bluuebunny/crossref_metadata_2025_split huggingface dataset:
The independent Influence of aerobic fitness and running economy on thermoregulation during running (1104.3)
Authors: Smoljanic Jovana , Dervis Sheila , Morris Nathan , Jay Ollie 
Published: June 2021

This study assessed the independent influence of aerobic fitness (VO2max) and running economy (RE) on changes in esophageal (∆Tes) and rectal (∆Tre) temperatures, and whole body sweat losses (WBSL) during treadmill running. 5 unfit (UF: 45±3 mlO2•kg‐1•min‐1) and 5 fit (F: 61±5 mlO2•kg‐1•min‐1) males, matched for body mass (UF: 78.9±5.5 kg; F: 78.0±5.9 kg) ran at 1) a metabolic heat production (Hprod) of 640 W and 2) 60%VO2max. Also, 5 high RE (HI‐RE: 185±17 mlO2•kg‐1•km‐1) and 5 low RE (LO‐RE: 221±9 mlO2•kg‐1•km‐1) males, matched for mass and VO2max (HI‐RE: 73.8±7.2 kg, 60±4 mlO2•kg‐1•min‐1; LO‐RE: 73.5±6.9 kg, 61±7 mlO2•kg‐1•min‐1) ran at a 1) Hprod of 640 W and 2) fixed speed of 10.5 km•h‐1. Ambient conditions were 25.4±0.8°C, 37±12% RH. At 640 W, similar ∆Tes (F: 0.65±0.24°C; UF: 0.58±0.24°C), ∆Tre (F: 0.92±0.25°C; UF: 0.92±0.26°C), and WBSL (446±147 mL; HI: 528±52 mL) were observed irrespective of VO2max. At 60%VO2max, greater ∆Tes (F: 1.04±0.23°C; UF: 0.66±0.43°C), ∆Tre (F: 1.14±0.34°C; UF: 0.86±0.26°C) and WBSL (F: 859±152 mL; UF: 564±91 mL) were observed in the F group. At 10.5 km•h‐1, greater Hprod (LO‐RE: 992±109 W; HI‐RE: 822±107 W), ∆Tes (LO‐RE: 1.27±0.29°C; HI‐RE: 0.84±0.16°C), ∆Tre (LO‐RE: 1.49±0.29°C; HI‐RE: 0.96±0.34°C) and WBSL (LO‐RE: 861±57 mL; HI‐RE: 663±131 mL) were observed in the LO‐RE group. In conclusion, thermoregulatory responses are altered by RE due to differences in Hprod, but not VO2peak.Grant Funding Source: Supported by NSERC (Dr. Ollie Jay ‐ Grant Holder)
Skin temperature responses following a warm‐weather road race (1104.4)
Authors: Belval Luke , Comstock Brett , Huggins Robert , Stearns Rebecca , Hosokawa Yuri , McKenzie Amy , Earp Jacob , Casa Douglas 
Published: June 2021

Purpose: To quantify the skin temperature changes following intense exercise in warm‐weather. Methods: Anterior thermal images and gastrointestinal temperature (TGI) from 20 male runners (mean±SD; 73.5 ± 10.9 kg) participating in a 11.2 km road race were collected before and immediately after the race. Wet‐bulb globe temperature (WBGT) and wind speed were recorded at the finish line. Infrared thermal images were divided into 11 distinct regions, superior torso (ST), inferior torso (IT), face (F), right forearm (RF), left forearm (LF), right upper arm (RUA), left upper arm (LUA), right thigh (RT), left thigh (LT), right lower leg (RLL) and left lower leg (LLL). Mean weighted anterior skin temperature (MWST) was calculated via approximation of body surface area. Paired samples t‐tests were performed to compare pre‐ and post‐race values. Correlation analysis was performed to evaluate the relationship between MWST and TGI. Results: Mean WBGT was 27.04 ± 1.20 °C. Mean wind speed was 1.38 ± 0.87 km/h. TGI significantly increased from pre‐ to post‐race (pre: 37.18 ± 0.37 °C, post: 39.39 ± 0.73 °C, p<0.001). MWST decreased, approaching significance (pre: 30.46 ± 1.77 °C, post: 29.48 ± 0.95 °C, p=0.059). Mean skin temperature for ST (p=0.001), IT (p<0.001), RUA (p=0.015) and LUA (p=0.004) significantly decreased from pre‐race values. There was no relationship between Post‐TGI and Post‐MWST (r=0.052, p=0.848). Conclusions: Despite a significant increase in TGI, skin temperature decreased compared to pre‐race measures. ST, IT, RUA and LUA may represent the areas with the greatest potential for heat loss, given the air to skin temperature gradient.Grant Funding Source: Supported by The Falmouth Road Race, The American Physiological Society and a UConn SURF Award
Effects of housing temperature on stress‐induced hyperthermia in mice, and the associated change in voluntary motor activity (1105.1)
Authors: Boily Patrice , Ring Daniel 
Published: June 2021

