Light masking of circadian rhythms of heat production, heat loss, and body temperature in squirrel monkeys

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.

1999 ◽  
Vol 276 (5) ◽  
pp. R1397-R1407 ◽  
Author(s):  
Edward L. Robinson ◽  
Charles A. Fuller

Whole body heat production (HP) and heat loss (HL) were examined to determine if the free-running circadian rhythm in body temperature (Tb) results from coordinated changes in HP and HL rhythms in thermoneutrality (27°C) as well as mild cold (17°C). Squirrel monkey metabolism ( n = 6) was monitored by both indirect and direct calorimetry, with telemetered measurement of Tb and activity. Feeding was also measured. Rhythms of HP, HL, and conductance were tightly coupled with the circadian Tb rhythm at both ambient temperatures (TA). At 17°C, increased HP compensated for higher HL at all phases of the Tb rhythm, resulting in only minor changes to Tb. Parallel compensatory changes of HP and HL were seen at all rhythm phases at both TA. Similar time courses of Tb, HP, and HL in their respective rhythms and the relative stability of Tb during both active and rest periods suggest action of the circadian timing system on Tb set point.


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).


2014 ◽  
Vol 39 (7) ◽  
pp. 843-843
Author(s):  
Daniel Gagnon

The current thesis examined whether sex differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrated that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W·°C−1, p = 0.05) during exercise performed at a fixed rate of metabolic heat production. The second study showed that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W·m−2 (496 ± 139 vs. 483 ± 185 W·m−2·°C−1, p = 0.91) and 300 W·m−2 (283 ± 70 vs. 211 ± 66 W·m−2·°C−1, p = 0.17), only becoming greater in males at a requirement for heat loss of 350 W·m−2 (197 ± 61 vs. 82 ± 27 W·m−2·°C−1, p = 0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg·min−1·cm−2, p = 0.02) and methacholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg·min−1·cm−2, p = 0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.


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.


2008 ◽  
Vol 294 (5) ◽  
pp. R1586-R1592 ◽  
Author(s):  
Ollie Jay ◽  
Daniel Gagnon ◽  
Michel B. DuCharme ◽  
Paul Webb ◽  
Francis D. Reardon ◽  
...  

Previous studies report greater postexercise heat loss responses during active recovery relative to inactive recovery despite similar core temperatures between conditions. Differences have been ascribed to nonthermal factors influencing heat loss response control since elevations in metabolism during active recovery are assumed to be insufficient to change core temperature and modify heat loss responses. However, from a heat balance perspective, different rates of total heat loss with corresponding rates of metabolism are possible at any core temperature. Seven male volunteers cycled at 75% of V̇o2peak in the Snellen whole body air calorimeter regulated at 25.0°C, 30% relative humidity (RH), for 15 min followed by 30 min of active (AR) or inactive (IR) recovery. Relative to IR, a greater rate of metabolic heat production (Ṁ − Ẇ) during AR was paralleled by a greater rate of total heat loss (ḢL) and a greater local sweat rate, despite similar esophageal temperatures between conditions. At end-recovery, rate of body heat storage, that is, [(Ṁ − Ẇ) − ḢL] approached zero similarly in both conditions, with Ṁ − Ẇ and ḢL elevated during AR by 91 ± 26 W and 93 ± 25 W, respectively. Despite a higher Ṁ − Ẇ during AR, change in body heat content from calorimetry was similar between conditions due to a slower relative decrease in ḢL during AR, suggesting an influence of nonthermal factors. In conclusion, different levels of heat loss are possible at similar core temperatures during recovery modes of different metabolic rates. Evidence for nonthermal influences upon heat loss responses must therefore be sought after accounting for differences in heat production.


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).


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 < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P < .001) and 5 mm Hg (F6,24 = 5.4, P < .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F1,12 = 44.7, P < .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.


PEDIATRICS ◽  
1979 ◽  
Vol 63 (6) ◽  
pp. 926-928

Pediatricians may be able to bring the dangers of accidental hypothermia to the attention of their patients at the time of a sports, camp, or college "physical." People who spend time outdoors must learn to recognize hypothermia-producing weather and water; to know that shivering indicates heat loss exceeding available insulation and body heat production; and to understand that loss of good judgment and hand coordination soon follow uncontrollable shivering. They must not go into areas in which, without proper gear, unfavorable weather conditions or dangerous water may develop, and they must understand that most tragedies from cold result from failure to make camp or to return to safety when weather conditions become unfavorable.


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