scholarly journals The Impact of Central and Peripheral Cyclooxygenase Enzyme Inhibition on Exercise-Induced Elevations in Core Body Temperature

2017 ◽  
Vol 12 (5) ◽  
pp. 662-667 ◽  
Author(s):  
Matthijs T.W. Veltmeijer ◽  
Dineke Veeneman ◽  
Coen C.C.W. Bongers ◽  
Mihai G. Netea ◽  
Jos W. van der Meer ◽  
...  

Purpose:Exercise increases core body temperature (TC) due to metabolic heat production. However, the exercise-induced release of inflammatory cytokines including interleukin-6 (IL-6) may also contribute to the rise in TC by increasing the hypothalamic temperature set point. This study investigated whether the exercise-induced increase in TC is partly caused by an altered hypothalamic temperature set point.Methods:Fifteen healthy, active men age 36 ± 14 y were recruited. Subjects performed submaximal treadmill exercise in 3 randomized test conditions: (1) 400 mg ibuprofen and 1000 mg acetaminophen (IBU/APAP), (2) 1000 mg acetaminophen (APAP), and (3) a control condition (CTRL). Acetaminophen and ibuprofen were used to block the effect of IL-6 at a central and peripheral level, respectively. TC, skin temperature, and heart rate were measured continuously during the submaximal exercise tests.Results:Baseline values of TC, skin temperature, and heart rate did not differ across conditions. Serum IL-6 concentrations increased in all 3 conditions. A significantly lower peak TC was observed in IBU/APAP (38.8°C ± 0.4°C) vs CTRL (39.2°C ± 0.5°C, P = .02) but not in APAP (38.9°C ± 0.4°C) vs CTRL. Similarly, a lower ΔTC was observed in IBU/APAP (1.7°C ± 0.3°C) vs CTRL (2.0°C ± 0.5°C, P < .02) but not in APAP (1.7°C ± 0.5°C) vs CTRL. No differences were observed in skin temperature and heart-rate responses across conditions.Conclusions:The combined administration of acetaminophen and ibuprofen resulted in an attenuated increase in TC during exercise compared with a CTRL. This observation suggests that a prostaglandin-E2-induced elevated hypothalamic temperature set point may contribute to the exercise-induced rise in TC.

2018 ◽  
Vol 99 ◽  
pp. 1-6 ◽  
Author(s):  
Alexander P. Welles ◽  
Xiaojiang Xu ◽  
William R. Santee ◽  
David P. Looney ◽  
Mark J. Buller ◽  
...  

1997 ◽  
Vol 272 (4) ◽  
pp. R1178-R1188 ◽  
Author(s):  
K. Krauchi ◽  
C. Cajochen ◽  
D. Mori ◽  
P. Graw ◽  
A. Wirz-Justice

The phase-shifting capacity and thermoregulatory effects of a single oral administration at 18 h of melatonin (5 mg) or S-20098, a melatonin agonist (5 or 100 mg), was investigated in eight healthy young men in a double-blind placebo crossover design. The unmasking conditions of a shortened constant-routine protocol (mini-CR) were used to collect evening phase markers of physiological parameters. In comparison to placebo, all three drug administrations induced an earlier dim-light melatonin onset (DLMO), an earlier increase in distal skin temperature, and an earlier decrease in core body temperature (CBT), heart rate, and proximal skin temperature. This indicates that administration at 18 h of both melatonin and S-20098 (more pronounced with 100 than 5 mg) induced an earlier regulation of the endogenous circadian nocturnal decline in CBT. On the posttreatment day a second mini-CR revealed persistent significantly phase-advanced circadian rhythms as estimated by DLMO, as well as by the midrange crossing time of CBT and heart rate decline. There were no significant differences between the two doses of S-20098. The data suggest that, in addition to immediate thermoregulatory changes, a phase advance of the circadian system had occurred and that the phase advance could still be measured on the posttreatment day.


2017 ◽  
Vol 20 (2) ◽  
pp. 202-207 ◽  
Author(s):  
Matthijs T.W. Veltmeijer ◽  
Thijs M.H. Eijsvogels ◽  
Wideke Barteling ◽  
Kitty Verbeek–Knobbe ◽  
Waander L. van Heerde ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Kazuyuki Miyamoto ◽  
Keisuke Suzuki ◽  
Hirokazu Ohtaki ◽  
Motoyasu Nakamura ◽  
Hiroki Yamaga ◽  
...  

Abstract Background Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure. Methods Mildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS. Results The survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage. Conclusions We developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.


