Pub Date : 2016-04-02DOI: 10.1080/23328940.2016.1179380
N. Vargas, F. Marino
ABSTRACT Exercise in heat stress exacerbates performance decrements compared to normothermic environments. It has been documented that the performance decrements are associated with reduced efferent drive from the central nervous system (CNS), however, specific factors that contribute to the decrements are not completely understood. During exertional heat stress, blood flow is preferentially distributed away from the intestinal area to supply the muscles and brain with oxygen. Consequently, the gastrointestinal barrier becomes increasingly permeable, resulting in the release of lipopolysaccharides (LPS, endotoxin) into the circulation. LPS leakage stimulates an acute-phase inflammatory response, including the release of interleukin (IL)-6 in response to an increasingly endotoxic environment. If LPS translocation is too great, heat shock, neurological dysfunction, or death may ensue. IL-6 acts initially in a pro-inflammatory manner during endotoxemia, but can attenuate the response through signaling the hypothalamic pituitary adrenal (HPA)-axis. Likewise, IL-6 is believed to be a thermoregulatory sensor in the gut during the febrile response, hence highlighting its role in periphery – to – brain communication. Recently, IL-6 has been implicated in signaling the CNS and influencing perceptions of fatigue and performance during exercise. Therefore, due to the cascade of events that occur during exertional heat stress, it is possible that the release of LPS and exacerbated response of IL-6 contributes to CNS modulation during exertional heat stress. The purpose of this review is to evaluate previous literature and discuss the potential role for IL-6 during exertional heat stress to modulate performance in favor of whole body preservation.
{"title":"Heat stress, gastrointestinal permeability and interleukin-6 signaling — Implications for exercise performance and fatigue","authors":"N. Vargas, F. Marino","doi":"10.1080/23328940.2016.1179380","DOIUrl":"https://doi.org/10.1080/23328940.2016.1179380","url":null,"abstract":"ABSTRACT Exercise in heat stress exacerbates performance decrements compared to normothermic environments. It has been documented that the performance decrements are associated with reduced efferent drive from the central nervous system (CNS), however, specific factors that contribute to the decrements are not completely understood. During exertional heat stress, blood flow is preferentially distributed away from the intestinal area to supply the muscles and brain with oxygen. Consequently, the gastrointestinal barrier becomes increasingly permeable, resulting in the release of lipopolysaccharides (LPS, endotoxin) into the circulation. LPS leakage stimulates an acute-phase inflammatory response, including the release of interleukin (IL)-6 in response to an increasingly endotoxic environment. If LPS translocation is too great, heat shock, neurological dysfunction, or death may ensue. IL-6 acts initially in a pro-inflammatory manner during endotoxemia, but can attenuate the response through signaling the hypothalamic pituitary adrenal (HPA)-axis. Likewise, IL-6 is believed to be a thermoregulatory sensor in the gut during the febrile response, hence highlighting its role in periphery – to – brain communication. Recently, IL-6 has been implicated in signaling the CNS and influencing perceptions of fatigue and performance during exercise. Therefore, due to the cascade of events that occur during exertional heat stress, it is possible that the release of LPS and exacerbated response of IL-6 contributes to CNS modulation during exertional heat stress. The purpose of this review is to evaluate previous literature and discuss the potential role for IL-6 during exertional heat stress to modulate performance in favor of whole body preservation.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77384265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-04-02DOI: 10.1080/23328940.2016.1139961
S. Maloney
I thank the editors of Temperature for the opportunity to provide an editorial comment on the recent article by Solym ar et al. We have known for some time that, when endothermic animals are fasted, their energy expenditure pathways are altered in a way that results in a decrease in core body temperature during the inactive phase of their daily activity cycle. The decrease in body temperature generally is viewed as adaptive, since the closer the animal’s body temperature is to ambient temperature, the less energy is required to defend body temperature. In the laboratory mouse, a few days of fasting takes body temperature to below 31 C, which, according to the definition employed in the paper under discussion, means that the mice enter torpor. There is no change (at least initially) in the core body temperature during the active phase of the daily cycle; that is counterintuitive but seems to be what occurs to the body temperature rhythm whenever mammals run low on energy. Mammals with normal body fat content run low on energy soon after starting to fast, and display heterothermy within a day or two of fast initiation. What happens to obese animals, which have a store of energy in body fat? That is what Solym ar et al. have investigated, for the first time. In the face of a complete fast, mice previously made obese did not enter torpor until their body mass approached that of the normal-mass mice, a process that took several weeks; the obese mice started with a body mass more than double that of the control lean mice Figure. 2 of the paper by Solym ar and colleagues shows, though, that less-dramatic but distinct changes in the temperature rhythm of the obese mice happened long before that, as do cardiovascular changes in fasted obese mice. Indeed, heart rate, blood pressure, and oxygen consumption fell more rapidly during a fast in obese mice than they did in lean mice, albeit from a higher baseline. Thermal physiologists certainly would want to know what signal to the thermoregulatory system differed, during the first days of fasting, between the obese and lean animals. Neither the obese nor the lean mice were eating, and so presumably the gut-derived peptides that have been implicated in the shortterm control of appetite and energy expenditure did not differ. It would be valuable to test that hypothesis by measuring those peptides. A better candidate would be leptin, the adipose-derived cytokine that has been implicated in the hypothermia of fasting. Leptin replacement in underfed and ob/ob mice reduces the incidence of torpor, and mice without dopamine b hydroxylase (an enzyme in the pathway to epinephrine and norepinephrine production) show neither a fall in leptin nor torpor when fasted Though Solym ar and colleagues did not measure leptin concentrations in their mice, it seems quite possible that the obese mice, with surplus energy, had a delayed fall in leptin with fasting. There don’t appear to be any long-term data on leptin concentrations