Many studies that investigate stress‐induced hyperthermia (SIH) in rodents were conducted on mice housed under ambient temperatures (Ta) of 20‐22°C, which can induce chronic stress due to cold exposure. Further, SIH in mice is associated with an increase in voluntary motor activity (VMA). Given that VMA can be affected by Ta and that VMA can be a major source of heat production, we hypothesized that the amplitude of SIH, and the relationship between SIH and VMA, is affected by Ta. Two groups of 8 male mice, housed either at 21 or 27°C, were exposed to treatments known to induce varying levels of stress. For both groups. the treatments resulted The treatments for both groups resulted in an increasing SIH (control<handling<water spill<cage switch<clean cage) that was correlated to VMA; the slopes of the relationship between SIH and VMA did not differ between groups. The absolute amplitude of SIH of mice housed at 27ºC was significantly higher (by 0.45°C) than mice housed at 21°C, but the relative amplitude (during ‐ before stress) did not differ between groups. Within the range of Ta studied, we conclude that housing temperatures have minor effects on the stress response of mice.Grant Funding Source: Supported by a CSU‐AAUP grant
Gender difference in thermal perception and the role of estrogen in mice (1105.3)
Authors: Nagasihma Kei , Marui Shuri , Tsunakawa Mizuki , Obata Chisa , Matsushita Haruka , Waki Naoya , Harada Hiroyoshi 
Published: June 2021

The present study aimed to assess if there is a gender difference in thermal perception, and estrogen is involved in the mechanism. MethodsMale (M group) and female ICR mice were used (n=6 and 18, respectively). Each mouse was placed a device for temperature measurement in the abdominal cavity under general anesthesia. Female mice were divided to three groups: two groups were bilaterally ovariectomized with and without estradiol replacement (E2 and N groups) and one sham‐operated (F group). Mice were placed in an experiment box (50x12x15 cm), of which 5 Pertier boards at the bottom. Each board temperature was controlled by computer program, and changed each 6 min for 90 min. The temperature was selected from either of 28°C, 31°C, 34°C, 37°C, and 40°C with a difference from that of the other boards. Abdominal temperature (Tabd) and the position of a mouse and its board temperature were recorded every 1 min. Experiment was started after 60‐min baseline period with all boards set at 34°C. Mice were habituated to the box 2‐3 times before the experiment. ResultsDuring the housing period before the experiment, there were no differences in Tabd among the groups; however, during the experiment, Tabd was higher in the F group than in the M group. In addition, the F group preferred 40°C board, but the M group 34°C board. There were no differences in Tabd and temperature preference of the board among the F, E2 and N groups. Conclusion In this experimental condition, male mice showed higher environmental condition than female mice. However, estradiol is not likely mechanism for the difference.Grant Funding Source: MEXT.KIBANKEISEI
Role of rat vascular KATP channels in setting microvascular oxygen pressure at the onset of contractions (1106.15)
Authors: Holdsworth Clark , Ferguson Scott , Wright Jennifer , Fees Alexander , Poole David , Musch Timothy 
Published: June 2021

