Pub Date : 2016-04-02DOI: 10.1080/23328940.2016.1165786
P. Laursen
Like many of us, I love sport. I care deeply about athlete performance. It is my job to. That passion has enabled me to wear a number of hats in the arena. I’ve been an athlete (triathlon and cycling), a coach, a professor, and an applied sport scientist. Residing in this sometimes messy, often fun, middle-space, between research, theory and application, which do not always align, I’ve been able to make some observations, identify some problems, and foster some solutions. The topic of this editorial is a story about how I’ve assisted to bridge a small gap between science and practice, by mixing scientific understanding and ingenuity to alter athlete temperature. Last year I delivered two presentations in Paris on this topic, entitled: Keeping your cool: How fluid temperature affects thermal comfort and performance in the heat. My opening slide included the picture, shown as Figure 1. Here we have two of today’s world-best triathletes, Andrea Hewitt and Rachel Klamer, racing in the Gold Coast World Series Race in Australia (April 2015). In this race, it was 28 Celsius, with high humidity. To me, this picture speaks volumes about what’s really important when maximizing performance in hot environments. Consider the following question: what’s essential to these athletes when they have cold fluid in their hands? Are they thirsty and dehydrated, or is it more likely that their brain/body is overheating? If these athletes were thirsty, and fluid consumption mattered to their brain at that point, then surely they would be more interested in drinking that fluid; but clearly they are not. When it’s on, with metabolic heat production sky high, (as it is in most of the Olympic sports we deal with) it’s brain temperature, or perhaps more accurately the brain’s recognition of a body that’s overheating that matters. So let’s go back in time a bit and allow me to tell you the story about how I became involved in discovering the importance of fluid temperature for performance in the heat. While employed as a lecturer at Edith Cowen University (ECU) in Perth Australia, I enjoyed collaborating with Dr David Martin, an Australian Institute of Sport Senior Physiologist, in the area of precooling athletes before competition in the heat in order to improve performance. It was 2006, and the Beijing Olympics were at the forefront of our minds. We’d put our heads together previously for the Athens’ Games strategy where we had arrived at the position that the best precooling strategy possible, was a combining a plunge pool maneuver with an ice jacket to retain body coolness. Beijing, expected to be just as hot, was up next, and we were still searching for something effective and practical to keep athletes cool. Meanwhile, a sport scientist up in Darwin, named Matt Brearly, was doing some experimentation during his bike rides. Of course, it doesn’t get much hotter in Australia than this place. Very simply, he was looking at what happened to his performance times riding home
{"title":"From science to practice: Development of a thermally-insulated ice slushy dispensing bottle that helps athletes “keep their cool” in hot temperatures","authors":"P. Laursen","doi":"10.1080/23328940.2016.1165786","DOIUrl":"https://doi.org/10.1080/23328940.2016.1165786","url":null,"abstract":"Like many of us, I love sport. I care deeply about athlete performance. It is my job to. That passion has enabled me to wear a number of hats in the arena. I’ve been an athlete (triathlon and cycling), a coach, a professor, and an applied sport scientist. Residing in this sometimes messy, often fun, middle-space, between research, theory and application, which do not always align, I’ve been able to make some observations, identify some problems, and foster some solutions. The topic of this editorial is a story about how I’ve assisted to bridge a small gap between science and practice, by mixing scientific understanding and ingenuity to alter athlete temperature. Last year I delivered two presentations in Paris on this topic, entitled: Keeping your cool: How fluid temperature affects thermal comfort and performance in the heat. My opening slide included the picture, shown as Figure 1. Here we have two of today’s world-best triathletes, Andrea Hewitt and Rachel Klamer, racing in the Gold Coast World Series Race in Australia (April 2015). In this race, it was 28 Celsius, with high humidity. To me, this picture speaks volumes about what’s really important when maximizing performance in hot environments. Consider the following question: what’s essential to these athletes when they have cold fluid in their hands? Are they thirsty and dehydrated, or is it more