{"title":"Energy signaling in obese mice delays the impact of fasting on thermoregulation","authors":"S. Maloney","doi":"10.1080/23328940.2016.1139961","DOIUrl":"https://doi.org/10.1080/23328940.2016.1139961","url":null,"abstract":"I thank the editors of Temperature for the opportunity to provide an editorial comment on the recent article by Solym ar et al. We have known for some time that, when endothermic animals are fasted, their energy expenditure pathways are altered in a way that results in a decrease in core body temperature during the inactive phase of their daily activity cycle. The decrease in body temperature generally is viewed as adaptive, since the closer the animal’s body temperature is to ambient temperature, the less energy is required to defend body temperature. In the laboratory mouse, a few days of fasting takes body temperature to below 31 C, which, according to the definition employed in the paper under discussion, means that the mice enter torpor. There is no change (at least initially) in the core body temperature during the active phase of the daily cycle; that is counterintuitive but seems to be what occurs to the body temperature rhythm whenever mammals run low on energy. Mammals with normal body fat content run low on energy soon after starting to fast, and display heterothermy within a day or two of fast initiation. What happens to obese animals, which have a store of energy in body fat? That is what Solym ar et al. have investigated, for the first time. In the face of a complete fast, mice previously made obese did not enter torpor until their body mass approached that of the normal-mass mice, a process that took several weeks; the obese mice started with a body mass more than double that of the control lean mice Figure. 2 of the paper by Solym ar and colleagues shows, though, that less-dramatic but distinct changes in the temperature rhythm of the obese mice happened long before that, as do cardiovascular changes in fasted obese mice. Indeed, heart rate, blood pressure, and oxygen consumption fell more rapidly during a fast in obese mice than they did in lean mice, albeit from a higher baseline. Thermal physiologists certainly would want to know what signal to the thermoregulatory system differed, during the first days of fasting, between the obese and lean animals. Neither the obese nor the lean mice were eating, and so presumably the gut-derived peptides that have been implicated in the shortterm control of appetite and energy expenditure did not differ. It would be valuable to test that hypothesis by measuring those peptides. A better candidate would be leptin, the adipose-derived cytokine that has been implicated in the hypothermia of fasting. Leptin replacement in underfed and ob/ob mice reduces the incidence of torpor, and mice without dopamine b hydroxylase (an enzyme in the pathway to epinephrine and norepinephrine production) show neither a fall in leptin nor torpor when fasted Though Solym ar and colleagues did not measure leptin concentrations in their mice, it seems quite possible that the obese mice, with surplus energy, had a delayed fall in leptin with fasting. There don’t appear to be any long-term data on leptin concentrations","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81831970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-30DOI: 10.1080/23328940.2016.1166310
S. Hrometz, Jeremy A. Ebert, K. E. Grice, Sara M. Nowinski, E. Mills, B. Myers, J. E. Sprague
ABSTRACT Fatal hyperthermia as a result of 3,4-methylenedioxymethamphetamine (MDMA) use involves non-esterified free fatty acids (NEFA) and the activation of mitochondrial uncoupling proteins (UCP). NEFA gain access into skeletal muscle via specific transport proteins, including fatty acid translocase (FAT/CD36). FAT/CD36 expression is known to increase following chronic exercise. Previous studies have demonstrated the essential role of NEFA and UCP3 in MDMA-induced hyperthermia. The aims of the present study were to use a chronic exercise model (swimming for two consecutive hours per day, five days per wk for six wk) to increase FAT/CD36 expression in order to: 1) determine the contribution of FAT/CD36 in MDMA (20 mg/kg, s.c.)-mediated hyperthermia; and 2) examine the effects of the FAT/CD36 inhibitor, SSO (sulfo-N-succinimidyl oleate), on MDMA-induced hyperthermia in chronic exercise and sedentary control rats. MDMA administration resulted in hyperthermia in both sedentary and chronic exercise animals. However, MDMA-induced hyperthermia was significantly potentiated in the chronic exercise animals compared to sedentary animals. Additionally, chronic exercise significantly reduced body weight, increased FAT/CD36 protein expression levels and reduced plasma NEFA levels. The FAT/CD36 inhibitor, SSO (40 mg/kg, ip), significantly attenuated the hyperthermia mediated by MDMA in chronic exercised but not sedentary animals. Plasma NEFA levels were elevated in sedentary and exercised animals treated with SSO prior to MDMA suggesting attenuation of NEFA uptake into skeletal muscle. Chronic exercise did not alter skeletal muscle UCP3 protein expression levels. In conclusion, chronic exercise potentiates MDMA-mediated hyperthermia in a FAT/CD36 dependent fashion.