2021 ◽  
Vol 7 (1) ◽  
pp. e000907
Author(s):  
Giovanni Polsinelli ◽  
Angelo Rodio ◽  
Bruno Federico

IntroductionThe measurement of heart rate is commonly used to estimate exercise intensity. However, during endurance performance, the relationship between heart rate and oxygen consumption may be compromised by cardiovascular drift. This physiological phenomenon mainly consists of a time-dependent increase in heart rate and decrease in systolic volume and may lead to overestimate absolute exercise intensity in prediction models based on heart rate. Previous research has established that cardiovascular drift is correlated to the increase in core body temperature during prolonged exercise. Therefore, monitoring body temperature during exercise may allow to quantify the increase in heart rate attributable to cardiovascular drift and to improve the estimate of absolute exercise intensity. Monitoring core body temperature during exercise may be invasive or inappropriate, but the external auditory canal is an easily accessible alternative site for temperature measurement.Methods and analysisThis study aims to assess the degree of correlation between trends in heart rate and in ear temperature during 120 min of steady-state cycling with intensity of 59% of heart rate reserve in a thermally neutral indoor environment. Ear temperature will be monitored both at the external auditory canal level with a contact probe and at the tympanic level with a professional infrared thermometer.Ethics and disseminationThe study protocol was approved by an independent ethics committee. The results will be submitted for publication in academic journals and disseminated to stakeholders through summary documents and information meetings.


2014 ◽  
Vol 112 (9) ◽  
pp. 2199-2217 ◽  
Author(s):  
Nabil El Bitar ◽  
Bernard Pollin ◽  
Daniel Le Bars

In thermal neutral condition, rats display cyclic variations of the vasomotion of the tail and paws, synchronized with fluctuations of blood pressure, heart rate, and core body temperature. “On-” and “off-” cells located in the rostral ventromedial medulla, a cerebral structure implicated in somatic sympathetic drive, 1) exhibit similar spontaneous cyclic activities in antiphase and 2) are activated and inhibited by thermal nociceptive stimuli, respectively. We aimed at evaluating the implication of such neurons in autonomic regulation by establishing correlations between their firing and blood pressure, heart rate, and skin and core body temperature variations. When, during a cycle, a relative high core body temperature was reached, the on-cells were activated and within half a minute, the off-cells and blood pressure were depressed, followed by heart rate depression within a further minute; vasodilatation of the tail followed invariably within ∼3 min, often completed with vasodilatation of hind paws. The outcome was an increased heat loss that lessened the core body temperature. When the decrease of core body temperature achieved a few tenths of degrees, sympathetic activation switches off and converse variations occurred, providing cycles of three to seven periods/h. On- and off-cell activities were correlated with inhibition and activation of the sympathetic system, respectively. The temporal sequence of events was as follows: core body temperature → on-cell → off-cell ∼ blood pressure → heart rate → skin temperature → core body temperature. The function of on- and off-cells in nociception should be reexamined, taking into account their correlation with autonomic regulations.


1984 ◽  
Vol 57 (6) ◽  
pp. 1738-1741 ◽  
Author(s):  
T. G. Waldrop ◽  
D. E. Millhorn ◽  
F. L. Eldridge ◽  
L. E. Klingler

Respiratory responses to increased skin temperatures were recorded in anesthetized cerebrate and in unanesthetized decerebrate cats. All were vagotomized, glomectomized, and paralyzed. Core body temperature and end-tidal Pco2 were kept constant with servoncontrollers. Stimulation of cutaneous nociceptors by heating the skin to 46 degrees C caused respiration to increase in both cerebrate and decerebrate cats. An even larger facilitation of respiration occurred when the skin temperature was elevated to 51 degrees C. However, respiration did not increase in either group of cats when the skin was heated to 41 degrees C to activate cutaneous warm receptors. The phenomenon of sensitization of nociceptors was observed. Spinal transection prevented all the respiratory responses to cutaneous heating. We conclude that noxious, but not nonnoxious, increases in skin temperature cause increases in respiratory output.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Peng Zhou ◽  
Maricela Robles-Murguia ◽  
Deepa Mathew ◽  
Giles E. Duffield

Inhibitor of DNA binding 2 (ID2) is a helix-loop-helix transcriptional repressor rhythmically expressed in many adult tissues. Our previous studies have demonstrated thatId2null mice have sex-specific elevated glucose uptake in brown adipose tissue (BAT). Here we further explored the role ofId2in the regulation of core body temperature over the circadian cycle and the impact ofId2deficiency on genes involved in insulin signaling and adipogenesis in BAT. We discovered a reduced core body temperature inId2−/− mice. Moreover, inId2−/− BAT, 30 genes includingIrs1,PPARs, andPGC-1s were identified as differentially expressed in a sex-specific pattern. These data provide valuable insights into the impact ofId2deficiency on energy homeostasis of mice in a sex-specific manner.


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