Статті в журналах: "Whole body heat"

1

Pretorius, Thea, Gerald K. Bristow, Alan M. Steinman, and Gordon G. Giesbrecht. "Thermal effects of whole head submersion in cold water on nonshivering humans." Journal of Applied Physiology 101, no. 2 (August 2006): 669–75. http://dx.doi.org/10.1152/japplphysiol.01241.2005.

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This study isolated the effect of whole head submersion in cold water, on surface heat loss and body core cooling, when the confounding effect of shivering heat production was pharmacologically eliminated. Eight healthy male subjects were studied in 17°C water under four conditions: the body was either insulated or uninsulated, with the head either above the water or completely submersed in each body-insulation subcondition. Shivering was abolished with buspirone (30 mg) and meperidine (2.5 mg/kg), and subjects breathed compressed air throughout all trials. Over the first 30 min of immersion, exposure of the head increased core cooling both in the body-insulated conditions (head out: 0.47 ± 0.2°C, head in: 0.77 ± 0.2°C; P < 0.05) and the body-exposed conditions (head out: 0.84 ± 0.2°C and head in: 1.17 ± 0.5°C; P < 0.02). Submersion of the head (7% of the body surface area) in the body-exposed conditions increased total heat loss by only 10%. In both body-exposed and body-insulated conditions, head submersion increased core cooling rate much more (average of 42%) than it increased total heat loss. This may be explained by a redistribution of blood flow in response to stimulation of thermosensitive and/or trigeminal receptors in the scalp, neck and face, where a given amount of heat loss would have a greater cooling effect on a smaller perfused body mass. In 17°C water, the head does not contribute relatively more than the rest of the body to surface heat loss; however, a cold-induced reduction of perfused body mass may allow this small increase in heat loss to cause a relatively larger cooling of the body core.

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2

POIRIER, MARTIN P., DANIEL GAGNON, BRIAN J. FRIESEN, STEPHEN G. HARDCASTLE, and GLEN P. KENNY. "Whole-Body Heat Exchange during Heat Acclimation and Its Decay." Medicine & Science in Sports & Exercise 47, no. 2 (February 2015): 390–400. http://dx.doi.org/10.1249/mss.0000000000000401.

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3

Brothers, R. Matthew, Paul S. Bhella, Shigeki Shibata, Jonathan E. Wingo, Benjamin D. Levine, and Craig G. Crandall. "Cardiac systolic and diastolic function during whole body heat stress." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (April 2009): H1150—H1156. http://dx.doi.org/10.1152/ajpheart.01069.2008.

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During a whole body heat stress, stroke volume is either maintained or slightly elevated despite reduced ventricular filling pressures and central blood volume, suggestive of improved cardiac diastolic and/or systolic function. Heat stress improves cardiac systolic and diastolic function in patients with congestive heart failure, although it remains unknown whether similar responses occur in healthy individuals, which is the hypothesis to be tested. Nine male volunteers underwent a whole body heat stress. Echocardiographic indexes of diastolic and systolic function were performed following a supine resting period, and again following an increase in internal temperature of ∼1.0°C via passive heat stress. Despite previous reports of heat stress-induced decreases in ventricular filling pressures and central blood volume, no changes in indexes of diastolic function were identified during heating [i.e., unchanged early diastolic mitral annular tissue velocity (E′), mitral inflow during the early diastolic phase (E), the E/E′ ratio, and isovolumetric relaxation time]. Heat stress increased late diastolic septal ( P = 0.03) and lateral ( P = 0.01) mitral annular tissue velocities (A′), mitral inflow velocity during atrial contraction ( P < 0.001), and the relative contribution of atrial contraction to left ventricular filling during diastole ( P = 0.01), all indicative of improved atrial systolic function. Furthermore, indexes of ventricular systolic function were increased by heat stress [i.e., increased septal ( P = 0.001) and lateral ( P = 0.01) mitral annular systolic velocities and isovolumic acceleration at the septal ( P = 0.03) and lateral ( P < 0.001) mitral annulus]. These data are suggestive of improved atrial and ventricular systolic function by the heat stress. Together these data support previous findings, which used the less precise measure of ejection fraction, that heat stress improves indexes of systolic function, while diastolic function is maintained.

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4

Low, David A., David M. Keller, Jonathan E. Wingo, R. Matthew Brothers, and Craig G. Crandall. "Sympathetic nerve activity and whole body heat stress in humans." Journal of Applied Physiology 111, no. 5 (November 2011): 1329–34. http://dx.doi.org/10.1152/japplphysiol.00498.2011.

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We and others have shown that moderate passive whole body heating (i.e., increased internal temperature ∼0.7°C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature ∼1.3°C, while either MSNA ( n = 8) or SSNA ( n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Δ∼5°C, P < 0.001), internal temperature (Δ∼1.3°C, P < 0.001), mean body temperature (Δ∼2.0°C, P < 0.001), heart rate (Δ∼40 beats/min, P < 0.001), and cutaneous vascular conductance [Δ∼1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained ( P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Δ core temperature 0.63 ± 0.01°C) when expressed as burst frequency (26 ± 14 to 45 ± 16 bursts/min, P = 0.001), burst incidence (39 ± 13 to 48 ± 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 ± 170 to 489 ± 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 ± 15 bursts/min, P = 0.01; burst incidence: 56 ± 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 ± 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 ± 472 to mid heat stress 6,467 ± 5,256 units/min, P = 0.03) and continued to increase until the end of heat stress (11,217 ± 6,684 units/min, P = 0.002 vs. mid-heat stress). These results indicate that both MSNA and SSNA continue to increase as internal temperature is elevated above previously reported values.

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5

Cui, Jian, Cheryl Blaha, and Lawrence I. Sinoway. "Whole body heat stress attenuates the pressure response to muscle metaboreceptor stimulation in humans." Journal of Applied Physiology 121, no. 5 (November 1, 2016): 1178–86. http://dx.doi.org/10.1152/japplphysiol.00212.2016.

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The effects of whole body heat stress on sympathetic and cardiovascular responses to stimulation of muscle metaboreceptors and mechanoreceptors remains unclear. We examined the muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate in 14 young healthy subjects during fatiguing isometric handgrip exercise, postexercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed under normothermic and whole body heat stress (increase internal temperature ~0.6°C via a heating suit) conditions. Heat stress increased the resting MSNA and heart rate. Heat stress did not alter the mean blood pressure (MAP), heart rate, and MSNA responses (i.e., changes) to fatiguing exercise. During PECO, whole body heat stress accentuated the heart rate response [change (Δ) of 5.8 ± 1.5 to Δ10.0 ± 2.1 beats/min, P = 0.03], did not alter the MSNA response (Δ16.4 ± 2.8 to Δ17.3 ± 3.8 bursts/min, P = 0.74), and lowered the MAP response (Δ20 ± 2 to Δ12 ± 1 mmHg, P < 0.001). Under normothermic conditions, passive stretch during PECO evoked significant increases in MAP and MSNA (both P < 0.001). Of note, heat stress prevented the MAP and MSNA responses to stretch during PECO (both P > 0.05). These data suggest that whole body heat stress attenuates the pressor response due to metaboreceptor stimulation, and the sympathetic nerve response due to mechanoreceptor stimulation.