使用3,4-亚甲基二氧基甲基苯丙胺(MDMA)导致的致命性高热涉及非酯化游离脂肪酸(NEFA)和线粒体解偶联蛋白(UCP)的激活。NEFA通过特定的转运蛋白，包括脂肪酸转位酶(FAT/CD36)进入骨骼肌。已知脂肪/CD36表达在长期运动后增加。先前的研究已经证实了NEFA和UCP3在mdma诱导的热疗中的重要作用。本研究的目的是使用慢性运动模型(每天连续游泳2小时，每周5天，连续6周)增加FAT/CD36表达，以便:1)确定FAT/CD36在MDMA (20 mg/kg, s.c)介导的热疗中的作用;2)研究FAT/CD36抑制剂SSO(磺基- n -琥珀酰油酸酯)对慢性运动和久坐对照大鼠mdma诱导的高温的影响。在久坐和长期运动的动物中，MDMA均导致高热。然而，与久坐不动的动物相比，mdma诱导的热疗在慢性运动动物中显著增强。此外，慢性运动显著降低体重，增加脂肪/CD36蛋白表达水平，降低血浆NEFA水平。FAT/CD36抑制剂SSO (40 mg/kg, ip)可显著降低MDMA介导的慢性运动而非久坐动物的高热。在MDMA之前，久坐和运动的动物接受SSO治疗，血浆NEFA水平升高，表明骨骼肌对NEFA的吸收减弱。慢性运动不改变骨骼肌UCP3蛋白表达水平。总之，慢性运动以FAT/CD36依赖的方式增强mdma介导的热疗。
{"title":"Potentiation of Ecstasy-induced hyperthermia and FAT/CD36 expression in chronically exercised animals","authors":"S. Hrometz, Jeremy A. Ebert, K. E. Grice, Sara M. Nowinski, E. Mills, B. Myers, J. E. Sprague","doi":"10.1080/23328940.2016.1166310","DOIUrl":"https://doi.org/10.1080/23328940.2016.1166310","url":null,"abstract":"ABSTRACT Fatal hyperthermia as a result of 3,4-methylenedioxymethamphetamine (MDMA) use involves non-esterified free fatty acids (NEFA) and the activation of mitochondrial uncoupling proteins (UCP). NEFA gain access into skeletal muscle via specific transport proteins, including fatty acid translocase (FAT/CD36). FAT/CD36 expression is known to increase following chronic exercise. Previous studies have demonstrated the essential role of NEFA and UCP3 in MDMA-induced hyperthermia. The aims of the present study were to use a chronic exercise model (swimming for two consecutive hours per day, five days per wk for six wk) to increase FAT/CD36 expression in order to: 1) determine the contribution of FAT/CD36 in MDMA (20 mg/kg, s.c.)-mediated hyperthermia; and 2) examine the effects of the FAT/CD36 inhibitor, SSO (sulfo-N-succinimidyl oleate), on MDMA-induced hyperthermia in chronic exercise and sedentary control rats. MDMA administration resulted in hyperthermia in both sedentary and chronic exercise animals. However, MDMA-induced hyperthermia was significantly potentiated in the chronic exercise animals compared to sedentary animals. Additionally, chronic exercise significantly reduced body weight, increased FAT/CD36 protein expression levels and reduced plasma NEFA levels. The FAT/CD36 inhibitor, SSO (40 mg/kg, ip), significantly attenuated the hyperthermia mediated by MDMA in chronic exercised but not sedentary animals. Plasma NEFA levels were elevated in sedentary and exercised animals treated with SSO prior to MDMA suggesting attenuation of NEFA uptake into skeletal muscle. Chronic exercise did not alter skeletal muscle UCP3 protein expression levels. In conclusion, chronic exercise potentiates MDMA-mediated hyperthermia in a FAT/CD36 dependent fashion.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81852610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-16DOI: 10.1080/23328940.2016.1156215
K. N. Thomas, A. V. Van rij, S. Lucas, A. R. Gray, J. Cotter
ABSTRACT Exercise induces arterial flow patterns that promote functional and structural adaptations, improving functional capacity and reducing cardiovascular risk. While heat is produced by exercise, local and whole-body passive heating have recently been shown to generate favorable flow profiles and associated vascular adaptations in the upper limb. Flow responses to acute heating in the lower limbs have not yet been assessed, or directly compared to exercise, and other cardiovascular effects of lower-limb heating have not been fully characterized. Lower-limb heating by hot-water immersion (30 min at 42°C, to the waist) was compared to matched-duration treadmill running (65-75% age-predicted heart rate maximum) in 10 healthy, young adult volunteers. Superficial femoral artery shear rate assessed immediately upon completion was increased to a greater extent following immersion (mean ± SD: immersion +252 ± 137% vs. exercise +155 ± 69%, interaction: p = 0.032), while superficial femoral artery flow-mediated dilation was unchanged in either intervention. Immersion increased heart rate to a lower peak than during exercise (immersion +38 ± 3 beats·min-1 vs. exercise +87 ± 3 beats·min-1, interaction: p < 0.001), whereas only immersion reduced mean arterial pressure after exposure (−8 ± 3 mmHg, p = 0.012). Core temperature increased twice as much during immersion as exercise (+1.3 ± 0.4°C vs. +0.6 ± 0.4°C, p < 0.001). These data indicate that acute lower-limb hot-water immersion has potential to induce favorable shear stress patterns and cardiovascular responses within vessels prone to atherosclerosis. Whether repetition of lower-limb heating has long-term beneficial effects in such vasculature remains unexplored.
