scholarly journals The Role of Volume Regulation and Thermoregulation in AKI during Marathon Running

2019 ◽  
Vol 14 (9) ◽  
pp. 1297-1305 ◽  
Author(s):  
Sherry G. Mansour ◽  
Thomas G. Martin ◽  
Wassim Obeid ◽  
Rachel W. Pata ◽  
Karen M. Myrick ◽  
...  
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Marathon Running ◽  
Marathon Runners ◽  
Volume Balance ◽  
Blood And Urine Samples ◽  
Core Body ◽  
Urine Microscopy ◽  
Sweat Sodium

Background and objectivesMarathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage.Design, setting, participants, & measurementsTo investigate the etiology, we examined volume and thermoregulatory responses as possible mechanisms in runners’ AKI using a prospective cohort of runners in the 2017 Hartford Marathon. Vitals, blood, and urine samples were collected in 23 runners 1 day premarathon and immediately and 1 day postmarathon. We measured copeptin at each time point. Continuous core body temperature, sweat sodium, and volume were assessed during the race. The primary outcome of interest was AKI, defined by AKIN criteria.ResultsRunners ranged from 22 to 63 years old; 43% were men. Runners lost a median (range) of 2.34 (0.50–7.21) g of sodium and 2.47 (0.36–6.81) L of volume via sweat. After accounting for intake, they had a net negative sodium and volume balance at the end of the race. The majority of runners had increases in core body temperature to 38.4 (35.8–41)°C during the race from their baseline. Fifty-five percent of runners developed AKI, yet 74% had positive urine microscopy for acute tubular injury. Runners with more running experience and increased participation in prior marathons developed a rise in creatinine as compared with those with lesser experience. Sweat sodium losses were higher in runners with AKI versus non-AKI (median, 3.41 [interquartile range (IQR), 1.7–4.8] versus median, 1.4 [IQR, 0.97–2.8] g; P=0.06, respectively). Sweat volume losses were higher in runners with AKI versus non-AKI (median, 3.89 [IQR, 1.49–5.09] versus median, 1.66 [IQR, 0.72–2.84] L; P=0.03, respectively). Copeptin was significantly higher in runners with AKI versus those without (median, 79.9 [IQR, 25.2–104.4] versus median, 11.3 [IQR, 6.6–43.7]; P=0.02, respectively). Estimated temperature was not significantly different.ConclusionsAll runners experienced a substantial rise in copeptin and body temperature along with salt and water loss due to sweating. Sodium and volume loss via sweat as well as plasma copeptin concentrations were associated with AKI in runners.PodcastThis article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2019_08_13_CJASNPodcast_19_09_.mp3

Assessing the role of nocturnal core body temperature dysregulation as a biomarker of neurodegeneration

2019 ◽  
Vol 29 (5) ◽  
Author(s):  
Arabella K. Raupach ◽  
Kaylena A. Ehgoetz Martens ◽  
Negar Memarian ◽  
George Zhong ◽  
Elie Matar ◽  
...  
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Core Body

scholarly journals Dual orexin receptor antagonist induces changes in core body temperature in rats after exercise

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tristan Martin ◽  
Yves Dauvilliers ◽  
Ouma-Chandrou Koumar ◽  
Valentine Bouet ◽  
Thomas Freret ◽  
...  
Keyword(s):  
Body Temperature ◽  
Receptor Antagonist ◽  
Core Body Temperature ◽  
Treadmill Running ◽  
Orexin Receptors ◽  
Dose Effects ◽  
Male Wistar Rats ◽  
Core Body ◽  
Dose Dependent

AbstractHypothalamic orexin neurons are involved in various physiological functions, including thermoregulation. The orexinergic system has been considered as a potent mediator of the exercise response. The present study describes how the antagonization of the orexinergic system by a dual orexin receptor antagonist (DORA) modifies the thermoregulatory process during exercise. Core Body Temperature (CBT) and Spontaneous Locomotor Activity (SLA) of 12 male Wistar rats were recorded after either oral administration of DORA (30 mg/kg or 60 mg/kg) or placebo solution, both at rest and in exercise conditions with treadmill running. DORA ingestion decreased SLA for 8 hours (p < 0.001) and CBT for 4 hours (p < 0.01). CBT (°C) response was independent of SLA. The CBT level decreased from the beginning to the end of exercise when orexin receptors were antagonized, with a dose-dependent response (39.09 ± 0.36 and 38.88 ± 0.28 for 30 and 60 mg/kg; p < 0.001) compared to placebo (39.29 ± 0.31; p < 0.001). CBT increased during exercise was also blunted after DORA administration, but without dose effects of DORA. In conclusion, our results favor the role of orexin in the thermoregulation under stress related to exercise conditions.

