Thermometry, Calorimetry, and Mean Body Temperature during Heat Stress

2013 ◽  
pp. 1689-1719 ◽  
Author(s):  
Glen P. Kenny ◽  
Ollie Jay
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Mean Body Temperature

IMPAIRMENT OF SWEAT SECRETION IN MALNOURISHED INFANTS

PEDIATRICS ◽  
1954 ◽  
Vol 14 (6) ◽  
pp. 659-662
Author(s):  
E. KAHN ◽  
M. D. RAND ◽  
A. R. P. WALKER
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Close Correlation ◽  
Peripheral Circulation ◽  
Sweat Glands ◽  
Severe Malnutrition ◽  
Mean Body Temperature ◽  
Sweat Secretion ◽  
The Mean

Severely malnourished African infants are often feverish during hot summer weather. To elucidate the cause of this phenomenon, malnourished infants and controls were studied under standard conditions of heat stress with regard to sweat secretion and rise of body temperature. There was a marked impairment in the function of the sweat glands in the malnourished infants and the mean body temperature rose higher than that of the controls. The derangement of the sweat secretion was not related to the extent of the nutritional oedema. There was no close correlation between impairment of sweat secretion and rise in body temperature. The possible reasons for these observations are discussed. It is suggested that dysfunction of the sweat glands in severe malnutrition is caused by a poor peripheral circulation.

Mean body temperature does not modulate eccrine sweat rate during upright tilt

2005 ◽  
Vol 98 (4) ◽  
pp. 1207-1212 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Peroneal Nerve ◽  
Sweat Rate ◽  
Control Site ◽  
Body Temperatures ◽  
Mean Body Temperature ◽  
Head Up Tilt ◽  
Treated Site ◽  
Eccrine Sweat

Conflicting reports exist about the role of baroreflexes in efferent control of eccrine sweat rate. These conflicting reports may be due to differing mean body temperatures between studies. The purpose of this project was to test the hypothesis that mean body temperature modulates the effect of head-up tilt on sweat rate and skin sympathetic nerve activity (SSNA). To address this question, mean body temperature (0.9·internal temperature + 0.1·mean skin temperature), SSNA (microneurography of peroneal nerve, n = 8), and sweat rate (from an area innervated by the peroneal nerve and from two forearm sites, one perfused with neostigmine to augment sweating at lower mean body temperatures and the second with the vehicle, n = 12) were measured in 13 subjects during multiple 30° head-up tilts during whole body heating. At the end of the heat stress, mean body temperature (36.8 ± 0.1 to 38.0 ± 0.1°C) and sweat rate at all sites were significantly elevated. No significant correlations were observed between mean body temperature and the change in SSNA during head-up tilt ( r = 0.07; P = 0.62), sweating within the innervated area ( r = 0.06; P = 0.56), sweating at the neostigmine treated site ( r = 0.04; P = 0.69), or sweating at the control site ( r = 0.01; P = 0.94). Also, for each tilt throughout the heat stress, there were no significant differences in sweat rate (final tilt sweat rates were 0.69 ± 0.11 and 0.68 ± 0.11 mg·cm−2·min−1 within the innervated area; 1.04 ± 0.16 and 1.06 ± 0.16 mg·cm−2·min−1 at the neostigmine-treated site; and 0.85 ± 0.15 and 0.85 ± 0.15 mg·cm−2·min−1 at the control site, for supine and tilt, respectively). Hence, these data indicate that mean body temperature does not modulate eccrine sweat rate during baroreceptor unloading induced via 30° head-up tilt.