运动诱导动脉血流模式，促进功能和结构适应，提高功能能力，降低心血管风险。虽然热量是通过运动产生的，但最近的研究表明，局部和全身被动加热可以在上肢产生有利的血流分布和相关的血管适应性。下肢急性加热的血流反应尚未被评估，或与运动直接比较，下肢加热对心血管的其他影响尚未完全表征。将10名健康的年轻成年志愿者的下肢热水浸泡加热(42°C 30分钟，腰部)与匹配持续时间的跑步机跑步(65-75%的年龄预测心率最大值)进行比较。完成后立即评估的股浅动脉剪切率在浸泡后增加到更大程度(平均±SD:浸泡+252±137% vs运动+155±69%，相互作用:p = 0.032)，而股浅动脉血流介导的扩张在两种干预中都没有变化。浸泡将心率提高到比运动时更低的峰值(浸泡+38±3次·min-1 vs运动+87±3次·min-1，相互作用:p < 0.001)，而只有浸泡降低了暴露后的平均动脉压(- 8±3 mmHg, p = 0.012)。浸泡时的核心温度升高是运动时的两倍(+1.3±0.4°C vs +0.6±0.4°C, p < 0.001)。这些数据表明，急性下肢热水浸泡有可能在容易发生动脉粥样硬化的血管中诱导有利的剪切应力模式和心血管反应。下肢反复加热是否对此类脉管系统有长期的有益影响尚不清楚。
{"title":"Substantive hemodynamic and thermal strain upon completing lower-limb hot-water immersion; comparisons with treadmill running","authors":"K. N. Thomas, A. V. Van rij, S. Lucas, A. R. Gray, J. Cotter","doi":"10.1080/23328940.2016.1156215","DOIUrl":"https://doi.org/10.1080/23328940.2016.1156215","url":null,"abstract":"ABSTRACT Exercise induces arterial flow patterns that promote functional and structural adaptations, improving functional capacity and reducing cardiovascular risk. While heat is produced by exercise, local and whole-body passive heating have recently been shown to generate favorable flow profiles and associated vascular adaptations in the upper limb. Flow responses to acute heating in the lower limbs have not yet been assessed, or directly compared to exercise, and other cardiovascular effects of lower-limb heating have not been fully characterized. Lower-limb heating by hot-water immersion (30 min at 42°C, to the waist) was compared to matched-duration treadmill running (65-75% age-predicted heart rate maximum) in 10 healthy, young adult volunteers. Superficial femoral artery shear rate assessed immediately upon completion was increased to a greater extent following immersion (mean ± SD: immersion +252 ± 137% vs. exercise +155 ± 69%, interaction: p = 0.032), while superficial femoral artery flow-mediated dilation was unchanged in either intervention. Immersion increased heart rate to a lower peak than during exercise (immersion +38 ± 3 beats·min-1 vs. exercise +87 ± 3 beats·min-1, interaction: p < 0.001), whereas only immersion reduced mean arterial pressure after exposure (−8 ± 3 mmHg, p = 0.012). Core temperature increased twice as much during immersion as exercise (+1.3 ± 0.4°C vs. +0.6 ± 0.4°C, p < 0.001). These data indicate that acute lower-limb hot-water immersion has potential to induce favorable shear stress patterns and cardiovascular responses within vessels prone to atherosclerosis. Whether repetition of lower-limb heating has long-term beneficial effects in such vasculature remains unexplored.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86471823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-03DOI: 10.1080/23328940.2016.1159772
M. R. Che Jusoh, S. Stannard, T. Mündel
ABSTRACT The present study determined whether 0.8g/kg bodyweight sago ingested before (Pre-Sago) or during (Dur-Sago) exercise under warm-humid conditions (30 ± 2°C, 78 ± 3 % RH; 20 km·h−1 frontal airflow) conferred a performance and/or physiological benefit compared to a control (Control) condition. Eight trained, male cyclists/triathletes (45 ± 4 y, VO2peak: 65 ± 10 ml·kg−1·min−1, peak aerobic power: 397 ± 71 W) completed 3 15-min time-trials (∼75% VO2peak) pre-loaded with 45 min of steady-state (∼55% VO2peak) cycling following > 24 h standardization of training and diet. Measures of work completed, rectal and mean skin temperatures, heart rate, expiratory gases and venous blood samples were taken. Compared to Control, Pre-Sago resulted in a smaller rise in rectal temperature (0.3 ± 0.5°C) while heart rate increased to a greater extent (6 ± 13 beats·min−1) during exercise (both P < 0.05), however, compared to Control time-trial performance remained unaffected (Pre-Sago: −0.5 ± 4.0%, P > 0.05). During exercise, plasma glucose concentrations were maintained higher for Dur-Sago than Control (P < 0.05), however substrate oxidation rates remained similar (P > 0.05). Dur-Sago also resulted in a higher plasma sodium concentration (2 ± 2 mmol·l1) and lower whole-body sweat loss (544 ± 636 g) and, therefore, reduced plasma volume contraction (all P < 0.05). Heart rate increased to a greater extent (5 ± 13 beats·min−1) during Dur-Sago, yet compared to Control time-trial performance remained unaffected (+0.9 ± 2.3%, P > 0.05). Uniquely, these results indicate that during exercise heat stress feeding sago can result in some ‘beneficial’ physiological responses, however these do not translate to changes in exercise performance when performed in a post-prandial state.