Modification of circadian body temperature rhythm during the luteal menstrual phase: role of melatonin

1996 ◽  
Vol 80 (1) ◽  
pp. 25-29 ◽  
Author(s):  
A. Cagnacci ◽  
R. Soldani ◽  
G. A. Laughlin ◽  
S. S. Yen
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Menstrual Phase ◽  
Temperature Rhythm ◽  
Melatonin Administration ◽  
Early Follicular Phase ◽  
Body Temperature Rhythm ◽  
The Mean ◽  
Core Body

In women during early follicular phase (FP), the rise of melatonin at night accounts for 40% of the nocturnal core body temperature (Tc) decline. In seven normal-cycling women, the circadian rhythms of Tc and melatonin of the FP were compared with those of the luteal phase (LP). In addition, in both phases the Tc response to daytime melatonin administration was investigated. Melatonin levels were comparable during the two menstrual phases, but the nocturnal melatonin onset was delayed by 90 min in the LP (P < 0.01). This was accompanied by a delay of the nadir of the Tc circadian rhythm (P < 0.002), a 0.3 degrees C elevation (P < 0.005) of the mean 24-h value, and a 40% blunting (P < 0.002) of the amplitude. This attenuation of circadian Tc in LP women was replicated in two estrogen-treated hypogonadal women by the administration of medroxyprogesterone acetate. The daytime administration of melatonin (2.5 mg) decreased Tc during the FP (P < 0.01) but was ineffective in the LP. Present data indicate that in LP, in association with high progesterone levels, an attenuated and phase-delayed circadian Tc rhythm may, in part, be due to a reduced effect of melatonin.

Acute starvation alters lipopolysaccharide-induced fever in leptin-dependent and -independent mechanisms in rats

2010 ◽  
Vol 299 (6) ◽  
pp. R1709-R1719 ◽  
Author(s):  
Wataru Inoue ◽  
Giamal N. Luheshi
Keyword(s):  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Physiological Responses ◽  
Prolonged Fever ◽  
Acute Starvation ◽  
Fever Response ◽  
Core Body ◽  
Fasted Rats

A decrease in leptin levels with the onset of starvation triggers a myriad of physiological responses including immunosuppression and hypometabolism/hypothermia, both of which can counteract the fever response to pathogens. Here we examined the role of leptin in LPS-induced fever in rats that were fasted for 48 h prior to inflammation with or without leptin replacement (12 μg/day). The preinflammation fasting alone caused a progressive hypothermia that was almost completely reversed by leptin replacement. The LPS (100 μg/kg)-induced elevation in core body temperature ( T core) was attenuated in the fasted animals at 2–6 h after the injection, an effect that was not reversed by leptin replacement. Increasing the LPS dose to 1,000 μg/kg caused a long-lasting fever that remained unabated for up to 36 h after the injection in the fed rats. This sustained response was strongly attenuated in the fasted rats whose T core started to decrease by 18 h after the injection. Leptin replacement almost completely restored the prolonged fever. The attenuation of the prolonged fever in the fasted animals was accompanied by the diminution of proinflammatory PGE2 in the cerebrospinal fluid and mRNA of proopiomelanocortin (POMC) in the hypothalamus. Leptin replacement prevented the fasting-induced reduction of POMC but not PGE2. Moreover, the leptin-dependent fever maintenance correlated closely with hypothalamic POMC levels ( r = 0.77, P < 0.001). These results suggest that reduced leptin levels during starvation attenuate the sustained fever response by lowering hypothalamic POMC tone but not PGE2 synthesis.

scholarly journals Regular exercise counteracts circadian shifts in core body temperature during long-duration bed rest

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Stefan Mendt ◽  
Hanns-Christian Gunga ◽  
Dieter Felsenberg ◽  
Daniel L. Belavy ◽  
Mathias Steinach ◽  
...  
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Space Station ◽  
Bed Rest ◽  
Resistive Exercise ◽  
Long Duration ◽  
Human Exploration ◽  
Core Body

AbstractWith NASA’s plans for the human exploration of Mars, astronauts will be exposed to mission durations much longer than current spaceflight missions on the International Space Station. These mission durations will increase the risk for circadian misalignment. Exercise has gained increasing interest as a non-pharmacological aid to entrain the circadian system. To assess the potential of exercise as a countermeasure to mitigate the risk for circadian disorders during spaceflight, we investigated the effects of long-term head-down tilt bed rest (HDBR) with and without exercise on the circadian rhythm of core body temperature. Core body temperature was recorded for 24 h using a rectal probe in sixteen healthy men (age: 30.5 ± 7.5 years (mean ± SD)) after 7 days and 49 days of HDBR. Five participants underwent HDBR only (CTR), five participants underwent HDBR and performed resistive exercises (RE), and six participants underwent HDBR and performed resistive exercises superimposed with vibrations (RVE). The exercise was scheduled three times per week. CTR showed a phase delay of 0.69 h. In contrast, both exercise groups were characterized by a phase advance (0.45 h for RE and 0.45 h for RVE; p = 0.026 for interaction between time and group). These findings suggest that resistive exercise (with or without vibration) may also serve as a countermeasure during spaceflight to mitigate circadian misalignments. The results could also be important for increasing awareness about the role of circadian disorders in long-term bedridden patients.