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6

Kimball, Amy L., and Richard K. Shields. "Whole Body Heat Exposure Modulates Acute Glucose Homeostasis." Medicine & Science in Sports & Exercise 46 (May 2014): 549. http://dx.doi.org/10.1249/01.mss.0000495112.06143.87.

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7

Low, David A., David M. Keller, Jonathan E. Wingo, R. Matthew Brothers, and Craig G. Crandall. "Sympathetic Nerve Activity and Whole-Body Heat Stress." Medicine & Science in Sports & Exercise 40, Supplement (May 2008): S334. http://dx.doi.org/10.1249/01.mss.0000323337.69719.54.

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8

Kimball, Amy L., Patrick M. McCue, Michael A. Petrie, and Richard K. Shields. "Whole body heat exposure modulates acute glucose metabolism." International Journal of Hyperthermia 35, no. 1 (October 10, 2018): 644–51. http://dx.doi.org/10.1080/02656736.2018.1516303.

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9

Kinsht, D. N. "Modeling of heat transfer in whole-body hyperthermia." Biophysics 51, no. 4 (August 2006): 659–63. http://dx.doi.org/10.1134/s0006350906040221.

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10

Hall, David M., Garry R. Buettner, Larry W. Oberley, Linjing Xu, Ronald D. Matthes, and Carl V. Gisolfi. "Mechanisms of circulatory and intestinal barrier dysfunction during whole body hyperthermia." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H509—H521. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h509.

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This work tested the hypotheses that splanchnic oxidant generation is important in determining heat tolerance and that inappropriate ·NO production may be involved in circulatory dysfunction with heat stroke. We monitored colonic temperature (Tc), heart rate, mean arterial pressure, and splanchnic blood flow (SBF) in anesthetized rats exposed to 40°C ambient temperature. Heating rate, heating time, and thermal load determined heat tolerance. Portal blood was regularly collected for determination of radical and endotoxin content. Elevating Tc from 37 to 41.5°C reduced SBF by 40% and stimulated production of the radicals ceruloplasmin, semiquinone, and penta-coordinate iron(II) nitrosyl-heme (heme-·NO). Portal endotoxin concentration rose from 28 to 59 pg/ml ( P < 0.05). Compared with heat stress alone, heat plus treatment with the nitric oxide synthase (NOS) antagonist N ω-nitro-l-arginine methyl ester (l-NAME) dose dependently depressed heme-·NO production and increased ceruloplasmin and semiquinone levels. l-NAME also significantly reduced lowered SBF, increased portal endotoxin concentration, and reduced heat tolerance ( P < 0.05). The NOS II and diamine oxidase antagonist aminoguanidine, the superoxide anion scavenger superoxide dismutase, and the xanthine oxidase antagonist allopurinol slowed the rates of heme-·NO production, decreased ceruloplasmin and semiquinone levels, and preserved SBF. However, only aminoguanidine and allopurinol improved heat tolerance, and only allpourinol eliminated the rise in portal endotoxin content. We conclude that hyperthermia stimulates xanthine oxidase production of reactive oxygen species that activate metals and limit heat tolerance by promoting circulatory and intestinal barrier dysfunction. In addition, intact NOS activity is required for normal stress tolerance, whereas overproduction of ·NO may contribute to the nonprogrammed splanchnic dilation that precedes vascular collapse with heat stroke.

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11

Hall, David M., Kirk R. Baumgardner, Terry D. Oberley, and Carl V. Gisolfi. "Splanchnic tissues undergo hypoxic stress during whole body hyperthermia." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (May 1, 1999): G1195—G1203. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1195.

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Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O2saturation, splanchnic arterial-venous O2difference, and venous[Formula: see text], while decreasing venous O2saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased ∼20%. Two hours after heat exposure, the splanchnic arterial-venous O2difference remained elevated in heat-stressed animals despite normal Tc. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [3H]misonidazole. Liver and intestine were biopsied, and [3H]misonidazole content was quantified. Heat stress increased tissue [3H]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [3H]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.

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12

Vertrees, Roger A., Angela Leeth, Mark Girouard, John D. Roach, and Joseph B. Zwischenberger. "Whole-body hyperthermia: a review of theory, design and application." Perfusion 17, no. 4 (July 2002): 279–90. http://dx.doi.org/10.1191/0267659102pf588oa.

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The intentional induction of elevated body temperature to treat malignant lesions has its origins in the 18th century. The mechanism of heat-induced cell death is not clear; however, heat induces a variety of cellular changes. For heat to exert a therapeutic effect, pathogens (bacteria, viruses, or neoplastic tissues) need to be susceptible within temperature ranges that do not exert deleterious effects on normal tissues. Hyperthermia has been used successfully to treat isolated neoplastic lesions of the head and neck, regional tumors such as melanoma of the limb, and is under investigation as either an adjunct to, or therapy for, locally disseminated and systemic diseases. The clinical utility of perfusion hyperthermia has evolved into three approaches -isolated organ or limb, tumorous invasion of a cavity, and systemic or metastatic spread. When whole-body hyperthermic treatment has been tried, it has been induced in the patient by submersion in hot wax or liquid, wrapping in plastic, encasement in a high-flow water perfusion suit, or by extracorporeal perfusion. Our group has developed an extracorporeal method, veno-venous perfusion-induced systemic hyperthermia, that was used first to safely heat swine homogenously to an average body temperature of 43°C for 2 h. More recently, a Phase I clinical trial has been completed in which all patients were safely heated to 42 or 42.5°C for 2 h and survived the 30-day study period. We have been sufficiently encouraged by these results and are continuing to develop this technology.

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13

Zagorski, Nick. "Whole-Body Heat Shows Potential in Treating Depressive Symptoms." Psychiatric News 51, no. 13 (July 2016): 1. http://dx.doi.org/10.1176/appi.pn.2016.6b16.

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14

Lou, Zheng, and Wen-Jei Yang. "Whole body heat balance during the human thoracic hyperthermia." Medical & Biological Engineering & Computing 28, no. 2 (March 1990): 171–81. http://dx.doi.org/10.1007/bf02441774.

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15

Cui, Jian, Manabu Shibasaki, Scott L. Davis, David A. Low, David M. Keller, and Craig G. Crandall. "Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia." Journal of Applied Physiology 106, no. 4 (April 2009): 1125–31. http://dx.doi.org/10.1152/japplphysiol.00135.2008.

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Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature ∼ 0.7°C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (−4.34 ± 0.40 to −3.57 ± 0.31 units·beat−1·mmHg−1, respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating ( P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation.

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16

Ponikowska, Irena, Henryk Mikołaj Kozłowski, Przemysław Adamczyk, and Sylwia Wrotek. "Whole Body Hyperthermotherapy – Application in Medicine." Acta Balneologica 61, no. 4 (2019): 269–73. http://dx.doi.org/10.36740/abal201904108.

