from skin tissue underneath the vest. The purpose of this study is to investigate whether thermal stress is equal when a ventilated vest is worn compared to a no-vest situation with similar dry thermal resistance. Methods Nine healthy males walked on a treadmill (7 km h−1) for 45 min in a desert climate (34 °C, 20% relative humidity) with and without ventilated vest. Gastrointestinal temperature (Tgi), heart rate (HR), and skin temperature (Tsk) were continuously monitored. Local sweat rate (LSR) was assessed two times on six skin locations. Subjective ratings were assessed every 10 min. Results Final Tgi (37.6 ± 0.1 °C for vest and 37.6 ± 0.1 °C for no-vest), HR (133 ± 7 bpm and 133 ± 9 bpm) and mean Tsk (34.8 ± 0.7 °C and 34.9 ± 0.6 °C) were not different between conditions (p ≥ 0.163). Scapula skin temperature (Tscapula) under the vest tended to be lower (baseline to final: ΔTscapula = 0.35 ± 0.37 °C) than without vest (ΔTscapula = 0.74 ± 0.62 °C, p = 0.096). LSR at locations outside the vest did not differ with and without vest (p ≥ 0.271). Likewise, subjective responses did not differ between conditions (χ2 ≥ 0.143). Conclusions We conclude that two systems with similar dry thermal resistance and, therefore, similar required evaporation, resulted in similar thermal stress during paced walking in a hot-dry environment. Local ventilation did not alter the sweating response on locations outside the vest.

2005 ◽  
Vol 98 (3) ◽  
pp. 829-837 ◽  
Author(s):  
Yoshi-Ichiro Kamijo ◽  
Kichang Lee ◽  
Gary W. Mack

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40°C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3°C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVCBT) and sweat expulsion number increased at 38 and 40°C compared with 34°C ( P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40°C ( P < 0.05, different from 34°C). However, SSNA burst amplitude increased ( P < 0.05), whereas SSNA burst duration decreased ( P < 0.05), at the same time as we observed the increase in CVCBT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.


2014 ◽  
Vol 116 (8) ◽  
pp. 1088-1095 ◽  
Author(s):  
Nathan B. Morris ◽  
Anthony R. Bain ◽  
Matthew N. Cramer ◽  
Ollie Jay

Two studies were performed to 1) characterize changes in local sweat rate (LSR) following fluid ingestion of different temperatures during exercise, and 2) identify the potential location of thermoreceptors along the gastrointestinal tract that independently modify sudomotor activity. In study 1, 12 men cycled at 50% V̇o2peakfor 75 min while ingesting 3.2 ml/kg of 1.5°C, 37°C, or 50°C fluid 5 min before exercise; and after 15, 30, and 45-min of exercise. In study 2, 8 men cycled at 50% V̇o2peakfor 75 min while 3.2 ml/kg of 1.5°C or 50°C fluid was delivered directly into the stomach via a nasogastric tube (NG trials) or was mouth-swilled only (SW trials) after 15, 30, and 45 min of exercise. Rectal (Tre), aural canal (Tau), and mean skin temperature (Tsk); and LSR on the forehead, upper-back, and forearm were measured. In study 1, Tre, Tau, and Tskwere identical between trials, but after each ingestion, LSR was significantly suppressed at all sites with 1.5°C fluid and was elevated with 50°C fluid compared with 37°C fluid ( P < 0.001). The peak difference in mean LSR between 1.5°C and 50°C fluid after ingestion was 0.29 ± 0.06 mg·min−1·cm−2. In study 2, LSR was similar between 1.5°C and 50°C fluids with SW trials ( P = 0.738), but lower at all sites with 1.5°C fluid in NG trials ( P < 0.001) despite no concurrent differences in Tre, Tau, and Tsk. These data demonstrate that 1) LSR is transiently altered by cold and warm fluid ingestion despite similar core and skin temperatures; and 2) thermoreceptors that independently and acutely modulate sudomotor output during fluid ingestion probably reside within the abdominal area, but not the mouth.