{"title":"Physiologic and performance effects of sago supplementation before and during cycling in a warm-humid environment","authors":"M. R. Che Jusoh, S. Stannard, T. Mündel","doi":"10.1080/23328940.2016.1159772","DOIUrl":"https://doi.org/10.1080/23328940.2016.1159772","url":null,"abstract":"ABSTRACT The present study determined whether 0.8g/kg bodyweight sago ingested before (Pre-Sago) or during (Dur-Sago) exercise under warm-humid conditions (30 ± 2°C, 78 ± 3 % RH; 20 km·h−1 frontal airflow) conferred a performance and/or physiological benefit compared to a control (Control) condition. Eight trained, male cyclists/triathletes (45 ± 4 y, VO2peak: 65 ± 10 ml·kg−1·min−1, peak aerobic power: 397 ± 71 W) completed 3 15-min time-trials (∼75% VO2peak) pre-loaded with 45 min of steady-state (∼55% VO2peak) cycling following > 24 h standardization of training and diet. Measures of work completed, rectal and mean skin temperatures, heart rate, expiratory gases and venous blood samples were taken. Compared to Control, Pre-Sago resulted in a smaller rise in rectal temperature (0.3 ± 0.5°C) while heart rate increased to a greater extent (6 ± 13 beats·min−1) during exercise (both P < 0.05), however, compared to Control time-trial performance remained unaffected (Pre-Sago: −0.5 ± 4.0%, P > 0.05). During exercise, plasma glucose concentrations were maintained higher for Dur-Sago than Control (P < 0.05), however substrate oxidation rates remained similar (P > 0.05). Dur-Sago also resulted in a higher plasma sodium concentration (2 ± 2 mmol·l1) and lower whole-body sweat loss (544 ± 636 g) and, therefore, reduced plasma volume contraction (all P < 0.05). Heart rate increased to a greater extent (5 ± 13 beats·min−1) during Dur-Sago, yet compared to Control time-trial performance remained unaffected (+0.9 ± 2.3%, P > 0.05). Uniquely, these results indicate that during exercise heat stress feeding sago can result in some ‘beneficial’ physiological responses, however these do not translate to changes in exercise performance when performed in a post-prandial state.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79490814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.1080/23328940.2016.1157668
J. Deuis, I. Vetter
ABSTRACT Rodent models are frequently used to improve our understanding of the molecular mechanisms of pain and to develop novel analgesics. Robust behavioral assays that quantify nociceptive responses to different sensory modalities, such has heat, are therefore needed. Here, we describe a novel behavioral assay to quantify thermal paw withdrawal thresholds in mice, called the thermal probe test, and compared it with other methods commonly used to measure heat thresholds, namely the Hargreaves test and the dynamic and conventional hot plate tests. In the thermal probe test, a slightly rounded 2.5 mm diameter metal probe that heats on contact at a rate of 2.5°C/sec, is applied to the plantar surface of the hind paw in mice at a starting temperature of ∼37°C, and the temperature at which a withdrawal response occurs, designated as the paw withdrawal temperature, is automatically recorded. The thermal probe test is effective at quantifying thermal allodynia in carrageenan-induced inflammation (paw withdrawal temperature 3 h: contralateral, 50.3 ± 0.6°C; ipsilateral, 43.1 ± 1.0°C), burns injury (paw withdrawal temperature 3 d: contralateral, 50.8 ± 0.5°C; ipsilateral, 43.2 ± 0.6°C) and after topical capsaicin (paw withdrawal temperature: vehicle control, 49.7 ± 0.6°C; capsaicin, 44.8 ± 1.2°C), giving comparable results to the Hargreaves test. In addition, the thermal probe test can detect opioid mediated analgesia in carrageenan-induced inflammation. Therefore the thermal probe test is a novel behavioral assay effective for quantifying thermal allodynia and analgesia in mouse models of pain.