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This article is devoted to the use of a thermal factor in procedures called systemic hypertermotherapy. Different methods leading to increase in body temperature have been presented. The course of various therapies based on outside heat is described. A short review of the therapeutic effects of overheating has been made. In addition, both indications for using this type of treatment were given and attention was paid to existing contraindications. The facts cited in the article indicate that systemic hyperthermotherapy may be a perfect complement to the treatment procedures of patients suffering from diseases such as hypertension, depression, fibromyalgia, rheumatological and cancer diseases and others.

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17

Devarakonda, Surendra Balaji, Pallavi Bulusu, Marwan Al-rjoub, Amit Bhattacharya, and Rupak Kumar Banerjee. "Influence of external head cooling on the head, core body and blood temperatures using 3D whole-body model." International Journal of Numerical Methods for Heat & Fluid Flow 28, no. 10 (October 1, 2018): 2491–504. http://dx.doi.org/10.1108/hff-11-2017-0442.

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Purpose The purpose of this study is to evaluate the impact of external head cooling on alleviating the heat stress in the human body by analyzing the temperatures of the core body (Tc), blood (Tblood) and head (Th) during exercise conditions using 3D whole body model. Design/methodology/approach Computational study is conducted to comprehend the influence of external head cooling on Tc, Tblood and Th. The Pennes bioheat and energy balance equations formulated for the whole-body model are solved concurrently to obtain Tc, Tblood and Th for external head cooling values from 33 to 233 W/m2. Increased external head cooling of 404 W/m2 is used to compare the numerical and experimental Th data. Findings Significant reductions of 0.21°C and 0.38°C are observed in Th with external head cooling of 233 and 404 W/m2, respectively. However, for external head cooling of 233 W/m2, lesser reductions of 0.03°C and 0.06°C are found in Tc and Tblood, respectively. Computational results for external head cooling of 404 W/m2 show a difference of 15 per cent in Th compared to experimental values from literature. Originality/value The development of stress because of heat generated within human body is major concern for athletes exercising at high intensities. This study provides an insight into the effectiveness of external head cooling in regulating the head and body temperatures during exercise conditions.

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18

Lee, D. T., and E. M. Haymes. "Exercise duration and thermoregulatory responses after whole body precooling." Journal of Applied Physiology 79, no. 6 (December 1, 1995): 1971–76. http://dx.doi.org/10.1152/jappl.1995.79.6.1971.

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Whole body precooling was hypothesized to reduce thermoregulatory and metabolic responses, thereby enhancing running time. Fourteen male runners completed two high-intensity running tests consisting of resting in 24 degrees C (normothermic condition; NC) or 5 degrees C (hypothermic condition; HC) for 30 min followed by 10–16 min of rest at 24 degrees C and then an exercise bout (24 degrees C) at 82% maximal aerobic capacity to exhaustion. Rectal temperature (Tre) before exercise was lower (by 0.37 degrees C; P < 0.005) and exercise duration was longer (by 121 +/- 24%; P < 0.05) in HC than in NC. Tre and mean skin (Tsk) and mean body (Tb) temperatures remained lower during HC (P < 0.01). Pre- and postexercise changes for Tsk, Tb, thermal gradient (Tre-Tsk), and heart rate (HR) were larger in HC than in NC (P < 0.05). Final Tre, Tre-Tsk, HR, and blood lactate were similar between HC and NC. During exercise, heat storage was greater (P < 0.01) in HC than in NC (173 +/- 46 and 143 +/- 38 W/m2, respectively) and subjects sweated more in NC than in HC (P < 0.01). O2 consumption was lower initially in HC than in NC (P < 0.05), but O2 pulse was not different. It was concluded that precooling results in greater exercise endurance with enhanced heat storage rate and less stress on metabolic and cardiovascular systems.

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19

Wilson, Thad E., Jian Cui, Rong Zhang, and Craig G. Crandall. "Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (November 2006): R1443—R1448. http://dx.doi.org/10.1152/ajpregu.00712.2005.

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Orthostatic tolerance is reduced in the heat-stressed human. This study tested the following hypotheses: 1) whole body heat stress reduces cerebral blood velocity (CBV) and increases cerebral vascular resistance (CVR); and 2) reductions in CBV and increases in CVR in response to an orthostatic challenge will be greater while subjects are heat stressed. Fifteen subjects were instrumented for measurements of CBV (transcranial ultrasonography), mean arterial blood pressure (MAP), heart rate, and internal temperature. Whole body heating increased both internal temperature (36.4 ± 0.1 to 37.3 ± 0.1° C) and heart rate (59 ± 3 to 90 ± 3 beats/min); P < 0.001. Whole body heating also reduced CBV (62 ± 3 to 53 ± 2 cm/s) primarily via an elevation in CVR (1.35 ± 0.06 to 1.63 ± 0.07 mmHg · cm−1 · s); P < 0.001. A subset of subjects ( n = 8) were exposed to lower-body negative pressure (LBNP 10, 20, 30, 40 mmHg) in both normothermic and heat-stressed conditions. During normothermia, LBNP of 30 mmHg (highest level of LBNP achieved by the majority of subjects in both thermal conditions) did not significantly alter CBV, CVR, or MAP. During whole body heating, this LBNP decreased MAP (81 ± 2 to 75 ± 3 mmHg), decreased CBV (50 ± 4 to 39 ± 1 cm/s), and increased CVR (1.67 ± 0.17 to 1.92 ± 0.12 mmHg · cm−1 · s); P < 0.05. These data indicate that heat stress decreases CBV, and the reduction in CBV for a given orthostatic challenge is greater during heat stress. These outcomes reduce the reserve to buffer further decreases in cerebral perfusion before presyncope. Increases in CVR during whole body heating, coupled with even greater increases in CVR during orthostasis and heat stress, likely contribute to orthostatic intolerance.

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20

Broderick, Tom L. "Whole-body heat shock protects the ischemic rat heart by stimulating mitochondria respiration." Canadian Journal of Physiology and Pharmacology 84, no. 8-9 (September 2006): 929–33. http://dx.doi.org/10.1139/y06-039.

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Whole-body heat shock (HS) leads to an enhancement of postischemic mechanical function and an improvement in glucose use by the rat heart. Here, we examine the effect of HS on isolated mitochondrial metabolism during reperfusion in the working rat heart. Rats were anesthetized, and their body temperature was raised to 41–42 °C for 15 min. Control rats were treated the same way but were not exposed to hyperthermia. Twenty-fours after HS or sham treatment, rats were reanesthetized and the hearts were removed for perfusion with Krebs–Henseleit buffer, containing 11 mmol glucose/L and 1.2 mmol palmitate/L prebound to 3% albumin. Hearts were subjected to 25 min of global ischemia followed by 30 min of reperfusion. At the end of reperfusion, heart mitochondria were isolated using differential centrifugation and respiration measured in the presence of pyruvate, glutamate, or palmitoylcarnitine. Hearts subjected to HS showed an enhanced recovery of function, expressed as aortic flow, during the reperfusion period, compared with sham hearts. This improved functional status was associated with a significant increase in state 3 respiration in the presence of pyruvate, glutamate, or palmitoylcarnitine. These results show that HS offers protection against ischemic damage, and that a possible mechanism might be the enhanced myocardial metabolism of fuels.