Effective blood‐muscle O2 flux demands a sufficient microvascular O2 driving pressure (PO2mv) which is set by the ratio of O2 delivery‐O2 utilization. Smooth muscle cell hyperpolarization contributes to exercise induced increases in skeletal muscle O2 delivery mediated, in part, by ATP‐sensitive K+ (KATP) channels. We hypothesized that KATP channel blockade via glibenclamide (GLI) would speed the fall of PO2mv following the onset of skeletal muscle contractions. Spinotrapezius PO2mv (phosphorescence quenching) was measured in 12 adult male Sprague Dawley rats at rest and during 180 s of 1 Hz twitch contractions (~7 V) under control (CON) and GLI (5 mg/kg) conditions. GLI increased mean arterial pressure (ΔCON: 2 ± 1, ΔGLI: 17 ± 4 mmHg, p < 0.05) and decreased heart rate (ΔCON: 3 ± 2, ΔGLI: ‐9 ± 3 bpm, p < 0.05) but did not change baseline PO2mv (CON: 34.0 ± 2.2, GLI: 33.7 ± 1.6 mmHg, p > 0.05). Following the onset of contractions the time constant, mean response time and contracting steady‐state PO2mv were not different between conditions (p > 0.05 for all). However, a clearly defined undershoot (p < 0.05) of the contracting steady‐state PO2mv was evident with GLI (8.0 ± 2.6 %) but not during CON (1.6 ± 1.1 %). Our data indicate that blockade of KATP channels does not impact PO2mv kinetics parameters during small muscle mass electrical stimulation, but can cause transient mismatch of O2 delivery‐O2 utilization prior to stabilizing at the contracting steady‐state PO2mv. This suggests that KATP channels contribute substantially to skeletal muscle microvascular function during the crucial rest to contraction transition and therefore have the potential to mediate skeletal muscle performance decrements evident in disease states.Grant Funding Source: Supported by AHA Midwest Affiliate 0750090Z, NIH HL‐108328
Adenosine receptor activation influences postexercise skin blood flow (1106.20)
Authors: McGinn Ryan , Fujii Naoto , Kenny Glen 
Published: June 2021

Adenosine receptor activation influences postexercise skin blood flow R. N. McGinn, N. Fujii, G. P. Kenny Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, ON, K1N 6N5 Studies show that postexercise skin blood flow (SkBF) is reduced despite persistent hyperthermia. We have ascribed this to altered active vasodilation rather than adrenergic vasoconstriction (Kenny, Front Bio 15:259 2010). However, recent work shows that adenosine receptors mediates the decrease in SkBF following passive heat stress (Swift et al, Exp Phys, Epub 2013), thus it is plausible that adenosine receptors may also modulate postexercise SkBF. Eight males cycled for 15 min (85% VO2max) and then rested for 60 min at 25°C. Four microdialysis probes were inserted in the forearm and infused with: a) Ringer’s Lactate (CON); b) L‐NAME (nitric oxide synthase inhibitor); c) bretylium tosylate (BT; sympathetic nerve transmission inhibitor) or d) theophylline (THEO; adenosine receptor inhibitor). Cutaneous vascular conductance (CVC) was calculated as SkBF divided by mean arterial pressure. End‐exercise CVC was similar at all sites except L‐NAME (18% lower, P<0.01). CVC returned to resting levels after 20 min of recovery in CON (P=0.11). Compared with CON, CVC was reduced at L‐NAME at 10 min of recovery (P=0.03) and was increased at BT for the first 30 min of recovery (P<0.05). However, THEO was elevated throughout recovery (P蠄0.01) compared to CON. We show recovery SkBF to be modulated by nitric oxide (10 min) and adrenergic vasoconstriction (30 min), but adenosine receptors exerts a more prolonged effect (60 min).Abstract body: 1216/1220 characters Total: 1464/1720 charactersGrant Funding Source: Supported by: Natural Sciences and Engineering Research Council of Canada
The endothelial responses to low‐ and high‐intensity cycling with diesel exhaust exposure (1106.21)
Authors: Giles Luisa , Richard Normand , Ruan Jian , Tebbutt Scott , Carlsten Christopher , Koehle Michael 
Published: June 2021