likely that their brain/body is overheating? If these athletes were thirsty, and fluid consumption mattered to their brain at that point, then surely they would be more interested in drinking that fluid; but clearly they are not. When it’s on, with metabolic heat production sky high, (as it is in most of the Olympic sports we deal with) it’s brain temperature, or perhaps more accurately the brain’s recognition of a body that’s overheating that matters. So let’s go back in time a bit and allow me to tell you the story about how I became involved in discovering the importance of fluid temperature for performance in the heat. While employed as a lecturer at Edith Cowen University (ECU) in Perth Australia, I enjoyed collaborating with Dr David Martin, an Australian Institute of Sport Senior Physiologist, in the area of precooling athletes before competition in the heat in order to improve performance. It was 2006, and the Beijing Olympics were at the forefront of our minds. We’d put our heads together previously for the Athens’ Games strategy where we had arrived at the position that the best precooling strategy possible, was a combining a plunge pool maneuver with an ice jacket to retain body coolness. Beijing, expected to be just as hot, was up next, and we were still searching for something effective and practical to keep athletes cool. Meanwhile, a sport scientist up in Darwin, named Matt Brearly, was doing some experimentation during his bike rides. Of course, it doesn’t get much hotter in Australia than this place. Very simply, he was looking at what happened to his performance times riding home","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"12 1","pages":"187 - 190"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88620633","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: 10.1080/23328940.2016.1174794
M. Farrell
ABSTRACT Functional brain imaging of responses to thermal challenge in humans provides a viable method to implicate widespread neuroanatomical regions in the processes of thermoregulation. Thus far, functional neuroimaging techniques have been used infrequently in humans to investigate thermoregulation, although preliminary outcomes have been informative and certainly encourage further forays into this field of enquiry. At this juncture, sustained regional brain activations in response to prolonged changes in body temperature are yet to be definitively characterized, but it would appear that thermoregulatory regions are widely distributed throughout the hemispheres of the human brain. Of those autonomic responses to thermal challenge investigated so far, the loci of associated brainstem responses in human are homologous with other species. However, human imaging studies have also implicated a wide range of forebrain regions in thermal sensations and autonomic responses that extend beyond outcomes reported in other species. There is considerable impetus to continue human functional neuroimaging of thermoregulatory responses because of the unique opportunities presented by the method to survey regions across the whole brain in compliant, conscious participants.
{"title":"Regional brain responses in humans during body heating and cooling","authors":"M. Farrell","doi":"10.1080/23328940.2016.1174794","DOIUrl":"https://doi.org/10.1080/23328940.2016.1174794","url":null,"abstract":"ABSTRACT Functional brain imaging of responses to thermal challenge in humans provides a viable method to implicate widespread neuroanatomical regions in the processes of thermoregulation. Thus far, functional neuroimaging techniques have been used infrequently in humans to investigate thermoregulation, although preliminary outcomes have been informative and certainly encourage further forays into this field of enquiry. At this juncture, sustained regional brain activations in response to prolonged changes in body temperature are yet to be definitively characterized, but it would appear that thermoregulatory regions are widely distributed throughout the hemispheres of the human brain. Of those autonomic responses to thermal challenge investigated so far, the loci of associated brainstem responses in human are homologous with other species. However, human imaging studies have also implicated a wide range of forebrain regions in thermal sensations and autonomic responses that extend beyond outcomes reported in other species. There is considerable impetus to continue human functional neuroimaging of thermoregulatory responses because of the unique opportunities presented by the method to survey regions across the whole brain in compliant, conscious participants.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"1 1","pages":"220 - 231"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89790633","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: 10.1080/23328940.2016.1185206
