Effect of heating rate on evaporative heat loss in the microwave-exposed mouse

1982 ◽  
Vol 53 (2) ◽  
pp. 316-323 ◽  
Author(s):  
C. J. Gordon

Male CBA/J mice were administered heat loads of 0–28 J X g-1 at specific absorption rates (SARs) of either 47 or 93 W X kg-1 by exposure to 2,450-MHz microwave radiation at an ambient temperature of 30 degrees C while evaporative heat loss (EHL) was continuously monitored with dew-point hygrometry. At an SAR of 47 W X kg-1 a threshold heat load of 10.5 J X g-1 had to be exceeded before EHL increased. An approximate doubling of SAR to 93 W X kg-1 reduced the threshold to 5.2 J X g-1. Above threshold the slopes of the regression lines were 1.15 and 0.929 for the low- and high-SAR groups, respectively. Thus the difference in threshold and not slope attributes to the significant increase in EHL when mice are exposed at a high SAR (P less than 0.02). In separate experiments a SAR of 47 W X kg-1 raised the deep body temperature of anesthetized mice at a rate of 0.026 degrees C X s-1, whereas 93 W X kg-1 raised temperature at 0.049 degrees C X s-1. Hence the sensitivity of the EHL mode of heat dissipation is directly proportional to the rate of heat absorption and to the rate of rise in body temperature. These data contradict the notion that mammals have control over whole-body heat exchange only (i.e., thermoregulation) but instead indicate that the EHL system is highly responsive to the rate of heat absorption (i.e., temperature regulation).

1999 ◽  
Vol 276 (2) ◽  
pp. R298-R307 ◽  
Author(s):  
Edward L. Robinson ◽  
Charles A. Fuller

Whole body heat production (HP) and heat loss (HL) were examined to determine their relative contributions to light masking of the circadian rhythm in body temperature (Tb). Squirrel monkey metabolism ( n = 6) was monitored by both indirect and direct calorimetry, with telemetered measurement of body temperature and activity. Feeding was also measured. Responses to an entraining light-dark (LD) cycle (LD 12:12) and a masking LD cycle (LD 2:2) were compared. HP and HL contributed to both the daily rhythm and the masking changes in Tb. All variables showed phase-dependent masking responses. Masking transients at L or D transitions were generally greater during subjective day; however, L masking resulted in sustained elevation of Tb, HP, and HL during subjective night. Parallel, apparently compensatory, changes of HL and HP suggest action by both the circadian timing system and light masking on Tb set point. Furthermore, transient HL increases during subjective night suggest that gain change may supplement set point regulation of Tb.


2020 ◽  
Vol 319 (2) ◽  
pp. E438-E446
Author(s):  
Vojtěch Škop ◽  
Naili Liu ◽  
Juen Guo ◽  
Oksana Gavrilova ◽  
Marc L. Reitman

Understanding mouse thermal physiology informs the usefulness of mice as models of human disease. It is widely assumed that the mouse tail contributes greatly to heat loss (as it does in rat), but this has not been quantitated. We studied C57BL/6J mice after tail amputation. Tailless mice housed at 22°C did not differ from littermate controls in body weight, lean or fat content, or energy expenditure. With acute changes in ambient temperature from 19 to 39°C, tailless and control mice demonstrated similar body temperatures (Tb), metabolic rates, and heat conductances and no difference in thermoneutral point. Treatment with prazosin, an α1-adrenergic antagonist and vasodilator, increased tail temperature in control mice by up to 4.8 ± 0.8°C. Comparing prazosin treatment in tailless and control mice suggested that the tail’s contribution to total heat loss was a nonsignificant 3.4%. Major heat stress produced by treatment at 30°C with CL316243, a β3-adrenergic agonist, increased metabolic rate and Tb and, at a matched increase in metabolic rate, the tailless mice showed a 0.72 ± 0.14°C greater Tb increase and 7.6% lower whole body heat conductance. Thus, the mouse tail is a useful biomarker of vasodilation and thermoregulation, but in our experiments contributes only 5–8% of whole body heat dissipation, less than the 17% reported for rat. Heat dissipation through the tail is important under extreme scenarios such as pharmacological activation of brown adipose tissue; however, non-tail contributions to heat loss may have been underestimated in the mouse.