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White, Andrea T., Scott L. Davis, and Thad E. Wilson. "Metabolic, thermoregulatory, and perceptual responses during exercise after lower vs. whole body precooling." Journal of Applied Physiology 94, no. 3 (March 1, 2003): 1039–44. http://dx.doi.org/10.1152/japplphysiol.00720.2002.

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The purpose of this investigation was to compare the thermoregulatory, metabolic, and perceptual effects of lower body (LBI) and whole body (WBI) immersion precooling techniques during submaximal exercise. Eleven healthy men completed two 30-min cycling bouts at 60% of maximal O2uptake preceded by immersion to the suprailiac crest (LBI) or clavicle (WBI) in 20°C water. WBI produced significantly lower rectal temperature (Tre) during minutes 24–30 of immersion and lower Tre, mean skin temperature, and mean body temperature for the first 24, 14, and 16 min of exercise, respectively. Body heat storage rates differed significantly for LBI and WBI during immersion and exercise, although no net differences were observed between conditions. For WBI, metabolic heat production and heart rate were significantly higher during immersion but not during exercise. Thermal sensation was significantly lower (felt colder) and thermal discomfort was significantly higher (less comfortable) for WBI during immersion and exercise. In conclusion, WBI and LBI attenuated Tre increases during submaximal exercise and produced similar net heat storage over the protocol. LBI minimized metabolic increases and negative perceptual effects associated with WBI.

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22

Robins, H. Ian, J. Paul Woods, Cynthia L. Schmitt, and Justin D. Cohen. "A new technological approach to radiant heat whole body hyperthermia." Cancer Letters 79, no. 2 (May 1994): 137–45. http://dx.doi.org/10.1016/0304-3835(94)90252-6.

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23

Sekiguchi, Yasuki, Courteney L. Benjamin, Elaine C. Lee, Jeb F. Struder, Ciara N. Manning, Margaret C. Morrissey, Michael R. Szymanski, Rebecca L. Stearns, Lawrence E. Armstrong, and Douglas J. Casa. "Effects of Heat Acclimation Following Heat Acclimatization on Whole Body Heat Exchange in Trained Endurance Athletes." International Journal of Environmental Research and Public Health 19, no. 11 (May 25, 2022): 6412. http://dx.doi.org/10.3390/ijerph19116412.

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The purpose of this study was to examine the changes in metabolic heat production (Hprod), evaporative heat loss (Hevap), and dry heat loss (Hdry), following heat acclimatization (HAz) and heat acclimation (HA). Twenty-two male endurance athletes (mean ± standard deviation; age, 37 ± 12 y; body mass, 73.4 ± 8.7 kg; height, 178.7 ± 6.8 cm; and VO2max, 57.1 ± 7.2 mL·kg−1·min−1) completed three trials (baseline; post-HAz; and post-HA), which consisted of 60 min steady state exercise at 59 ± 2% velocityVO2max in the heat (ambient temperature [Tamb], 35.2 ± 0.6 °C; relative humidity [%rh] 47.5 ± 0.4%). During the trial, VO2 and RER were collected to calculate Hprod, Hevap, and Hdry. Following the baseline trial, participants completed self-directed outdoor summer training followed by a post-HAz trial. Then, five days of HA were completed over eight days in the heat (Tamb, 38.7 ± 1.1 °C; %rh, 51.2 ± 2.3%). During the HA sessions, participants exercised to maintain hyperthermia (38.50 °C and 39.75 °C) for 60 min. Then, a post-HA trial was performed. There were no differences in Hprod between the baseline (459 ± 59 W·m−2), post-HAz (460 ± 61 W·m−2), and post-HA (464 ± 55 W·m−2, p = 0.866). However, Hevap was significantly increased post-HA (385 ± 84 W·m−2) compared to post-HAz (342 ± 86 W·m−2, p = 0.043) and the baseline (332 ± 77 W·m−2, p = 0.037). Additionally, Hdry was significantly lower at post-HAz (125 ± 8 W·m−2, p = 0.013) and post-HA (121 ± 10 W·m−2, p < 0.001) compared to the baseline (128 ± 7 W·m−2). Hdry at post-HA was also lower than post-HAz (p = 0.049). Hprod did not change following HAz and HA. While Hdry was decreased following HA, the decrease in Hdry was smaller than the increases in Hevap. Adaptations in body heat exchange can occur by HA following HAz.

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Crandall, C. G. "Carotid baroreflex responsiveness in heat-stressed humans." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (October 1, 2000): H1955—H1962. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1955.

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The effects of whole body heating on human baroreflex function are relatively unknown. The purpose of this project was to identify whether whole body heating reduces the maximal slope of the carotid baroreflex. In 12 subjects, carotid-vasomotor and carotid-cardiac baroreflex responsiveness were assessed in normothermia and during whole body heating. Whole body heating increased sublingual temperature (from 36.4 ± 0.1 to 37.4 ± 0.1°C, P < 0.01) and increased heart rate (from 59 ± 3 to 83 ± 3 beats/min, P < 0.01), whereas mean arterial blood pressure (MAP) was slightly decreased (from 88 ± 2 to 83 ± 2 mmHg, P < 0.01). Carotid-vasomotor and carotid-cardiac responsiveness were assessed by identifying the maximal gain of MAP and heart rate to R wave-triggered changes in carotid sinus transmural pressure. Whole body heating significantly decreased the responsiveness of the carotid-vasomotor baroreflex (from −0.20 ± 0.02 to −0.13 ± 0.02 mmHg/mmHg, P < 0.01) without altering the responsiveness of the carotid-cardiac baroreflex (from −0.40 ± 0.05 to −0.36 ± 0.02 beats · min−1 · mmHg−1, P = 0.21). Carotid-vasomotor and carotid-cardiac baroreflex curves were shifted downward and upward, respectively, to accommodate the decrease in blood pressure and increase in heart rate that accompanied the heat stress. Moreover, the operating point of the carotid-cardiac baroreflex was shifted closer to threshold ( P = 0.02) by the heat stress. Reduced carotid-vasomotor baroreflex responsiveness, coupled with a reduction in the functional reserve for the carotid baroreflex to increase heart rate during a hypotensive challenge, may contribute to increased susceptibility to orthostatic intolerance during a heat stress.

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Nelson, Michael D., Mark J. Haykowsky, Stewart R. Petersen, Darren S. DeLorey, Michael K. Stickland, June Cheng-Baron, and Richard B. Thompson. "Aerobic fitness does not influence the biventricular response to whole body passive heat stress." Journal of Applied Physiology 109, no. 5 (November 2010): 1545–51. http://dx.doi.org/10.1152/japplphysiol.00769.2010.