N. Morris, O. Jay
It’s almost that time again. With the 2016 summer Olympics in Rio just around the corner, the season of dreams is upon us. It’s the time when we watch seemingly real life super heroes push themselves to the limit, while bringing back early memories of when we wanted to be those athletes on TV that children look up to. At the Rio games, not only will these super humans compete against each other, they must also contend with the hot and balmy conditions. Some of us, during sporting activities, may be familiar with battling against our own minds and dealing with the oppressive force of the heat, when we would happily accept any measure that alleviates the discomfort of our exertions. With respect to endurance sports in the heat, this relief can come with sipping cool water, spraying our face with a cool mist, or wrapping an ice towel around our necks. The cover photo of this edition of Temperature illustrates a scenario of two elite triathletes, Andrea Hewitt (on the left) and Rachel Klamer (on the right), dousing themselves with water from their bottles in order to cope with both the internal heat they are producing through muscular contractions, and the external heat from the surrounding environment. We sometimes see athletes self-dousing with water, or have done it ourselves, in order to attain an immediate relief from the heat rather than taking the time to drink. But is this a smart move? Shouldn’t we just drink the water instead, or even better – drink iced water? To answer this question, we must consider how much heat we can lose to water in its various forms. The most straightforward way is to do so via conduction following the ingestion of cold water. The amount of heat lost is determined by the temperature difference between the ingested water and the body core, the volume of water drunk, and the specific heat capacity of water, i.e. the amount of heat energy needed to warm up 1 g of water by 1 C, which is 4.184 J/g/ C. We can dramatically increase the amount of heat lost to water by adding ice into the mix, as the amount of heat required to melt ice, known as the latent heat of fusion, is much greater than the specific heat capacity of water at 334 J/g. It is this much greater potential for heat loss that has led to the recent trend of athletes consuming ice slurry drinks, a mixture of shredded ice and water, before or during their athletic activities. Despite this improved potential for heat dissipation, melting ice is still a far cry from the amount of heat we can lose through the evaporation of water, as just one gram of evaporated water results in the liberation of a massive 2430 J of latent heat energy. To put these different cooling strategies into context, we can directly compare heat loss potential with a fixed volume of water (Fig. 1). Assuming a core body temperature of 38 C, drinking one glass (250 ml) of 1 C water would result in a net heat loss of 39 kJ. Whereas if the contents of that glass were changed to half-water and hal
又快到那个时候了。随着2016年里约夏季奥运会的临近，我们迎来了梦想的季节。在这段时间里，我们看着看似真实的超级英雄把自己推向极限，同时回想起我们想成为孩子们崇拜的电视上的运动员的早期记忆。在里约奥运会上，这些超级人类不仅要相互竞争，还必须与炎热和温暖的环境作斗争。在体育活动中，我们中的一些人可能熟悉与自己的思想作斗争和应对高温的压迫力，当我们高兴地接受任何减轻我们努力时的不适的措施时。在炎热的天气里进行耐力运动，可以喝点凉水，在脸上喷点凉雾，或者在脖子上围一条冰巾。这期《温度》杂志的封面照片描绘了两名优秀的铁人三项运动员安德里亚·休伊特(左)和雷切尔·克莱默(右)的场景，他们从瓶子里拿水浸泡自己，以应对肌肉收缩产生的内部热量和周围环境产生的外部热量。我们有时会看到运动员自己用水洗澡，或者自己用水洗澡，目的是为了立即解暑，而不是花时间喝水。但这是明智之举吗?难道我们不应该直接喝水，或者更好的办法是——喝冰水吗?要回答这个问题，我们必须考虑有多少热量散失给各种形式的水。最直接的方法是在摄入冷水后通过传导。失去的热量是由摄入水和身体之间的温差核心,水的体积醉了,和水的比热容,即所需的热能加热1克水1 C,它是4.184 J / g / C .我们可以显著增加的热量损失向混合,水通过添加冰融化冰所需的热量,称为熔化潜热,比水的334 J/g比热容大得多。正是这种更大的热量流失的可能性，导致了最近运动员在运动前或运动期间喝冰浆饮料的趋势，冰浆饮料是一种碎冰和水的混合物。尽管在散热方面有了很大的提高，但冰的融化与水的蒸发所能损失的热量相比仍然相去甚远，因为仅仅一克蒸发的水就能释放出2430焦的巨大潜热能量。为了将这些不同的冷却策略置于背景中，我们可以直接比较固定体积的水的热损失潜力(图1)。假设核心体温为38℃，饮用一杯(250毫升)1℃的水将导致39千焦的净热损失。然而，如果杯子的内容物变成一半水一半冰，潜在的热损失将增加一倍以上，达到81千焦。然而，如果我们能把这250毫升的水扩散到皮肤表面，让它全部蒸发掉，最终的热量损失将达到惊人的607千焦。需要注意的是，虽然摄入水分而不洒出来相对容易，但要确保250毫升的水分布在皮肤上，使其全部蒸发就困难得多。然而，重要的是要记住，即使只有15%的水从皮肤上蒸发掉，热量损失仍然比摄入整个250毫升冰浆要大。另一个需要考虑的问题是，根据水蒸发的可能性，我们进行运动的方式和环境可能会改变用水浸泡的效果。例如，干燥的空气和高风速极大地促进了蒸发，因此在沙漠中骑行可能是用水自浇的理想情况，因为大部分水很可能蒸发掉。相反，高水平的环境湿度和低空气