Outdoor exercisers are frequently exposed to air pollution. How the endothelium responds to exercise in air pollution, and how these responses change with exercise intensity is unknown. The purpose of this study was to determine the endothelial responses to low‐ and high‐intensity cycling with diesel exhaust (DE) exposure. Eighteen males aged 24.56.2 yrs performed 30‐minute trials of low (30% of power at VO2peak) and high‐intensity (60% of power at VO2peak) cycling, and rest. For each subject, each trial was performed once breathing filtered air (FA) and once breathing DE (300ug/m3 of PM2.5) for a total of six trials, each separated by 7‐days. Prior to, immediately following, and 1 hour, and 2 hours post‐exposure flow‐mediated dilation (FMD), plasma nitrite/nitrate (NOx), intercellular adhesion molecule (ICAM)‐1, and vascular cell adhesion molecule (VCAM)‐1 were measured. Data were analyzed using repeated‐measures ANOVA. There were no main or interaction effects for FMD. DE exposure did not affect plasma VCAM‐1. Compared to the FA exposure, DE led to lower ICAM‐1 levels following high‐intensity exercise (p<0.05), while plasma NOx was increased (p<0.05). DE exposure does not differentially affect FMD post‐exercise, yet there are significant differences in key biomarkers that warrant further investigation.Grant Funding Source: Supported by: CASEM, Health Canada, the Fraser Basin Council, NSERC
Pre‐exercise whole‐body cooling decreases blood volume and oxygenated hemoglobin content in skeletal muscle during submaximal exercise (1106.7)
Authors: Gagnon Dominique , Kyröläinen Heikki , Gagnon Sheila , Herzig Karl‐Heinz , Rintamäki Hannu , Peltonen Juha 
Published: June 2021

Dynamic exercise and whole‐body cooling independently increase skeletal muscle tissue deoxygenation, yet their combined effects in muscular circulation are unknown. We investigated the effects of a cold environment on skeletal muscle blood volume and deoxygenation in eleven participants at 50% (walking) or 70% (running) of their peak VO2 for 60 min, in 22°C (NT), and 0°C without (CO) and with (PC) a pre‐exercise whole‐body cooling, which induced an increase in VO2 to 15%VO2peak. Near‐infrared spectroscopy (NIRS) derived signals for hemoglobin changes were measured continuously with NIRS on the vastus lateralis (VL) and the gastrocnemius (GM) muscles to determine changes in oxygenated (O2Hb), deoxygenated (HHb: indicating deoxygenation) and total (tHb: indicating blood volume) myo/hemoglobin concentrations (∆µM.L‐1). Total Hb was lower in PC (‐10.1±5.9 and ‐8.0±7.1 µM.L‐1) compared to NT (‐3.9±3.1 and ‐1.8±4.8 µM.L‐1) and CO (‐3.9±6.6 and 1.9±6.3 µM.L‐1) in walking and running respectively, in the VL but not in GM (p蠄0.001). This change in tHb was matched by O2Hb (p蠄0.001). No differences between conditions were observed in HHb. In conclusion, pre‐exercise whole‐body cooling decreased skeletal muscle blood volume which limited oxygenated hemoglobin availability but deoxygenation of the muscle during submaximal exercise was unaffected by the cold.Grant Funding Source: Supported by the Jenny and Antti Wihurin Foundation
Chronic carbon monoxide inhalation has a transient effect to reduce weight gain in mice fed a high fat diet (1107.3)
Authors: Hosick Peter , Ahmed Elhaitham , Gousset Monette , Granger Joey , Stec David 
Published: June 2021