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We examined biventricular function during passive heat stress in endurance trained (ET) and untrained (UT) men to evaluate whether aerobic fitness alters the volumetric response. Body temperature was elevated ∼0.8°C above baseline in 20 healthy men (10 ET, 64.4 ± 3.0 ml·kg−1·min−1; and 10 UT, 46.3 ± 6.2 ml·kg−1·min−1) by circulating warm water (50°C) throughout a tube-lined suit. Cardiac magnetic resonance imaging was used to measure biventricular volumes, function, filling velocities, volumetric flow rates, and left ventricular (LV) twist and circumferential strain at baseline (BL) and after 45 min of heat stress. In both groups, passive heat stress reduced biventricular end-diastolic (ET, −19.5 ± 24.0 ml; UT, −25.1 ± 23.8 ml) and end-systolic (ET, −15.9 ± 8.8 ml; UT, −17.6 ± 7.9 ml) volumes and left atrial volume (ET, −19.2 ± 11.6 ml; UT, −15.0 ± 12.7 ml) and significantly increased heart rate (ET, 29.3 ± 9.0 beats/min; UT, 31.7 ± 10.4 beats/min) and cardiac output (ET, 3.8 ± 2.2 l/min; UT, 3.2 ± 1.4 l/min) similarly, while biventricular stroke volume was unchanged. There were no between-group differences in any parameter. Heat stress increased ( P < 0.05), as a percentage of baseline values, biventricular ejection fraction (ET, 3.4 ± 5.3%; UT, 4.4 ± 3.7%), annular systolic tissue velocities (ET, 32.5 ± 34.9%; UT, 44.0 ± 38.1%), and peak LV twist (ET, 51.6 ± 59.7%; UT, 59.7 ± 54.2%) and untwisting rates (ET, 45.5 ± 42.3%; UT, 51.8 ± 55.0%) similarly in both groups. Early LV diastolic tissue and blood velocities, volumetric flow rates, and strain rates (diastole) were unchanged with heat stress in both groups. The present findings indicate that aerobic fitness does not influence the biventricular response to passive heat stress.

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Notley, Sean R., Sheila Dervis, Martin P. Poirier, and Glen P. Kenny. "Menstrual cycle phase does not modulate whole body heat loss during exercise in hot, dry conditions." Journal of Applied Physiology 126, no. 2 (February 1, 2019): 286–93. http://dx.doi.org/10.1152/japplphysiol.00735.2018.

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Menstrual cycle phase has long been thought to modulate thermoregulatory function. However, information pertaining to the effects of menstrual phase on time-dependent changes in whole body dry and evaporative heat exchange during exercise-induced heat stress and the specific heat load at which menstrual phase modulates whole body heat loss remained unavailable. We therefore used direct calorimetry to continuously assess whole body dry and evaporative exchange in 12 habitually active, non-endurance-trained, eumenorrheic women [21 ± 3 (SD) yr] within the early-follicular, late-follicular, and midluteal menstrual phases during three 30-min bouts of cycling at increasing fixed exercise intensities of 40% (Low), 55% (Moderate), and 70% (High) peak oxygen uptake, each followed by a 15-min recovery, in hot, dry conditions (40°C, 15% relative humidity). This model elicited equivalent rates of metabolic heat production among menstrual phases ( P = 0.80) of ~250 (Low), ~340 (Moderate), and ~430 W (High). However, dry and evaporative heat exchange and the resulting changes in net heat loss (dry ± evaporative heat exchange) were similar among phases (all P > 0.05), with net heat loss averaging 216 ± 43 (Low), 287 ± 63 (Moderate), and 331 ± 75 W (High) across phases. Accordingly, cumulative body heat storage (summation of heat production and loss) across all exercise bouts was similar among phases ( P = 0.55), averaging 464 ± 122 kJ. For some time, menstrual cycle phase has been thought to modulate heat dissipation; however, we show that menstrual cycle phase does not influence the contribution of whole body dry and evaporative heat exchange or the resulting changes in net heat loss or body heat storage, irrespective of the heat load. NEW & NOTEWORTHY Menstrual phase has long been thought to modulate thermoregulatory function in eumenorrheic women during exercise-induced heat stress. Contrary to that perception, we show that when assessed in young, non-endurance-trained women within the early-follicular, late-follicular, and midluteal phases during three incremental exercise-induced heat loads in hot, dry conditions, menstrual phase does not modify whole body dry and evaporative heat exchange or the resulting changes in body heat storage, regardless of the heat load employed.

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Crandall, C. G., R. A. Etzel, and D. B. Farr. "Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (December 1, 1999): H2348—H2352. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2348.

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Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

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Crandall, C. G., R. Zhang, and B. D. Levine. "Effects of whole body heating on dynamic baroreflex regulation of heart rate in humans." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 5 (November 1, 2000): H2486—H2492. http://dx.doi.org/10.1152/ajpheart.2000.279.5.h2486.

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The purpose of this project was to identify whether dynamic baroreflex regulation of heart rate (HR) is altered during whole body heating. In 14 subjects, dynamic baroreflex regulation of HR was assessed using transfer function analysis. In normothermic and heat-stressed conditions, each subject breathed at a fixed rate (0.25 Hz) while beat-by-beat HR and systolic blood pressure (SBP) were obtained. Whole body heating significantly increased sublingual temperature, HR, and forearm skin blood flow. Spectral analysis of HR and SBP revealed that the heat stress significantly reduced HR and SBP variability within the high-frequency range (0.2–0.3 Hz), reduced SBP variability within the low-frequency range (0.03–0.15 Hz), and increased the ratio of low- to high-frequency HR variability (all P < 0.01). Transfer function gain analysis showed that the heat stress reduced dynamic baroreflex regulation of HR within the high-frequency range (from 1.04 ± 0.06 to 0.54 ± 0.6 beats · min−1 · mmHg−1; P < 0.001) without significantly affecting the gain in the low-frequency range ( P = 0.63). These data suggest that whole body heating reduced high-frequency dynamic baroreflex regulation of HR associated with spontaneous changes in blood pressure. Reduced vagal baroreflex regulation of HR may contribute to reduced orthostatic tolerance known to occur in humans during heat stress.

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Ganio, Matthew S., Daniel Gagnon, Jill Stapleton, Craig G. Crandall, and Glen P. Kenny. "Effect of Human Skin Grafts on Whole-Body Heat Loss During Exercise Heat Stress." Journal of Burn Care & Research 34, no. 4 (2013): e263-e270. http://dx.doi.org/10.1097/bcr.0b013e31826c32c0.

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Watkins, Austen M., Dennis J. Cheek, Alison E. Harvey, Darryn S. Willoughby, Kara E. Gillam, and Joel B. Mitchell. "The Relationship Between Cellular Heat Tolerance and Whole Body Heat Acclimation in Exercising Humans." Medicine & Science in Sports & Exercise 38, Supplement (May 2006): S355. http://dx.doi.org/10.1249/00005768-200605001-02384.

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Unnikrishnan, Ginu, Rajeev Hatwar, Samantha Hornby, Srinivas Laxminarayan, Tushar Gulati, Luke N. Belval, Gabrielle E. W. Giersch, Josh B. Kazman, Douglas J. Casa, and Jaques Reifman. "A 3-D virtual human thermoregulatory model to predict whole-body and organ-specific heat-stress responses." European Journal of Applied Physiology 121, no. 9 (June 5, 2021): 2543–62. http://dx.doi.org/10.1007/s00421-021-04698-1.