Heat intolerance as a function of percent of body surface involved with miliaria rubra

1980 ◽  
Vol 239 (3) ◽  
pp. R233-R240 ◽  
Author(s):  
K. B. Pandolf ◽  
T. B. Griffin ◽  
E. H. Munro ◽  
R. F. Goldman
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Body Surface ◽  
Heat Storage ◽  
Sweat Rate ◽  
Skin Surface ◽  
Specific Region ◽  
The Body ◽  
Heat Acclimatization ◽  
Mean Body Temperature

Twenty-four heat-acclimatized male volunteers were wrapped as previously described (Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R226-R232, 1980) but to produce miliaria rubra (heat rash) in specific regions of the body. Three experimental rash groups were involved: 1) the torso (17% total skin surface rashed, n = 6), 2) torso and arms (38%, n = 8), or 3) legs (41%, n = 6), while four subjects served as controls. All subjects were reexposed to walking in the heat on the 7th day after unwrapping, and again 14, 21, and 28 days after unwrapping. When compared to responses for the last heat acclimatization day, tolerance time and sweat rate were lower and mean body temperature and delta heat storage significantly higher for experimental rash subjects contrasted to the controls for up to 21 days; however, no significant differences between the three rashed groups were found. The critical amount of surface area for heat intolerance from heat rash appears to be related to the specific region of the body and associated sweating responses; smaller rashed areas of the trunk, because they have greater potential for abundant sweating, may produce similar responses to heat stress as larger rashed areas of the limbs. Heat intolerance due to rash was not resolved until after 21 days.

Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress

2002 ◽  
Vol 93 (6) ◽  
pp. 1947-1951 ◽  
Author(s):  
Manabu Shibasaki ◽  
Thad E. Wilson ◽  
Jian Cui ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
No Synthase ◽  
The Other ◽  
Whole Body ◽  
Cholinergic Nerves ◽  
Mean Body Temperature ◽  
Cutaneous Vasodilation ◽  
And Control ◽  
Treated Site

Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 μM), the second membrane was perfused with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (l-NAMENeo), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to ∼20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 ± 0.1 to 37.5 ± 0.1°C ( P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 ± 0.1°C, l-NAMENeo: 37.1 ± 0.1°C, control: 36.9 ± 0.1°C), whereas no significant threshold difference was observed between thel-NAMENeo-treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at thel-NAMENeo-treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.

scholarly journals Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Controlled Trial ◽  
Whole Body ◽  
Cord Injury ◽  
Whole Body Heat Stress ◽  
Body Heat

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.

The comparative performance of tropical crossbred and local shorthorn beef cattle on native pasture at Katherine, NT

1967 ◽  
Vol 7 (26) ◽  
pp. 217 ◽  
Author(s):  
MJT Norman
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Peanut Meal ◽  
Average Weight ◽  
Wet Season ◽  
Comparative Performance ◽  
Native Pasture ◽  
Weight Gains ◽  
Adaptation To Heat ◽  
Dressing Percentage

The liveweight performance and carcase characteristics of Brahman x Hereford, Africander x Hereford and Africander x Shorthorn F, crossbred spayed heifers were compared with those of local Shorthorn spayed heifers on native pasture at Katherine, N.T., between 1962 and 1965. The breed groups were divided for planes of winter nutrition, viz., with and without 2 lb a day of peanut meal from early June until the start of the wet season. Without supplement, the average weight gains of B x H, A x H, A x S, and Shorthorn cattle between June 1962 and May 1965 were 0.49, 0.37, 0.36, and 0.23 lb a day respectively. With supplement, cattle reached slaughter weight a year earlier ; the average weight gains of B x H, A x H, and Shorthorn cattle between June 1962 and May 1964 were 0.61, 0.63, and 0.50 lb a day respectively. (There was no A x S supplemented group). Without supplement, the dressing percentage and estimated proportion of fat of B x H cattle was higher and the estimated proportion of muscle and bone lower than those of other breeds. With supplement, there were no significant differences in dressing percentage or carcase composition between breeds. Measurements made of thermoregulatory attributes indicated that the local Shorthorn cattle, through body temperature control, showed adaptation to heat stress.

Differences in body temperature, cell viability, and HSP-70 concentrations between Pelibuey and Suffolk sheep under heat stress

2013 ◽  
Vol 45 (8) ◽  
pp. 1691-1696 ◽  
Author(s):  
Rosita Denny Romero ◽  
Arnulfo Montero Pardo ◽  
Hugo Horacio Montaldo ◽  
Ana Delia Rodríguez ◽  
Joel Hernández Cerón
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Cell Viability ◽  
Hsp 70 ◽  
Suffolk Sheep
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