We recently reported chronic treatment with carbon monoxide (CO) releasing molecules results in prevention of weight gain in mice fed a high fat diet. At present, we sought to determine the effect of chronic CO inhalation on 4 week old lean (Prevent) and 24 week old obese (Reverse) C57BL/6J mice fed a high diet. Two different CO inhalation exposures were used daily for 30 weeks; 28 parts per million (ppm) CO for 2 hours or 200 ppm CO for 1 hour. Body weight, fasted blood glucose and body composition were measured throughout the treatment. Food intake, O2 consumption, CO2 production, motor activity, and body heat production were measured at 28 weeks after the start of the experimental protocol. Compared to high fat diet controls inhalation treatment resulted in prevention and reversal of body weight (Prevent: 36.3gm vs. 42.6gm, p<0.05; Reverse: 45.6gm vs. 52.8gm; p<0.05), fat mass (Prevent: 14.8gm vs. 18.2gm, p<0.05; Reverse: 15.0gm vs. 18.6gm; p<0.05) and, blood glucose (Prevent: 110gm/dl vs. 150gm/dl, p<0.05; Reverse: 124gm/dl vs. 135gm/dl; p<0.05) over the first 10 weeks of treatment, however, this effect was not sustained. No differences were found in any other variables measured. Our results demonstrate that CO inhalation has a transient effect to prevent and reduce body weight which is not sustained in mice fed a high fat diet suggesting chronic CO inhalation therapy is not an effective treatment for long term weight loss.Grant Funding Source: Supported by grants from the NHLBI, PO1HL‐51971, HL088421 (D.E.S.) and 1T32HL105324 (P.A.H).
Intrauteruterine growth restriction increases tyrosine hydroxylase expression and propensity for addiction in low birth weight rats (1107.9)
Authors: Ondek Katelynn , Keen‐Rhinehart Erin 
Published: June 2021

Obesity is an epidemic of growing concern. Much research has focused on the roles of hypothalamic feeding peptides in energy balance and how these are affected by gestational programming, the impact of the intrauterine environment on adult physiology. Gestational programming may also affect the mesolimbocortical pathway, which projects from the ventral tegmental area (VTA) to the nucleus accumbens and prefrontal cortex in the brain and comprises a general reward system that reinforces natural behaviors such as eating, drinking, and sexual activity. Since low birth weight (LBW) humans tend to exhibit both obesity and a propensity toward addiction, we hypothesized that lack of maternal nutrition may cause baseline changes in dopaminergic activity that lead to perturbations in ingestive behavior. We utilized a traditional rat model of intrauterine growth restriction by placing dams on a 50% food‐restricted diet during the latter half of pregnancy. Offspring had significantly lower birth weights (5.6±0.08g vs. 6.5±0.06g, p<0.01) and significantly higher tyrosine hydroxylase (TH) immunoreactivity in the VTA than controls (159±19 vs. 454±88 A.U., p<0.05), suggesting that they would be more sensitive to rewarding stimuli. Therefore, we examined sucrose consumption in these animals over a 24 hour period and in a limited access paradigm where animals received 10% sucrose for 90 minute intervals. LBW offspring consumed significantly more (29±2ml vs. 23±1ml, p<0.05) when given limited access to sucrose. This suggests that LBW offspring increase ingestive behaviors when given limited access to substances with rewarding properties. Consequently, the dopaminergic reward system deserves closer examination to determine its role in LBW‐related obesity.Grant Funding Source: Supported by APS UGSRF Fellowship
Mitogen‐inducible gene 6 haploinsufficiency protects mice against streptozotocin‐induced diabetes (1108.11)
Authors: Chen Yi‐Chun , Colvin E. , Fueger Patrick 
Published: June 2021