{"title":"The thermal probe test: A novel behavioral assay to quantify thermal paw withdrawal thresholds in mice","authors":"J. Deuis, I. Vetter","doi":"10.1080/23328940.2016.1157668","DOIUrl":"https://doi.org/10.1080/23328940.2016.1157668","url":null,"abstract":"ABSTRACT Rodent models are frequently used to improve our understanding of the molecular mechanisms of pain and to develop novel analgesics. Robust behavioral assays that quantify nociceptive responses to different sensory modalities, such has heat, are therefore needed. Here, we describe a novel behavioral assay to quantify thermal paw withdrawal thresholds in mice, called the thermal probe test, and compared it with other methods commonly used to measure heat thresholds, namely the Hargreaves test and the dynamic and conventional hot plate tests. In the thermal probe test, a slightly rounded 2.5 mm diameter metal probe that heats on contact at a rate of 2.5°C/sec, is applied to the plantar surface of the hind paw in mice at a starting temperature of ∼37°C, and the temperature at which a withdrawal response occurs, designated as the paw withdrawal temperature, is automatically recorded. The thermal probe test is effective at quantifying thermal allodynia in carrageenan-induced inflammation (paw withdrawal temperature 3 h: contralateral, 50.3 ± 0.6°C; ipsilateral, 43.1 ± 1.0°C), burns injury (paw withdrawal temperature 3 d: contralateral, 50.8 ± 0.5°C; ipsilateral, 43.2 ± 0.6°C) and after topical capsaicin (paw withdrawal temperature: vehicle control, 49.7 ± 0.6°C; capsaicin, 44.8 ± 1.2°C), giving comparable results to the Hargreaves test. In addition, the thermal probe test can detect opioid mediated analgesia in carrageenan-induced inflammation. Therefore the thermal probe test is a novel behavioral assay effective for quantifying thermal allodynia and analgesia in mouse models of pain.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83633072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26eCollection Date: 2016-04-01DOI: 10.1080/23328940.2016.1156214
Toby Mündel, Aaron Raman, Zachary J Schlader
We tested the hypothesis that skin temperature, specifically of the head, is capable of modulating thermal behavior during exercise in the cold. Following familiarization 8 young, healthy, recreationally active males completed 3 trials, each consisting of 30 minutes of self-paced cycle ergometry in 6°C. Participants were instructed to control their exercise work rate to achieve and maintain thermal comfort. On one occasion participants wore only shorts and shoes (Control) and on the 2 other occasions their head was either warmed (Warming) or cooled (Cooling). Work rate, rate of metabolic heat production, thermal perceptions, rectal, mean weighted skin and head temperatures were measured. Exercise work rate was reduced during Warming and augmented during Cooling after the first and second minutes of exercise, respectively (P ≤ 0.04), with the rate of metabolic heat production mirroring work rate. At this early stage of exercise (≤5 min) the changes over time for rectal temperature were negligible and similar (0.1 ± 0.1°C, P = 0.51), while the decrease in mean skin temperature was not different between all trials (1.7 ± 0.6°C, P = 0.13). Mean head temperature was either decreased (Control: 1.5 ± 1.1°C, Cooling: 2.9 ± 0.8°C, both P < 0.01) or increased (Warming: 1.7 ± 0.9°C, P < 0.01). Head thermal perception was warmer and more comfortable in Warming and cooler and less comfortable in Cooling (P < 0.01). Participants achieved thermal comfort similarly in all trials (P > 0.09) after 10 ± 7 min and this was maintained until the end of exercise. These results indicate that peripheral temperatures modulate thermal behavior in the cold.
{"title":"Head temperature modulates thermal behavior in the cold in humans.","authors":"Toby Mündel, Aaron Raman, Zachary J Schlader","doi":"10.1080/23328940.2016.1156214","DOIUrl":"10.1080/23328940.2016.1156214","url":null,"abstract":"<p><p>We tested the hypothesis that skin temperature, specifically of the head, is capable of modulating thermal behavior during exercise in the cold. Following familiarization 8 young, healthy, recreationally active males completed 3 trials, each consisting of 30 minutes of self-paced cycle ergometry in 6°C. Participants were instructed to control their exercise work rate to achieve and maintain thermal comfort. On one occasion participants wore only shorts and shoes (Control) and on the 2 other occasions their head was either warmed (Warming) or cooled (Cooling). Work rate, rate of metabolic heat production, thermal perceptions, rectal, mean weighted skin and head temperatures were measured. Exercise work rate was reduced during Warming and augmented during Cooling after the first and second minutes of exercise, respectively (P ≤ 0.04), with the rate of metabolic heat production mirroring work rate. At this early stage of exercise (≤5 min) the changes over time for rectal temperature were negligible and similar (0.1 ± 0.1°C, P = 0.51), while the decrease in mean skin temperature was not different between all trials (1.7 ± 0.6°C, P = 0.13). Mean head temperature was either decreased (Control: 1.5 ± 1.1°C, Cooling: 2.9 ± 0.8°C, both P < 0.01) or increased (Warming: 1.7 ± 0.9°C, P < 0.01). Head thermal perception was warmer and more comfortable in Warming and cooler and less comfortable in Cooling (P < 0.01). Participants achieved thermal comfort similarly in all trials (P > 0.09) after 10 ± 7 min and this was maintained until the end of exercise. These results indicate that peripheral temperatures modulate thermal behavior in the cold.</p>","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4965003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79269142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.1080/23328940.2016.1156801
A. Hunt, D. Billing, M. J. Patterson, Joanne N. Caldwell
ABSTRACT Military activities in hot environments pose 2 competing demands: the requirement to perform realistic training to develop operational capability with the necessity to protect armed forces personnel against heat-related illness. To ascertain whether work duration limits for protection against heat-related illness restrict military activities, this study examined the heat strain and risks of heat-related illness when conducting a military activity above the prescribed work duration limits. Thirty-seven soldiers conducted a march (10 km; ∼5.5 km h−1) carrying 41.8 ± 3.6 kg of equipment in 23.1 ± 1.8°C wet-bulb globe temperature. Body core temperature was recorded throughout and upon completion, or withdrawal, participants rated their severity of heat-related symptoms. Twenty-three soldiers completed the march in 107 ± 6.4 min (Completers); 9 were symptomatic for heat exhaustion, withdrawing after 71.6 ± 10.1 min (Symptomatic); and five were removed for body core temperature above 39.0°C (Hyperthermic) after 58.4 ± 4.5 min. Body core temperature was significantly higher in the Hyperthermic (39.03 ± 0.26°C), than Symptomatic (38.34 ± 0.44°C; P = 0.007) and Completers (37.94 ± 0.37°C; P<0.001) after 50 min. Heat-related symptom severity was significantly higher among Symptomatic (28.4 ± 11.8) compared to Completers (15.0 ± 9.8, P = 0.006) and Hyperthermic (13.0 ± 9.6, P = 0.029). The force protection provided by work duration limits may be preventing the majority of personnel from conducting activities in hot environments, thereby constraining a commander's mandate to develop an optimised military force. The dissociation between heat-related symptoms and body core temperature elevation suggests that the physiological mechanisms underpinning exhaustion during exertional heat stress should be re-examined to determine the most appropriate physiological criteria for prescribing work duration limits.