Role of core body temperature in nephrolithiasis

2020 ◽  
Vol 126 (5) ◽  
pp. 620-624
Author(s):  
Sudarshan Srirangapatanam ◽  
Scott Wiener ◽  
Marshall L. Stoller
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Core Body

scholarly journals 0163 Investigating the Role of Vasoactive Intestinal Peptide-Containing Neurons of the Ventromedal Preoptic Area in Sleep-Wake Control

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A64-A64
Author(s):  
A Venner ◽  
P M Fuller
Keyword(s):  
Body Temperature ◽  
Vasoactive Intestinal Peptide ◽  
Rem Sleep ◽  
Preoptic Area ◽  
Viral Vector ◽  
Core Body Temperature ◽  
Cell Group ◽  
Anatomical Location ◽  
Core Body

Abstract Introduction A role for vasoactive intestinal peptide (VIP) in promoting rapid eye movement (REM) sleep has been suggested, but the anatomical location of the neurons that release VIP to promote REM sleep has not been identified. Here, we investigated the role of VIP-containing cell groups in the ventromedial preoptic area (VMPOVIP) in sleep-wake regulation. The VMPO has also previously been implicated in thermoregulation and the febrile response. Methods We first investigated the native firing activity of VMPOVIP neurons, over repeated sleep-wake cycles, using in vivo fiber photometry in VIP-ires-Cre mice. We next examined the afferent and efferent profile of this cell group using conditional retrograde (pseudotyped modified rabies) and anterograde (adeno-associated viral vector-based) tracers. We finally utilized a chemogenetic strategy to selectively activate VMPOVIP neurons cells while monitoring electroencephalogram/electromyogram activity and core body temperature, in order to determine their role in sleep-wake and thermoregulatory control. Results We found that VMPOVIP cells were predominantly and strikingly REM-active, that they received many synaptic inputs from surrounding hypothalamic regions (including the ventromedial hypothalamus, dorsomedial hypothalamus and the arcuate nucleus), and that they targeted established sleep-wake nodes, such as the ventrolateral preoptic nucleus, tuberomammillary nucleus, lateral hypothalamus and ventrolateral periaqueductal gray area. To our surprise, chemogenetic activation of the VMPOVIP cell population had little effect upon all measures of sleep-wake analysed and no effect upon core body temperature. Conclusion We conclude that VMPOVIP neurons do not promote REM sleep per se. However, their REM-active profile and anatomical connectivity suggest that these neurons may play a functional role in generating certain cardinal features of REM sleep, which is an active focus of on-going research in our laboratory. Support SRSF CDA #016-JP-17 to A.V. and NS073613, NS092652 and NS103161 to P.M.

scholarly journals Activation of neuronal adenosine A1 receptors causes hypothermia through central and peripheral mechanisms

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243986
Author(s):  
Haley S. Province ◽  
Cuiying Xiao ◽  
Allison S. Mogul ◽  
Ankita Sahoo ◽  
Kenneth A. Jacobson ◽  
...  
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Metabolic Stress ◽  
Specific Cell ◽  
Danger Signal ◽  
Extracellular Adenosine ◽  
Dorsomedial Hypothalamus ◽  
Mouse Response ◽  
Core Body

Extracellular adenosine, a danger signal, can cause hypothermia. We generated mice lacking neuronal adenosine A1 receptors (A1AR, encoded by the Adora1 gene) to examine the contribution of these receptors to hypothermia. Intracerebroventricular injection of the selective A1AR agonist (Cl-ENBA, 5'-chloro-5'-deoxy-N6-endo-norbornyladenosine) produced hypothermia, which was reduced in mice with deletion of A1AR in neurons. A non-brain penetrant A1AR agonist [SPA, N6-(p-sulfophenyl) adenosine] also caused hypothermia, in wild type but not mice lacking neuronal A1AR, suggesting that peripheral neuronal A1AR can also cause hypothermia. Mice expressing Cre recombinase from the Adora1 locus were generated to investigate the role of specific cell populations in body temperature regulation. Chemogenetic activation of Adora1-Cre-expressing cells in the preoptic area did not change body temperature. In contrast, activation of Adora1-Cre-expressing dorsomedial hypothalamus cells increased core body temperature, concordant with agonism at the endogenous inhibitory A1AR causing hypothermia. These results suggest that A1AR agonism causes hypothermia via two distinct mechanisms: brain neuronal A1AR and A1AR on neurons outside the blood-brain barrier. The variety of mechanisms that adenosine can use to induce hypothermia underscores the importance of hypothermia in the mouse response to major metabolic stress or injury.

Sign in / Sign up

Export Citation Format

Share Document