{"title":"To drink or to pour: How should athletes use water to cool themselves?","authors":"N. Morris, O. Jay","doi":"10.1080/23328940.2016.1185206","DOIUrl":"https://doi.org/10.1080/23328940.2016.1185206","url":null,"abstract":"It’s almost that time again. With the 2016 summer Olympics in Rio just around the corner, the season of dreams is upon us. It’s the time when we watch seemingly real life super heroes push themselves to the limit, while bringing back early memories of when we wanted to be those athletes on TV that children look up to. At the Rio games, not only will these super humans compete against each other, they must also contend with the hot and balmy conditions. Some of us, during sporting activities, may be familiar with battling against our own minds and dealing with the oppressive force of the heat, when we would happily accept any measure that alleviates the discomfort of our exertions. With respect to endurance sports in the heat, this relief can come with sipping cool water, spraying our face with a cool mist, or wrapping an ice towel around our necks. The cover photo of this edition of Temperature illustrates a scenario of two elite triathletes, Andrea Hewitt (on the left) and Rachel Klamer (on the right), dousing themselves with water from their bottles in order to cope with both the internal heat they are producing through muscular contractions, and the external heat from the surrounding environment. We sometimes see athletes self-dousing with water, or have done it ourselves, in order to attain an immediate relief from the heat rather than taking the time to drink. But is this a smart move? Shouldn’t we just drink the water instead, or even better – drink iced water? To answer this question, we must consider how much heat we can lose to water in its various forms. The most straightforward way is to do so via conduction following the ingestion of cold water. The amount of heat lost is determined by the temperature difference between the ingested water and the body core, the volume of water drunk, and the specific heat capacity of water, i.e. the amount of heat energy needed to warm up 1 g of water by 1 C, which is 4.184 J/g/ C. We can dramatically increase the amount of heat lost to water by adding ice into the mix, as the amount of heat required to melt ice, known as the latent heat of fusion, is much greater than the specific heat capacity of water at 334 J/g. It is this much greater potential for heat loss that has led to the recent trend of athletes consuming ice slurry drinks, a mixture of shredded ice and water, before or during their athletic activities. Despite this improved potential for heat dissipation, melting ice is still a far cry from the amount of heat we can lose through the evaporation of water, as just one gram of evaporated water results in the liberation of a massive 2430 J of latent heat energy. To put these different cooling strategies into context, we can directly compare heat loss potential with a fixed volume of water (Fig. 1). Assuming a core body temperature of 38 C, drinking one glass (250 ml) of 1 C water would result in a net heat loss of 39 kJ. Whereas if the contents of that glass were changed to half-water and hal","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"474 1","pages":"191 - 194"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74488497","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: 10.1080/23328940.2016.1171281
Gavin Travers, D. Nichols, A. Farooq, S. Racinais, J. Périard
ABSTRACT Aim: Intestinal temperature telemetry systems are promising monitoring and research tools in athletes. However, the additional equipment that must be carried to continuously record temperature data limits their use to training. The purpose of this study was to assess the validity and reliability of a new gastrointestinal temperature data logging and telemetry system (e-Celsius™) during water bath experimentation and exercise trials. Materials and Methods: Temperature readings of 23 pairs of e-Celsius (TeC) and VitalSense (TVS) ingestible capsules were compared to rectal thermistor responses (Trec) at 35, 38.5 and 42°C in a water bath. Devices were also assessed in vivo during steady-state cycling (n = 11) and intermittent running (n = 11) in hot conditions. Results: The water bath experiment showed TVS and TeC under-reported Trec (P<0.001). This underestimation of Trec also occurred during both cycling (mean bias vs TVS: 0.21°C, ICC: 0.84, 95% CI: 0.66–0.91; mean bias vs. TeC: 0.44°C, ICC: 0.68, 95% CI: 0.07–0.86, P<0.05) and running trials (mean bias vs. TVS: 0.15°C, ICC: 0.92, 95% CI: 0.83–0.96; mean bias vs. TeC: 0.25, ICC: 0.86, 95% CI: 0.61–0.94, P<0.05). However, calibrating the devices attenuated this difference during cycling and eliminated it during running. During recovery following cycling exercise, TeC and TVS were significantly lower than Trec despite calibration (P<0.01). Conclusion: These results indicate that both TeC and TVS under-report Trec during steady-state and intermittent exercise in the heat, with TeC predicting Trec with the least accuracy of the telemetry devices. It is therefore recommended to calibrate these devices at multiple temperatures prior to use.