2013 ◽  
Vol 305 (6) ◽  
pp. R619-R629 ◽  
Author(s):  
Joanie Larose ◽  
Heather E. Wright ◽  
Jill Stapleton ◽  
Ronald J. Sigal ◽  
Pierre Boulay ◽  
...  

Studies in young adults show that a greater proportion of heat is gained shortly following the start of exercise and that temporal changes in whole body heat loss during intermittent exercise have a pronounced effect on body heat storage. The consequences of short-duration intermittent exercise on heat storage with aging are unclear. We compared evaporative heat loss (H E) and changes in body heat content (ΔHb) between young (20–30 yr), middle-aged (40–45 yr), and older males (60–70 yr) of similar body mass and surface area, during successive exercise (4 × 15 min) and recovery periods (4 × 15 min) at a fixed rate of heat production (400 W) and under fixed environmental conditions (35°C/20% relative humidity). H E was lower in older males vs. young males during each exercise (Ex1: 283 ± 10 vs. 332 ± 11 kJ, Ex2: 334 ± 10 vs. 379 ± 5 kJ, Ex3: 347 ± 11 vs. 392 ± 5 kJ, and Ex4: 347 ± 10 vs. 387 ± 5 kJ, all P < 0.02), whereas H E in middle-aged males was intermediate to that measured in young and older adults (Ex1: 314 ± 13, Ex2: 355 ± 13, Ex3: 371 ± 13, and Ex4: 365 ± 8 kJ). H E was not significantly different between groups during the recovery periods. The net effect over 2 h was a greater ΔHb in older (267 ± 33 kJ; P = 0.016) and middle-aged adults (245 ± 16 kJ; P = 0.073) relative to younger counterparts (164 ± 20 kJ). As a result of a reduced capacity to dissipate heat during exercise, which was not compensated by a sufficiently greater rate of heat loss during recovery, both older and middle-aged males had a progressively greater rate of heat storage compared with young males over 2 h of intermittent exercise.


2011 ◽  
Vol 300 (4) ◽  
pp. R958-R968 ◽  
Author(s):  
Daniel Gagnon ◽  
Glen P. Kenny

Previous studies have suggested that greater core temperatures during intermittent exercise (Ex) are due to attenuated sweating [upper back sweat rate (SR)] and skin blood flow (SkBF) responses. We evaluated the hypothesis that heat loss is not altered during exercise-rest cycles (ER). Ten male participants randomly performed four 120-min trials: 1) 60-min Ex and 60-min recovery (60ER); 2) 3 × 20-min Ex separated by 20-min recoveries (20ER); 3) 6 × 10-min Ex separated by 10-min recoveries (10ER), or 4) 12 × 5-min Ex separated by 5-min recoveries (5ER). Exercise was performed at a workload of 130 W at 35°C. Whole body heat exchange was determined by direct calorimetry. Core temperature, SR (by ventilated capsule), and SkBF (by laser-doppler) were measured continuously. Evaporative heat loss (EHL) progressively increased with each ER, such that it was significantly greater ( P ≤ 0.05) at the end of the last compared with the first Ex for 5ER (299 ± 39 vs. 440 ± 41 W), 10ER (425 ± 51 vs. 519 ± 45 W), and 20ER (515 ± 63 vs. 575 ± 74 W). The slope of the EHL response against esophageal temperature significantly increased from the first to the last Ex within the 10ER (376 ± 56 vs. 445 ± 89 W/°C, P ≤ 0.05) and 20ER (535 ± 85 vs. 588 ± 28 W/°C, P ≤ 0.05) conditions, but not during 5ER (296 ± 96 W/°C vs. 278 ± 95 W/°C, P = 0.237). In contrast, the slope of the SkBF response against esophageal temperature did not significantly change from the first to the last Ex (5ER: 51 ± 23 vs. 54 ± 19%/°C, P = 0.848; 10ER: 53 ± 8 vs. 56 ± 21%/°C, P = 0.786; 20ER: 44 ± 20 vs. 50 ± 27%/°C, P = 0.432). Overall, no differences in body heat content and core temperature were observed. These results suggest that altered local and whole body heat loss responses do not explain the previously observed greater core temperatures during intermittent exercise.