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Abstract Objective This study aimed at assessing the risks associated with human exposure to heat-stress conditions by predicting organ- and tissue-level heat-stress responses under different exertional activities, environmental conditions, and clothing. Methods In this study, we developed an anatomically detailed three-dimensional thermoregulatory finite element model of a 50th percentile U.S. male, to predict the spatiotemporal temperature distribution throughout the body. The model accounts for the major heat transfer and thermoregulatory mechanisms, and circadian-rhythm effects. We validated our model by comparing its temperature predictions of various organs (brain, liver, stomach, bladder, and esophagus), and muscles (vastus medialis and triceps brachii) under normal resting conditions (errors between 0.0 and 0.5 °C), and of rectum under different heat-stress conditions (errors between 0.1 and 0.3 °C), with experimental measurements from multiple studies. Results Our simulations showed that the rise in the rectal temperature was primarily driven by the activity level (~ 94%) and, to a much lesser extent, environmental conditions or clothing considered in our study. The peak temperature in the heart, liver, and kidney were consistently higher than in the rectum (by ~ 0.6 °C), and the entire heart and liver recorded higher temperatures than in the rectum, indicating that these organs may be more susceptible to heat injury. Conclusion Our model can help assess the impact of exertional and environmental heat stressors at the organ level and, in the future, evaluate the efficacy of different whole-body or localized cooling strategies in preserving organ integrity.

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Wilson, Thad E., and Chester A. Ray. "Effect of thermal stress on the vestibulosympathetic reflexes in humans." Journal of Applied Physiology 97, no. 4 (October 2004): 1367–70. http://dx.doi.org/10.1152/japplphysiol.00403.2004.

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Both heat stress and vestibular activation alter autonomic responses; however, the interaction of these two sympathetic activators is unknown. To determine the effect of heat stress on the vestibulosympathetic reflex, eight subjects performed static head-down rotation (HDR) during normothermia and whole body heating. Muscle sympathetic nerve activity (MSNA; peroneal microneurography), mean arterial blood pressure (MAP), heart rate (HR), and internal temperature were measured during the experimental trials. HDR during normothermia caused a significant increase in MSNA (Δ5 ± 1 bursts/min; Δ53 ± 14 arbitrary units/min), whereas no change was observed in MAP, HR, or internal temperature. Whole body heating significantly increased internal temperature (Δ0.9 ± 0.1°C), MSNA (Δ10 ± 3 bursts/min; Δ152 ± 44 arbitrary units/min), and HR (Δ25 ± 6 beats/min), but it did not alter MAP. HDR during whole body heating increased MSNA (Δ16 ± 4 bursts/min; Δ233 ± 90 arbitrary units/min from normothermic baseline), which was not significantly different from the algebraic sum of HDR during normothermia and whole body heating (Δ15 ± 4 bursts/min; Δ205 ± 55 arbitrary units/min). These data suggest that heat stress does not modify the vestibulosympathetic reflex and that both the vestibulosympathetic and thermal reflexes are robust, independent sympathetic nervous system activators.

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Yellon, D. M., E. Iliodromitis, D. S. Latchman, D. M. V. Winkle, J. M. Downey, F. M. Williams, and T. J. Williams. "Whole body heat stress fails to limit infarct size in the reperfused rabbit heart." Cardiovascular Research 26, no. 4 (April 1, 1992): 342–46. http://dx.doi.org/10.1093/cvr/26.4.342.

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Brothers, R. Matthew, Jonathan E. Wingo, Kimberly A. Hubing, Juan Del Coso, and Craig G. Crandall. "Effect of whole body heat stress on peripheral vasoconstriction during leg dependency." Journal of Applied Physiology 107, no. 6 (December 2009): 1704–9. http://dx.doi.org/10.1152/japplphysiol.00711.2009.

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The venoarteriolar response (VAR) increases vascular resistance upon increases in venous transmural pressure in cutaneous, subcutaneous, and muscle vascular beds. During orthostasis, it has been proposed that up to 45% of the increase in systemic vascular tone is due to VAR-related local mechanism(s). The objective of this project was to test the hypothesis that heat stress attenuates VAR-mediated cutaneous and whole leg vasoconstriction. During normothermic conditions, measurements of cutaneous blood flow (laser-Doppler flowmetry) and femoral artery blood flow (Doppler ultrasound) were obtained from both legs during supine and leg-dependent conditions. These measurements were repeated following a whole body heat stress (increase in internal temperature of 1.4 ± 0.2°C). Before leg dependency, cutaneous (CVC) and femoral vascular conductances (FVC) were significantly elevated in both legs during heat stress relative to normothermia ( P < 0.001). During leg dependency the absolute decrease in CVC was attenuated during heat stress ( P < 0.01) while the absolute decrease in FVC was unaffected ( P = 0.90). When CVC and FVC data were analyzed as a relative change from their respective baseline values, heat stress significantly attenuated the magnitude of vasoconstriction due to leg dependency in the cutaneous and femoral circulations ( P < 0.001 for both variables). These data suggest that an attenuated local vasoconstriction, evoked via the venoarteriolar response, may contribute to reduced blood pressure control and thus reduced orthostatic tolerance that occurs in heat-stressed individuals.

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McDermott, Brendon P., Douglas J. Casa, Matthew S. Ganio, Rebecca M. Lopez, Susan W. Yeargin, Lawrence E. Armstrong, and Carl M. Maresh. "Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A Systematic Review." Journal of Athletic Training 44, no. 1 (January 1, 2009): 84–93. http://dx.doi.org/10.4085/1062-6050-44.1.84.

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Abstract Objective: To assess existing original research addressing the efficiency of whole-body cooling modalities in the treatment of exertional hyperthermia. Data Sources: During April 2007, we searched MEDLINE, EMBASE, Scopus, SportDiscus, CINAHL, and Cochrane Reviews databases as well as ProQuest for theses and dissertations to identify research studies evaluating whole-body cooling treatments without limits. Key words were cooling, cryotherapy, water immersion, cold-water immersion, ice-water immersion, icing, fanning, bath, baths, cooling modality, heat illness, heat illnesses, exertional heatstroke, exertional heat stroke, heat exhaustion, hyperthermia, hyperthermic, hyperpyrexia, exercise, exertion, running, football, military, runners, marathoner, physical activity, marathoning, soccer, and tennis. Data Synthesis: Two independent reviewers graded each study on the Physiotherapy Evidence Database (PEDro) scale. Seven of 89 research articles met all inclusion criteria and a minimum score of 4 out of 10 on the PEDro scale. Conclusions: After an extensive and critical review of the available research on whole-body cooling for the treatment of exertional hyperthermia, we concluded that ice-water immersion provides the most efficient cooling. Further research comparing whole-body cooling modalities is needed to identify other acceptable means. When ice-water immersion is not possible, continual dousing with water combined with fanning the patient is an alternative method until more advanced cooling means can be used. Until future investigators identify other acceptable whole-body cooling modalities for exercise-induced hyperthermia, ice-water immersion and cold-water immersion are the methods proven to have the fastest cooling rates.

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Wechalekar, H., B. P. Setchell, W. G. Breed, M. Ricci, C. Leigh, and E. Peirce. "437. Whole body heat stress induces selective germ cell apoptosis in mice." Reproduction, Fertility and Development 20, no. 9 (2008): 117. http://dx.doi.org/10.1071/srb08abs437.