{"title":"Validation of an ingestible temperature data logging and telemetry system during exercise in the heat","authors":"Gavin Travers, D. Nichols, A. Farooq, S. Racinais, J. Périard","doi":"10.1080/23328940.2016.1171281","DOIUrl":"https://doi.org/10.1080/23328940.2016.1171281","url":null,"abstract":"ABSTRACT Aim: Intestinal temperature telemetry systems are promising monitoring and research tools in athletes. However, the additional equipment that must be carried to continuously record temperature data limits their use to training. The purpose of this study was to assess the validity and reliability of a new gastrointestinal temperature data logging and telemetry system (e-Celsius™) during water bath experimentation and exercise trials. Materials and Methods: Temperature readings of 23 pairs of e-Celsius (TeC) and VitalSense (TVS) ingestible capsules were compared to rectal thermistor responses (Trec) at 35, 38.5 and 42°C in a water bath. Devices were also assessed in vivo during steady-state cycling (n = 11) and intermittent running (n = 11) in hot conditions. Results: The water bath experiment showed TVS and TeC under-reported Trec (P<0.001). This underestimation of Trec also occurred during both cycling (mean bias vs TVS: 0.21°C, ICC: 0.84, 95% CI: 0.66–0.91; mean bias vs. TeC: 0.44°C, ICC: 0.68, 95% CI: 0.07–0.86, P<0.05) and running trials (mean bias vs. TVS: 0.15°C, ICC: 0.92, 95% CI: 0.83–0.96; mean bias vs. TeC: 0.25, ICC: 0.86, 95% CI: 0.61–0.94, P<0.05). However, calibrating the devices attenuated this difference during cycling and eliminated it during running. During recovery following cycling exercise, TeC and TVS were significantly lower than Trec despite calibration (P<0.01). Conclusion: These results indicate that both TeC and TVS under-report Trec during steady-state and intermittent exercise in the heat, with TeC predicting Trec with the least accuracy of the telemetry devices. It is therefore recommended to calibrate these devices at multiple temperatures prior to use.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"14 1","pages":"208 - 219"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80794431","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: 10.1080/23328940.2016.1168535
B. Kingma
The human thermoregulatory apparatus has both autonomic and behavioral mechanisms at its disposal. Behavioral mechanisms include changing of clothes, moving to warmer/cooler/shaded areas and changing the environment by operating windows or the thermostat. For autonomous thermoregulation the body relies on metabolic responses to increase heat production, and besides sweating also on cardiovascular responses to increase heat loss and modulation of body tissue insulation. In this edition of Temperature, Schlader et al. identify that the hypoor hypertensive load on the cardiovascular system that is a consequence of autonomous thermoregulation may cause health risks for people that have problems with their heart. This is exemplified by increased mortality during cold spells or heat waves in healthcompromised populations; but also mild thermal challenges can have long lasting effects on systolic blood pressure in older adults. Schlader et al. indicate that instead of undergoing these internal perturbations, the body may minimize the cardiovascular load by behavioral thermoregulation to counteract or even preemptively avoid the thermal challenge. In this particular paper Schlader et al. describe how thermoregulatory behavior, by moving from a cool to a warm environment and vice versa, is preceded by small changes in blood pressure and moderate changes in skin blood flow. Thermal behavior is thus successful in avoiding large internal cardiovascular perturbations in a healthy subpopulation. Noteworthy, behavior initiated with minimal changes to core temperature, and Schlader et al. conclude that distal skin temperature (i.e., fingertip) may be the primary auxiliary signal for the body to initiate cold-defensive behavior. Based on their data a similar conclusion may be drawn for heat-defensive behavior, however, Schlader et al. discuss possible limitations from the methodology and point out that face and neck skin may have a stronger influence on thermal sensation in warm conditions. All in all, the data shows the strong coupling of modest changes to skin temperature in relation to initiation of thermal behavior. Moreover the behavioral thermopreferendum may work out as a second line of defense (after skin blood flow) to minimize the metabolic and water expenditure for body temperature regulation. But what if the thermosensory pathway is impaired, such as in older adults or diabetics? Could a lack of thermoregulatory response add to cardiovascular problems in these populations? The work of Schlader et al. gives clear clues on how to proceed with this matter and the link between autonomous and behavioral thermoregulation may prove critical especially in those populations who have impaired autonomous means of regulating body temperature. For instance, monitoring of temperature and cardiovascular parameters with wearables may be used to inform individuals, or their medical professionals, that they should show thermoregulatory behavior in order to avoid advers