Epidermal growth factor (EGF) and gastrin co‐administration is effective in correcting hyperglycemia and pancreatic beta cell mass deficiencies in various type 1 diabetes (T1D) rodent models, yet the failure in clinical translation of this treatment implies that EGF‐mediated tissue repair is a complicated process warranting further investigation. In this study, we aimed to determine if EGF receptor feedback inhibition by Mitogen‐inducible Gene 6 (Mig6) contributes to the development of T1D. We hypothesized that Mig6 haploinsufficiency, and hence heightened EGFR signaling, would abrogate T1D development in mice. To this end, we treated Mig6 haploinsufficient mice (Mig6+/‐) and their wild‐type littermates (Mig6+/+) with multiple low doses of streptozotocin (STZ) to induce beta cell death and diabetes. We found that whereas STZ‐treated Mig6+/+ mice became diabetic, STZ‐treated Mig6+/‐ mice remained fully glucose tolerant. Concurrently, STZ‐treated Mig6+/‐ mice exhibited preserved levels of circulating insulin following a glucose challenge. As insulin sensitivity was similar between Mig6+/‐ and Mig6+/+ mice, the preserved glucose tolerance in STZ‐treated Mig6+/‐ mice is likely the result of preserved beta cell function. Conversely, Mig6 overexpression in isolated islets compromises glucose‐stimulated insulin secretion. In vitro studies in 832/13 INS‐1 beta cells suggested that Mig6 hinders EGF receptor activation, thereby inhibiting EGF‐mediated DNA damage repair. Finally, STZ‐treated Mig6+/‐ mice have greater beta cell mass recovery at 20 days post‐STZ. These data demonstrate that a reduction in Mig6 promotes beta cell damage repair, thus abating the progression of T1D. Our work suggests that Mig6 may be a novel therapeutic target for T1D.Grant Funding Source: Supported by NIH grant DK078732 and a DeVault Fellowship from IUSM
GLP‐1 linked to an α2‐adrenergic antagonist enhances glucose disposal (1108.2)
Authors: Stein Lauren , Yosten Gina , Ananthakrishnan Kameswari , Wagner Josef , Lynch Ronald , Samson Willis 
Published: June 2021

β‐cells uniquely express both Glucagon Like Peptide‐1 (GLP‐1R) and α2Adrenergic Receptor (α2AR), as a combination. Activation of GLP‐1R potentiates, while α2AR agonists inhibit, glucose stimulated insulin secretion. We hypothesized that GLP‐1 linked to an α2AR antagonist Yohimbine (Yhb) would display enhanced binding and β‐cell specificity, and thus improve glucose disposal compared to GLP‐1 alone. Vehicle, or vehicle containing 1.0 nmole of GLP‐1, Yhb or the GLP‐1/Yhb conjugate were given i.a. 5 min before an i.a. infusion of 1 mg/kg glucose in conscious, unrestrained male rats. Blood was collected for plasma glucose monitoring and insulin determination via a jugular catheter prior to pretreatment, 5 min later prior to glucose infusion, and 1,5,10,15 and 30 min later. GLP‐1 or Yhb alone did not enhance glucose disposal compared to controls. However, glucose levels were cleared significantly faster in rats pretreated with the GLP‐1/Yhb conjugate, returning to baseline already 5 min after glucose infusion. Since, GLP‐1 did not potentiate recovery compared to the GLP‐1/Yhb at the same concentration, these findings are consistent with an increased affinity of GLP‐1, within the bivalent ligand, for binding to β‐cells in vivo. We conclude that the GLP‐1/Yhb conjugate, due to its enhanced β‐cell affinity and specificity, may be a promising therapeutic candidate for control of β‐cell function.Grant Funding Source: Juvenile Diabetes Research Foundation, NIH HL‐66023
Probing the intra‐islet control of beta cell function (1108.3)
Authors: Elrick Mollisa , Yosten Gina , Salvatori Alison , Samson W.K. 
Published: June 2021

Neuronostatin (NST) is produced in pancreatic delta cells from the somatostatin preprohormone, and has been shown to inhibit glucose‐stimulated insulin secretion from beta cells of primary islets, but not from isolated beta cell cultures. We have demonstrated that NST stimulates glucagon release and have hypothesized that this is necessary for the peptide’s in vivo effect to impair glucose tolerance. Here we demonstrate the action of NST to increase proglucagon message in alpha cells and identify a potential mechanism to be via phosphorylation of protein kinase A. The NST receptor, GPR107, is abundantly expressed in the pancreas, in particular in the alpha cell population and both the effect on proglucagon mRNA levels and PKA phosphrylation are absent in alpha cells in which the expression of the NST receptor has been compromised using siRNA. Taken together with our observation that NST infusion in conscious rats impairs glucose tolerance and that plasma levels of the peptide are elevated in the fasted compared to the fed or fasted‐refed state, our studies support the hypothesis that endogenous NST is a physiologically relevant determinant of islet cell function and may contribute to the hyperglucagonemia of the prediabetic state.Grant Funding Source: NIH HL66023