The effect of whole body heat exposure and of cooling the hypothalamus on antibody titre in the rat

1981 ◽  
Vol 391 (1) ◽  
pp. 25-27 ◽  
Author(s):  
M. Banet ◽  
D. Fischer ◽  
K. U. Hartmann ◽  
H. Hensel ◽  
Ursula Hilling
Keyword(s):  
Antibody Titre ◽  
Heat Exposure ◽  
Whole Body ◽  
Body Heat

Intermittent sequential pneumatic compression does not enhance whole-body heat loss in elderly adults during extreme heat exposure

2019 ◽  
Vol 44 (12) ◽  
pp. 1383-1386
Author(s):  
Andrew W. D’Souza ◽  
Sean R. Notley ◽  
Robert D. Meade ◽  
Glen P. Kenny
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Heat Loss ◽  
Lower Limb ◽  
Vascular Function ◽  
Heat Exposure ◽  
Extreme Heat ◽  
Whole Body ◽  
Elderly Adults ◽  
Body Heat

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss.

115. WHOLE BODY HEAT EXPOSURE INDUCES APOPTOSIS IN MOUSE CAUDAL EPIDIDYMAL SPERMATOZOA

2009 ◽  
Vol 21 (9) ◽  
pp. 34 ◽  
Author(s):  
H. Wechalekar ◽  
B. P. Setchell ◽  
W. G. Breed ◽  
M. Ricci ◽  
C. Leigh ◽  
...  
Keyword(s):  
Actinomycin D ◽  
Heat Exposure ◽  
Annexin V ◽  
Whole Body ◽  
Sperm Number ◽  
Sperm Preparation ◽  
Heat Treated ◽  
Epididymal Spermatozoa ◽  
And Control ◽  
Body Heat

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.

scholarly journals Whole-body heat exposure induces membrane changes in spermatozoa from the cauda epididymidis of laboratory mice

2010 ◽  
Vol 12 (4) ◽  
pp. 591-598 ◽  
Author(s):  
Harsha Wechalekar ◽  
Brian P. Setchell ◽  
Eleanor J. Peirce ◽  
Mario Ricci ◽  
Chris Leigh ◽  
...  
Keyword(s):  
Heat Exposure ◽  
Whole Body ◽  
Laboratory Mice ◽  
Membrane Changes ◽  
Cauda Epididymidis ◽  
Body Heat

Effects of whole-body heat on male germ cell development and sperm motility in the laboratory mouse

2016 ◽  
Vol 28 (5) ◽  
pp. 545 ◽  
Author(s):  
H. Wechalekar ◽  
B. P. Setchell ◽  
K. R. Pilkington ◽  
C. Leigh ◽  
W. G. Breed ◽  
...  
Keyword(s):  
Germ Cell ◽  
Sperm Motility ◽  
Cell Apoptosis ◽  
Heat Exposure ◽  
Male Germ Cell ◽  
Whole Body ◽  
Control Group ◽  
Germ Cell Apoptosis ◽  
Heat Treated ◽  
Body Heat

This study investigated the effects of high temperatures on male germ cell development and epididymal sperm motility of laboratory mice. In Experiment 1, adult males (n = 16) were exposed to whole-body heat of 37–38°C for 8 h day–1 for 3 consecutive days, whereas controls (n = 4) were left at 23–24°C. In Experiment 2, adult mice (n = 6) were exposed to 37–38°C for a single 8-h period with controls (n = 6) left at 23–24°C. Experiment 2 was conducted as a continuation of previous study that showed changes in spermatozoa 16 h after exposure to heat of 37–38°C for 8 h day–1 for 3 consecutive days. In the present study, in Experiment 1, high temperature reduced testes weights 16 h and 14 days after exposure, whereas by Day 21 testes weights were similar to those in the control group (P = 0.18). At 16 h, 7 and 14 days after exposure, an increase in germ cell apoptosis was noticeable in early and late stages (I–VI and XI–XII) of the cycle of the seminiferous epithelium. However, apoptosis in intermediate stages (VII–X) was evident 16 h after heat exposure (P < 0.05), without any change at other time periods. By 21 days, there were no significant differences between heat-treated groups and controls. Considerably more caspase-3-positive germ cells occurred in heat-treated mice 16 h after heat exposure compared with the control group (P < 0.0001), whereas 8 h after heat in Experiment 2, sperm motility was reduced with a higher percentage of spermatozoa showing membrane damage. In conclusion, the present study shows that whole-body heat of 37–38°C induces stage-specific germ cell apoptosis and membrane changes in spermatozoa; this may result in reduced fertility at particular times of exposure after heating.

scholarly journals Whole body heat exposure modulates acute glucose metabolism

2018 ◽  
Vol 35 (1) ◽  
pp. 644-651 ◽  
Author(s):  
Amy L. Kimball ◽  
Patrick M. McCue ◽  
Michael A. Petrie ◽  
Richard K. Shields
Keyword(s):  
Glucose Metabolism ◽  
Heat Exposure ◽  
Whole Body ◽  
Body Heat

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.

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