{"title":"Heat strain during military training activities: The dilemma of balancing force protection and operational capability","authors":"A. Hunt, D. Billing, M. J. Patterson, Joanne N. Caldwell","doi":"10.1080/23328940.2016.1156801","DOIUrl":"https://doi.org/10.1080/23328940.2016.1156801","url":null,"abstract":"ABSTRACT Military activities in hot environments pose 2 competing demands: the requirement to perform realistic training to develop operational capability with the necessity to protect armed forces personnel against heat-related illness. To ascertain whether work duration limits for protection against heat-related illness restrict military activities, this study examined the heat strain and risks of heat-related illness when conducting a military activity above the prescribed work duration limits. Thirty-seven soldiers conducted a march (10 km; ∼5.5 km h−1) carrying 41.8 ± 3.6 kg of equipment in 23.1 ± 1.8°C wet-bulb globe temperature. Body core temperature was recorded throughout and upon completion, or withdrawal, participants rated their severity of heat-related symptoms. Twenty-three soldiers completed the march in 107 ± 6.4 min (Completers); 9 were symptomatic for heat exhaustion, withdrawing after 71.6 ± 10.1 min (Symptomatic); and five were removed for body core temperature above 39.0°C (Hyperthermic) after 58.4 ± 4.5 min. Body core temperature was significantly higher in the Hyperthermic (39.03 ± 0.26°C), than Symptomatic (38.34 ± 0.44°C; P = 0.007) and Completers (37.94 ± 0.37°C; P<0.001) after 50 min. Heat-related symptom severity was significantly higher among Symptomatic (28.4 ± 11.8) compared to Completers (15.0 ± 9.8, P = 0.006) and Hyperthermic (13.0 ± 9.6, P = 0.029). The force protection provided by work duration limits may be preventing the majority of personnel from conducting activities in hot environments, thereby constraining a commander's mandate to develop an optimised military force. The dissociation between heat-related symptoms and body core temperature elevation suggests that the physiological mechanisms underpinning exhaustion during exertional heat stress should be re-examined to determine the most appropriate physiological criteria for prescribing work duration limits.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77777895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.1080/23328940.2016.1157665
J. Brock, R. McAllen
ABSTRACT We review the evidence for thermoregulatory temperature sensors in the mammalian spinal cord and reach the following conclusions. 1) Spinal cord temperature contributes physiologically to temperature regulation. 2) Parallel anterolateral ascending pathways transmit signals from spinal cooling and spinal warming: they overlap with the respective axon pathways of the dorsal horn neurons that are driven by peripheral cold- and warm-sensitive afferents. 3) We hypothesize that these ‘cold’ and ‘warm’ ascending pathways transmit all extracranial thermosensory information to the brain. 4) Cutaneous cold afferents can be activated not only by cooling the skin but also by cooling sites along their axons: we consider that this is functionally insignificant in vivo. 5) By a presynaptic action on their central terminals, local spinal cooling enhances neurotransmission from incoming ‘cold’ afferent action potentials to second order neurons in the dorsal horn; this effect disappears when the spinal cord is warm. 6) Spinal warm sensitivity is due to warm-sensitive miniature vesicular transmitter release from afferent terminals in the dorsal horn: this effect is powerful enough to excite second order neurons in the ‘warm’ pathway independently of any incoming sensory traffic. 7) Distinct but related presynaptic mechanisms at cold- and warm-sensitive afferent terminals can thus account for the thermoregulatory actions of spinal cord temperature.