1984 ◽  
Vol 56 (5) ◽  
pp. 1283-1288 ◽  
Author(s):  
J. M. Johnson ◽  
D. S. O'Leary ◽  
W. F. Taylor ◽  
M. K. Park

To find whether sweat rate (SR) and forearm skin blood flow ( SkBF ) were reflexly affected by skin temperature (Tsk) we used water-perfused suits to rapidly elevate Tsk during exercise. With this elevation in Tsk, there was a period of little net change in esophageal temperature (Tes) but marked responses in SR and SkBF . During this period a rise in Tsk of 4.2 +/- 0.3 degrees C was associated with an increase in SR of 0.44 +/- 0.09 mg X cm-2 X min-1 and an increase in SkBF of 3.27 +/- 0.42 ml X 100 ml-1 X min-1. Multiple linear regression analysis as well as comparison with control studies in which Tsk was kept cool also reveal a consistent role for Tsk in the reflex regulation of SR and SkBF . Responses in SR and FBF were much more marked at levels of Tsk below 33 degrees C. Below a Tsk of 33 degrees C, SR rose 0.30 +/- 0.06 mg X cm-2 X min-1 per degrees C rise in Tsk, whereas above 33 degrees SR rose only 0.05 +/- 0.01 mg X cm2 X min per degrees C. FBF rose 2.81 +/- 0.60 and 0.77 +/- 0.18 ml X 100 ml-1 X min-1 per degrees C rise in Tsk at the lower and upper ranges of Tsk, respectively.


2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.


1965 ◽  
Vol 20 (1) ◽  
pp. 31-36 ◽  
Author(s):  
C. H. Wyndham

The response characteristics have been studied of the curves relating heat conductance and sweat rate to change in rectal temperature at different levels of skin temperature, and vice versa. The increase in these responses with deviation in rectal temperature from the “neutral” setting is highly nonlinear; the neutral point and the curve shift to the right and the slope decreases with lowering of skin temperature and vice versa when it is raised. With further deviation of rectal temperature these responses reach maximum values, i.e., become “saturated.” All of these features are analogous to servomechanisms with negative feedback, giving sensitive and stable control. Control of these responses by skin temperature is more linear, characterizing passive control systems which are insensitive and less stable. Quantitatively, the effect at skin temperature of 26 C of 1 C rise in rectal temperature on heat conductance and sweat rate is 10 times greater than the same rise in skin temperature; at a neutral skin temperature of 33–34 C, a rise of 1 C in rectal temperature is 6–7 times greater; at a high skin temperature of 36 C, a rise in rectal temperature of 1 C is 4–5 times greater. relationship between heat conductance and a change in either rectal or skin temperatures; relationship between sweat rate and a change in either rectal or skin temperatures; response characteristics of curves relating heat conductance to change in either rectal or skin temperatures; response characteristics of curves relating sweat rate to change in either rectal or skin temperatures; assessment of the contribution of skin and rectal temperatures to man's temperature regulation Submitted on October 22, 1963


1976 ◽  
Vol 40 (5) ◽  
pp. 653-657 ◽  
Author(s):  
K. A. Smiles ◽  
R. S. Elizondo ◽  
C. C. Barney

A technique is presented for preparing a durable thermode implant in the hypothalamus of the rhesus monkey. In unanesthetized monkeys implanted with thermodes in the anterior hypothalamic area of the brain, a linear relation was found between local sweat rates on the general body surface and clamped hypothalamic temperature. Changes in skin temperature were found to shift the hypothalamic set-point temperature at which sweating began but did not alter the gain of the hypothalamic temperature-sweat rate relationship. This study provides direct support for the concept that central brain temperature and skin temperature interact additively in the control of sweating in higher primates. Due to the very close similarity between these responses and those seen with indirect measurements of brain temperature in men, the rhesus monkey is seen as an excellent experimental analogue for studying human thermoregulation.


1961 ◽  
Vol 157 (2) ◽  
pp. 363-369 ◽  
Author(s):  
D. F. Brebner ◽  
D. McK. Kerslake
Keyword(s):  

1962 ◽  
Vol 17 (1) ◽  
pp. 103-106 ◽  
Author(s):  
H. S. Belding ◽  
B. A. Hertig

Human subjects were transferred between environments imposing different levels of heat stress. Analyses of measurements obtained after a reasonably steady state had been achieved in each of several environments revealed equally good correlation between a) sweat rate and ear temperature (tympanic membrane), and b) sweat rate and calculated deep skin temperature (hypothetical). The correlations are consistent with adjustment of sweating in response to either hypothalamic temperature or temperature of skin receptors or some combination of the two. However, during the first 20 min after transfer, changes in sweat rate and skin temperature occurred together and in the same direction, but were not accompanied by any consistent change in ear temperature. Thus, to the extent that ear temperature represents hypothalamic temperature, an hypothesis of control of sweating based on hypothalamic temperature alone is not tenable. Alternative physiological explanations are given for data developed elsewhere and used in support of an hypothesis of sweat control solely from the hypothalamus. Submitted on August 14, 1961


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