{"title":"The link between autonomic and behavioral thermoregulation","authors":"B. Kingma","doi":"10.1080/23328940.2016.1168535","DOIUrl":"https://doi.org/10.1080/23328940.2016.1168535","url":null,"abstract":"The human thermoregulatory apparatus has both autonomic and behavioral mechanisms at its disposal. Behavioral mechanisms include changing of clothes, moving to warmer/cooler/shaded areas and changing the environment by operating windows or the thermostat. For autonomous thermoregulation the body relies on metabolic responses to increase heat production, and besides sweating also on cardiovascular responses to increase heat loss and modulation of body tissue insulation. In this edition of Temperature, Schlader et al. identify that the hypoor hypertensive load on the cardiovascular system that is a consequence of autonomous thermoregulation may cause health risks for people that have problems with their heart. This is exemplified by increased mortality during cold spells or heat waves in healthcompromised populations; but also mild thermal challenges can have long lasting effects on systolic blood pressure in older adults. Schlader et al. indicate that instead of undergoing these internal perturbations, the body may minimize the cardiovascular load by behavioral thermoregulation to counteract or even preemptively avoid the thermal challenge. In this particular paper Schlader et al. describe how thermoregulatory behavior, by moving from a cool to a warm environment and vice versa, is preceded by small changes in blood pressure and moderate changes in skin blood flow. Thermal behavior is thus successful in avoiding large internal cardiovascular perturbations in a healthy subpopulation. Noteworthy, behavior initiated with minimal changes to core temperature, and Schlader et al. conclude that distal skin temperature (i.e., fingertip) may be the primary auxiliary signal for the body to initiate cold-defensive behavior. Based on their data a similar conclusion may be drawn for heat-defensive behavior, however, Schlader et al. discuss possible limitations from the methodology and point out that face and neck skin may have a stronger influence on thermal sensation in warm conditions. All in all, the data shows the strong coupling of modest changes to skin temperature in relation to initiation of thermal behavior. Moreover the behavioral thermopreferendum may work out as a second line of defense (after skin blood flow) to minimize the metabolic and water expenditure for body temperature regulation. But what if the thermosensory pathway is impaired, such as in older adults or diabetics? Could a lack of thermoregulatory response add to cardiovascular problems in these populations? The work of Schlader et al. gives clear clues on how to proceed with this matter and the link between autonomous and behavioral thermoregulation may prove critical especially in those populations who have impaired autonomous means of regulating body temperature. For instance, monitoring of temperature and cardiovascular parameters with wearables may be used to inform individuals, or their medical professionals, that they should show thermoregulatory behavior in order to avoid advers","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"22 1","pages":"195 - 196"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81814788","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: 10.1080/23328940.2016.1163452
J. Roberts, Graeme Coulson, A. Munn, Michael R. Kearney
ABSTRACT Foraging time may be constrained by a suite of phenomena including weather, which can restrict a species' activity and energy intake. This is recognized as pivotal for many species whose distributions are known to correlate with climate, including kangaroos, although such impacts are rarely quantified. We explore how differences in shade seeking, a thermoregulatory behavior, of 2 closely-related kangaroo species, Macropus rufus (red kangaroos) and M. fuliginosus (western grey kangaroos), might reflect differences in their distributions across Australia. We observed foraging and shade-seeking behavior in the field and, together with local weather observations, calculated threshold radiant temperatures (based on solar and infrared radiant heat loads) over which the kangaroos retreated to shade. We apply these calculated tolerance thresholds to hourly microclimatic estimates derived from daily-gridded weather data to predict activity constraints across the Australian continent over a 10-year period. M. fuliginosus spent more time than M. rufus in the shade (7.6 ± 0.7 h versus 6.4 ± 0.9 h) and more time foraging (11.8 ± 0.5 h vs. 10.0 ± 0.6 h), although total time resting was equivalent (∼8.2 h). M. rufus tolerated 19°C higher radiant temperatures than M. fuliginosus (89°C versus 70°C radiant temperature). Across Australia, we predicted M. fuliginosus to be more restricted to shade than M. rufus, with higher absolute shade requirements farther north. These results corroborate previous findings that M. rufus is more adept at dealing with heat than M. fuliginosus and indicate that M. rufus is less dependent on shade on a continental scale.