{"title":"Spinal cord thermosensitivity: An afferent phenomenon?","authors":"J. Brock, R. McAllen","doi":"10.1080/23328940.2016.1157665","DOIUrl":"https://doi.org/10.1080/23328940.2016.1157665","url":null,"abstract":"ABSTRACT We review the evidence for thermoregulatory temperature sensors in the mammalian spinal cord and reach the following conclusions. 1) Spinal cord temperature contributes physiologically to temperature regulation. 2) Parallel anterolateral ascending pathways transmit signals from spinal cooling and spinal warming: they overlap with the respective axon pathways of the dorsal horn neurons that are driven by peripheral cold- and warm-sensitive afferents. 3) We hypothesize that these ‘cold’ and ‘warm’ ascending pathways transmit all extracranial thermosensory information to the brain. 4) Cutaneous cold afferents can be activated not only by cooling the skin but also by cooling sites along their axons: we consider that this is functionally insignificant in vivo. 5) By a presynaptic action on their central terminals, local spinal cooling enhances neurotransmission from incoming ‘cold’ afferent action potentials to second order neurons in the dorsal horn; this effect disappears when the spinal cord is warm. 6) Spinal warm sensitivity is due to warm-sensitive miniature vesicular transmitter release from afferent terminals in the dorsal horn: this effect is powerful enough to excite second order neurons in the ‘warm’ pathway independently of any incoming sensory traffic. 7) Distinct but related presynaptic mechanisms at cold- and warm-sensitive afferent terminals can thus account for the thermoregulatory actions of spinal cord temperature.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79927209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.1080/23328940.2016.1153360
J. Stephens, A. Schiemann, C. Roesl, Dorota M. Miller, S. Massey, N. Pollock, T. Bulger, K. Stowell
ABSTRACT Malignant hyperthermia manifests as a rapid and sustained rise in temperature in response to pharmacological triggering agents, e.g. inhalational anesthetics and the muscle relaxant suxamethonium. Other clinical signs include an increase in end-tidal CO2, increased O2 consumption, as well as tachycardia, and if untreated a malignant hyperthermia episode can result in death. The metabolic changes are caused by dysregulation of skeletal muscle Ca2+ homeostasis, resulting from a defective ryanodine receptor Ca2+ channel, which resides in the sarcoplasmic reticulum and controls the flux of Ca2+ ions from intracellular stores to the cytoplasm. Most genetic variants associated with susceptibility to malignant hyperthermia occur in the RYR1 gene encoding the ryanodine receptor type 1. While malignant hyperthermia susceptibility can be diagnosed by in vitro contracture testing of skeletal muscle biopsy tissue, it is advantageous to use DNA testing. Currently only 35 of over 400 potential variants in RYR1 have been classed as functionally causative of malignant hyperthermia and thus can be used for DNA diagnostic tests. Here we describe functional analysis of 2 RYR1 variants (c. 7042_7044delCAG, p.ΔGlu2348 and c.641C>T, p.Thr214Met) that occur in the same malignant hyperthermia susceptible family. The p.Glu2348 deletion, causes hypersensitivity to ryanodine receptor agonists using in vitro analysis of cloned human RYR1 cDNA expressed in HEK293T cells, while the Thr214Met substitution, does not appear to significantly alter sensitivity to agonist in the same system. We suggest that the c. 7042_7044delCAG, p.ΔGlu2348 RYR1 variant could be added to the list of diagnostic mutations for susceptibility to malignant hyperthermia.
{"title":"Functional analysis of RYR1 variants linked to malignant hyperthermia","authors":"J. Stephens, A. Schiemann, C. Roesl, Dorota M. Miller, S. Massey, N. Pollock, T. Bulger, K. Stowell","doi":"10.1080/23328940.2016.1153360","DOIUrl":"https://doi.org/10.1080/23328940.2016.1153360","url":null,"abstract":"ABSTRACT Malignant hyperthermia manifests as a rapid and sustained rise in temperature in response to pharmacological triggering agents, e.g. inhalational anesthetics and the muscle relaxant suxamethonium. Other clinical signs include an increase in end-tidal CO2, increased O2 consumption, as well as tachycardia, and if untreated a malignant hyperthermia episode can result in death. The metabolic changes are caused by dysregulation of skeletal muscle Ca2+ homeostasis, resulting from a defective ryanodine receptor Ca2+ channel, which resides in the sarcoplasmic reticulum and controls the flux of Ca2+ ions from intracellular stores to the cytoplasm. Most genetic variants associated with susceptibility to malignant hyperthermia occur in the RYR1 gene encoding the ryanodine receptor type 1. While malignant hyperthermia susceptibility can be diagnosed by in vitro contracture testing of skeletal muscle biopsy tissue, it is advantageous to use DNA testing. Currently only 35 of over 400 potential variants in RYR1 have been classed as functionally causative of malignant hyperthermia and thus can be used for DNA diagnostic tests. Here we describe functional analysis of 2 RYR1 variants (c. 7042_7044delCAG, p.ΔGlu2348 and c.641C>T, p.Thr214Met) that occur in the same malignant hyperthermia susceptible family. The p.Glu2348 deletion, causes hypersensitivity to ryanodine receptor agonists using in vitro analysis of cloned human RYR1 cDNA expressed in HEK293T cells, while the Thr214Met substitution, does not appear to significantly alter sensitivity to agonist in the same system. We suggest that the c. 7042_7044delCAG, p.ΔGlu2348 RYR1 variant could be added to the list of diagnostic mutations for susceptibility to malignant hyperthermia.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82933035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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