2019 ◽  
Vol 44 (3) ◽  
pp. 332-335 ◽  
Author(s):  
Andrew W. D’Souza ◽  
Sean R. Notley ◽  
Erin K. Brown ◽  
Martin P. Poirier ◽  
Glen P. Kenny

Using direct calorimetry, we determined if the Hexoskin shirt (Carré Technologies Inc., Que., Canada), a wearable device for monitoring physiological strain, would compromise whole-body heat loss and exacerbate body heat storage during moderate-intensity activity in hot-dry conditions. The shirt did not impair heat dissipation and resulted in similar body heat storage when worn alone relative to a semi-nude condition (214 vs. 211 kJ) or when worn underneath a work uniform compared with a cotton undershirt (307 vs. 318 kJ).


1983 ◽  
Vol 244 (6) ◽  
pp. R778-R784
Author(s):  
C. J. Gordon

Although heating rate is important for stimulating thermoregulatory reflexes, it is not known if the control system differentiates between total heat gain and rate of heat gain. Exposing animals to microwaves inside a waveguide permits continuous monitoring of whole-body heat absorption. Tail skin temperature of restrained mice was recorded during whole-body exposure to 2,450-MHz microwave radiation at specific absorption rates (SAR) of either 11.5, 21.7, or 43.5 W . kg-1 and whole-body heat loads of 0.3-14 J . g-1. The integration of tail skin temperature with time, defined as the skin temperature index (STI), was measured as a function of absorbed heat load. At ambient temperatures of 20 and 25 degrees C the STI, averaged with respect to heat load, increased significantly with SAR. Depending on SAR, the sensitivity of heat loss from the tail to microwave exposure increased 32-71% per 1 degree C elevation in ambient temperature. The data indicate that heat loss from the tail increases with the whole-body heat load accrued from microwave exposure. When heat loss is averaged with respect to heat load, the rate of heat absorption and ambient temperature increase the sensitivity of thermoregulatory centers that control peripheral heat loss from the tail of mice.


2014 ◽  
Vol 39 (3) ◽  
pp. 292-298 ◽  
Author(s):  
Jill M. Stapleton ◽  
Joanie Larose ◽  
Christina Simpson ◽  
Andreas D. Flouris ◽  
Ronald J. Sigal ◽  
...  

Heat waves are the cause of many preventable deaths around the world, especially among older adults and in countries with more temperate climates. In the present study, we examined the effects of age on whole-body heat loss and heat storage during passive exposure to environmental conditions representative of the upper temperature extremes experienced in Canada. Direct and indirect calorimetry measured whole-body evaporative heat loss and dry heat exchange, as well as the change in body heat content. Twelve younger (21 ± 3 years) and 12 older (65 ± 5 years) adults with similar body weight (younger: 72.0 ± 4.4 kg; older: 80.1 ± 4.2 kg) and body surface area (younger: 1.8 ± 0.1 m2; older: 2.0 ± 0.1 m2) rested for 2 h in a hot–dry [36.5 °C, 20% relative humidity (RH)] or hot–humid (36.5 °C, 60% RH) environment. In both conditions, evaporative heat loss was not significantly different between groups (dry: p = 0.758; humid: p = 0.814). However, the rate of dry heat gain was significantly greater (by approx. 10 W) for older adults relative to younger adults during the hot–dry (p = 0.032) and hot–humid exposure (p = 0.019). Consequently, the cumulative change in body heat content after 2 h of rest was significantly greater in older adults in the hot–dry (older: 212 ± 25 kJ; younger: 131 ± 27 kJ, p = 0.018) as well as the hot–humid condition (older: 426 ± 37 kJ; younger: 317 ± 45 kJ, p = 0.037). These findings demonstrate that older individuals store more heat during short exposures to dry and humid heat, suggesting that they may experience increased levels of thermal strain in such conditions than people of younger age.


2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P &lt; .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P &lt; .001) and 5 mm Hg (F6,24 = 5.4, P &lt; .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P &lt; .001) increased in the plasma (58% and 285%, respectively) (P &lt; .05). The HSP72 (F1,12 = 44.7, P &lt; .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.


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