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Introduction: In scrotal mammals, heat stress (43°C/ 20 min) to the scrotum results in germ cell death in the testes1, abnormal spermatozoa, and infertility2 whereas two days of whole body heating (36°C, 12 h/ day) reduces testes weight, sperm numbers and fertility3. The aim of the present study was to determine the intratesticular effects of whole body heating on germ cell maturation and apoptosis. Methods: C57BL/6 mice (n = 16) were housed at 37–38°C for 8 h/ day for 3 days while controls (n = 4) were kept at 23–24°C. Animals from heat treated (n = 4), and control groups (n = 1) were sacrificed at 16 h, 7, 14 and 21 days post exposure to heat. Testes were weighed and analysed by t-test. In testes from each animal, two sections 70µm apart were end labelled for TdT-mediated-dUTP nick (TUNEL). Apoptosis was determined in 200 seminiferous tubules by a colour threshold set in the particle analysis program (Olympus).The tubules were staged as I-VI (early), VII-VIII, IX-X and XI-XII (late) and results analysed using Wilcoxon test. Results: The weights of testes were significantly reduced in heat-treated animals (P < 0.05) at 16 h, 7 and 14 days with no significant difference at 21 days. Apoptosis was significantly higher in the heat-treated group in stages I-VI and XI-XII at 16 h, 7 and 14 days (P < 0.05). In addition, in stages VII-VIII and IX-X apoptosis was significantly higher at 16 h (P < 0.05) with no statistical difference between other time intervals. By day 21, the levels of apoptosis did not differ significantly from the controls in any of the stages (P > 0.05).Conclusion: Whole body heat stress can induce stage and cell specific degeneration of the germ cells in the seminiferous epithelium. The germ cells undergoing apoptosis are spermatogonia, primary spermatocytes and early spermatids. In addition, heat stress produces significant apoptosis of germ cells in the hormone dependent stages VII-VIII immediately after heat stress. (1) Rockett, J.C. et al. (2001) Biol. Reprod. 65:229–239. (2) Banks, S. et al. (2005) Reproduction 129:505–514. (3) Yaeram, J. et al. (2006) Reprod. Fert. Dev. 18:647–653.

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Amorim, Fabiano T., Paulette M. Yamada, Suzanne M. Schneider, and Pope L. Moseley. "Does Whole Body Heat Acclimation Change Peripheral Blood Mononuclear Cell Thermotolerance?" Medicine & Science in Sports & Exercise 40, Supplement (May 2008): S333—S334. http://dx.doi.org/10.1249/01.mss.0000323335.84966.42.

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Friesen, Brian J., Martin P. Poirier, Dallon T. Lamarche, Andrew W. D’Souza, Jung-Hyun Kim, and Glen P. Kenny. "Postexercise Activation of Muscle Metaboreceptors Modulates Whole-Body Evaporative Heat Loss." Medicine & Science in Sports & Exercise 49, no. 5S (May 2017): 449. http://dx.doi.org/10.1249/01.mss.0000518116.25047.ad.

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Gagnon, Daniel. "Sex-related differences in local and whole-body heat loss responses: Physical or physiological?" Applied Physiology, Nutrition, and Metabolism 39, no. 7 (July 2014): 843. http://dx.doi.org/10.1139/apnm-2014-0020.

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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.

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Cui, Jian, Thad E. Wilson, and Craig G. Crandall. "Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 1 (January 1, 2002): R252—R258. http://dx.doi.org/10.1152/ajpregu.00337.2001.

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To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature ( P < 0.01), MSNA ( P < 0.01), heart rate ( P< 0.01), and skin blood flow ( P < 0.001), whereas mean arterial blood pressure did not change significantly ( P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (−128.3 ± 13.9 U · beats−1 · mmHg−1) was similar ( P = 0.31) with normothermia (−140.6 ± 21.1 U · beats−1 · mmHg−1). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating.

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Luetkemeier, Maurie J., Dustin R. Allen, Mu Huang, Faith K. Pizzey, Iqra M. Parupia, Thad E. Wilson, and Scott L. Davis. "Skin tattooing impairs sweating during passive whole body heating." Journal of Applied Physiology 129, no. 5 (November 1, 2020): 1033–38. http://dx.doi.org/10.1152/japplphysiol.00427.2019.

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This study is the first to assess the reflex control of sweating in tattooed skin. The novel findings are twofold. First, attenuated increases in sweat rate were observed in tattooed skin compared with adjacent healthy non-tattooed skin in response to a moderate increase (1.0°C) in internal temperature during a passive whole body heat stress. Second, reduced sweating in tattooed skin is likely related to functional damage to the secretory mechanisms of eccrine sweat glands, rendering it less responsive to cholinergic stimulation.

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Dervis, Sheila, Martin P. Poirier, Pierre Boulay, Ronald J. Sigal, Janine Malcolm, Naoto Fujii, and Glen P. Kenny. "Does the Exercise-Induced Heat Load Influence Whole-Body Heat Loss in Type 1 Diabetes?" Medicine & Science in Sports & Exercise 49, no. 5S (May 2017): 18. http://dx.doi.org/10.1249/01.mss.0000516861.96340.87.

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43

Notley, Sean R., Andrew W. D’Souza, Robert D. Meade, Brodie J. Richards, and Glen P. Kenny. "Whole-body heat exchange in women during constant- and variable-intensity work in the heat." European Journal of Applied Physiology 120, no. 12 (September 9, 2020): 2665–75. http://dx.doi.org/10.1007/s00421-020-04486-3.

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44

NOTLEY, SEAN R., MARTIN P. POIRIER, STEPHEN G. HARDCASTLE, ANDREAS D. FLOURIS, PIERRE BOULAY, RONALD J. SIGAL, and GLEN P. KENNY. "Aging Impairs Whole-Body Heat Loss in Women under Both Dry and Humid Heat Stress." Medicine & Science in Sports & Exercise 49, no. 11 (November 2017): 2324–32. http://dx.doi.org/10.1249/mss.0000000000001342.

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45

Cui, Jian, Rong Zhang, Thad E. Wilson, and Craig G. Crandall. "Spectral analysis of muscle sympathetic nerve activity in heat-stressed humans." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 3 (March 2004): H1101—H1106. http://dx.doi.org/10.1152/ajpheart.00790.2003.

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Whole body heating increases muscle sympathetic nerve activity (MSNA); however, the effect of heat stress on spectral characteristics of MSNA is unknown. Such information may provide insight into mechanisms of heat stress-induced MSNA activation. The purpose of the present study was to test the hypothesis that heat stress-induced changes in systolic blood pressure variability parallel changes in MSNA variability. In 13 healthy subjects, MSNA, electrocardiogram, arterial blood pressure (via Finapres), and respiratory activity were recorded under both normothermic and heat stress conditions. Spectral characteristics of integrated MSNA, R-R interval, systolic blood pressure, and respiratory excursions were assessed in the low (LF; 0.03–0.15 Hz) and high (HF; 0.15–0.45 Hz) frequency components. Whole body heating significantly increased skin and core body temperature, MSNA burst rate, and heart rate, but not mean arterial blood pressure. Systolic blood pressure and R-R interval variability were significantly reduced in both the LF and HF ranges. Compared with normothermic conditions, heat stress significantly increased the HF component of MSNA, while the LF component of MSNA was not altered. Thus the LF-to-HF ratio of MSNA oscillatory components was significantly reduced. These data indicate that the spectral characteristics of MSNA are altered by whole body heating; however, heat stress-induced changes in MSNA do not parallel changes in systolic blood pressure variability. Moreover, the reduction in LF component of systolic blood pressure during heat stress is unlikely related to spectral changes in MSNA.

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46

Patel, Hemal H., Anna Hsu, and Garrett J. Gross. "Cardioprotection is strain dependent in rat in response to whole body hyperthermia." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (March 1, 2001): H1208—H1214. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1208.

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Previous results showed a genetic component to cardioprotection. Therefore, we investigated the heat shock response in Wistar and Sprague-Dawley (SD) rats at 24 and 48 h. Rats were subjected to whole body hyperthermia achieving colonic temperatures of 40 or 42°C for 20 min. After recovery hearts were excised for protein measurements or were subjected to 30 min of ischemia and then 2 h of reperfusion. Heat shock protein (HSP) expression was determined by Western blotting and infarct size was determined by triphenyltetrazolium staining. All groups of SD and Wistar rats demonstrated HSP72 and HSP90 induction at both time points in response to a heat stress of 42°C. At 24 h there was only a significant reduction in infarct size seen in control vs. small SD (60.0 ± 4.8 vs. 26.5 ± 2.3) rats. However, at 48 h control versus small SD (60.0 ± 4.8 vs. 17.6 ± 3.8) and Wistar (59.4 ± 4.3 vs. 29.8 ± 6.0) and control versus large SD (53.7 ± 2.6 vs. 19.8 ± 4.7) and Wistar (57.3 ± 1.6 vs. 34.5 ± 2.8) rats demonstrated a significant reduction in infarct size with a greater reduction observed in SD rats. We conclude that heat shock-induced cardioprotection in rats is dependent on strain, temperature, time after stress, and size.

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47

Budd, G. M., J. R. Brotherhood, A. L. Hendrie, and S. E. Jeffery. "Effects of fitness, fatness, and age on men's responses to whole body cooling in air." Journal of Applied Physiology 71, no. 6 (December 1, 1991): 2387–93. http://dx.doi.org/10.1152/jappl.1991.71.6.2387.

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Simple and multiple regression analyses were used to assess the influence of 12 white men's fitness (aerobic capacity 44–58 ml O2.min-1.kg fat-free mass-1), fatness (mean skin-fold thickness 5–20 mm, body fat content 15–36%), and age (26–52 yr) on their thermal, metabolic, cardiovascular, and subjective responses to 2 h of whole body cooling, nude, in air at 10 degrees C. Fitter men had slower heart rates, and fatter men had higher blood pressures. Fitness had no effect (P greater than 0.39) on any measured response to cold. Fatness was associated (P less than 0.01) with reduced heat loss, heat production, and mean skin temperature; unchanged heat debt; and increased tissue insulation. Age had the opposite effects. When the confounding effects of fatness were held constant by multiple regression, older men responded to cold as though they were 1 mm of skinfold thickness leaner for each 3–4 yr of age. We conclude that aging, even between the relatively youthful ages of 26 and 52 yr, is accompanied by a progressive weakening of the vasoconstrictor response to cold.

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48

Mamiya, Hiroaki, Yoshihiko Takeda, Takashi Naka, Naoki Kawazoe, Guoping Chen, and Balachandran Jeyadevan. "Practical Solution for Effective Whole-Body Magnetic Fluid Hyperthermia Treatment." Journal of Nanomaterials 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/1047697.

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Magnetic fluid hyperthermia therapy is considered as a promising treatment for cancers including unidentifiable metastatic cancers that are scattered across the whole body. However, a recent study on heat transfer simulated on a human body model showed a serious side effect: occurrences of hot spots in normal tissues due to eddy current loss induced by variation in the irradiated magnetic field. The indicated allowable upper limit of field amplitude Hac for constant irradiation over the entire human body corresponded to approximately 100 Oe at a frequency f of 25 kHz. The limit corresponds to the value Hacf of 2.5 × 106 Oe·s−1 and is significantly lower than the conventionally accepted criteria of 6 × 107 Oe·s−1. The present study involved evaluating maximum performance of conventional magnetic fluid hyperthermia cancer therapy below the afore-mentioned limit, and this was followed by discussing alternative methods not bound by standard frameworks by considering steady heat flow from equilibrium responses of stable nanoparticles. Consequently, the clarified potentials of quasi-stable core-shell nanoparticles, dynamic alignment of easy axes, and short pulse irradiation indicate that the whole-body magnetic fluid hyperthermia treatment is still a possible candidate for future cancer therapy.

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Iguchi, Masaki, Andrew E. Littmann, Shuo-Hsiu Chang, Lydia A. Wester, Jane S. Knipper, and Richard K. Shields. "Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans." Journal of Athletic Training 47, no. 2 (March 1, 2012): 184–90. http://dx.doi.org/10.4085/1062-6050-47.2.184.

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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.

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Wechalekar, H., B. P. Setchell, W. G. Breed, M. Ricci, C. Leigh, and E. Peirce. "115. WHOLE BODY HEAT EXPOSURE INDUCES APOPTOSIS IN MOUSE CAUDAL EPIDIDYMAL SPERMATOZOA." Reproduction, Fertility and Development 21, no. 9 (2009): 34. http://dx.doi.org/10.1071/srb09abs115.

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Introduction: The aim of the present study was to determine the immediate effects of whole body heating on sperm numbers, motility and apoptosis. Material and Methods: C57BL/6 mice (n=7) were exposed to 37-38oC (8 hours/day), for three consecutive days while control mice (n=7) were kept at 23-24oC. Caudal epididymal spermatozoa were collected from control and heat treated mice 16 hours after the last heat treatment to determine the sperm number and motility using a Neubauer haemocytometer and sperm apoptotic changes by dual colorflow cytometry using Annexin V/PE (Annexin V conjugated with phycoerythrin) and 7AAD (7-amino-actinomycin D) stains. Results: There were no significant differences (p>0.05) in sperm numbers between heat treated and control mice, however heating did result in a significant reduction in sperm motility (p<0.05). Apoptosis staining identified four different subpopulations of spermatozoa: (a) live spermatozoa (Annexin V-/7AAD-), (b) early apoptotic spermatozoa with exteriorized phosphotidylserine (PS) receptor and intact plasmalemma (Annexin V+/7AAD-), (c) late apoptotic spermatozoa with PS receptor translocation and leaky plasmalemma (Annexin V+/7AAD+) and (d) dead spermatozoa with damaged plasmalemma with no detectable PS receptor (Annexin V-/7AAD+). Heating resulted in significant reduction in the percentage of live spermatozoa (p<0.05), an increase in early apoptotic (p<0.05), late apoptotic (p<0.05), and dead spermatozoa (p<0.05). Conclusion: This study shows that mice exposed to whole body heat exposure of 37-38oC for 8 hours per day for three consecutive days exhibited early and late apoptotic changes to epididymal spermatozoa. These findings suggest possible adverse effects of exposure to high temperature on the viability of human spermatozoa in the epididymides. In addition, these findings reinforce the importance of temperature during sperm preparation procedures in infertility clinics, and research laboratories.

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