{"title":"A continent-wide analysis of the shade requirements of red and western grey kangaroos","authors":"J. Roberts, Graeme Coulson, A. Munn, Michael R. Kearney","doi":"10.1080/23328940.2016.1163452","DOIUrl":"https://doi.org/10.1080/23328940.2016.1163452","url":null,"abstract":"ABSTRACT Foraging time may be constrained by a suite of phenomena including weather, which can restrict a species' activity and energy intake. This is recognized as pivotal for many species whose distributions are known to correlate with climate, including kangaroos, although such impacts are rarely quantified. We explore how differences in shade seeking, a thermoregulatory behavior, of 2 closely-related kangaroo species, Macropus rufus (red kangaroos) and M. fuliginosus (western grey kangaroos), might reflect differences in their distributions across Australia. We observed foraging and shade-seeking behavior in the field and, together with local weather observations, calculated threshold radiant temperatures (based on solar and infrared radiant heat loads) over which the kangaroos retreated to shade. We apply these calculated tolerance thresholds to hourly microclimatic estimates derived from daily-gridded weather data to predict activity constraints across the Australian continent over a 10-year period. M. fuliginosus spent more time than M. rufus in the shade (7.6 ± 0.7 h versus 6.4 ± 0.9 h) and more time foraging (11.8 ± 0.5 h vs. 10.0 ± 0.6 h), although total time resting was equivalent (∼8.2 h). M. rufus tolerated 19°C higher radiant temperatures than M. fuliginosus (89°C versus 70°C radiant temperature). Across Australia, we predicted M. fuliginosus to be more restricted to shade than M. rufus, with higher absolute shade requirements farther north. These results corroborate previous findings that M. rufus is more adept at dealing with heat than M. fuliginosus and indicate that M. rufus is less dependent on shade on a continental scale.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"107 1","pages":"340 - 353"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85126068","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: 10.1080/23328940.2016.1176102
C. Gordon, Joanne N. Caldwell, N. A. Taylor
ABSTRACT Aim: Static muscle activation elicits intensity-dependent, non-thermal sweating that is presumably controlled by feedforward (central command) mechanisms. However, it is currently unknown how the size of the recruited muscle mass interacts with that mechanism. To investigate the possible muscle-size dependency of that non-thermal sweating, the recruitment of two muscle groups of significantly different size was investigated in individuals within whom steady-state thermal sweating had been established and clamped. Methods: Fourteen passively heated subjects (climate chamber and water-perfusion garment) performed 60-s, static handgrip and knee-extension activations at 30% and 50% of maximal voluntary force, plus a handgrip at 40% intensity (143.4 N) and a third knee extension at the same absolute force. Local sweating from four body segments (averaged to represent whole-body sudomotor activity), three deep-body and eight skin temperatures, heart rates and perceptions of physical effort were measured continuously, and analyzed over the final 30 s of exercise. Results: In the presence of thermal clamping and low-level, steady-state sweating, static muscle activation resulted in exercise-intensity dependent changes in the whole-body sudomotor response during these handgrip and knee-extension actions (P < 0.05). However, there was no evidence of a dependency on the size of the recruited muscle mass (P > 0.05), yet both dependencies were apparent for heart rate, and partially evident for the sensations of physical effort. Conclusion: These observations represent the first evidence that exercise-related sudomotor feedforward is not influenced by the size of the activated muscle mass, but is instead primarily dictated by the intensity of the exercise itself.
{"title":"Non-thermal modulation of sudomotor function during static exercise and the impact of intensity and muscle-mass recruitment","authors":"C. Gordon, Joanne N. Caldwell, N. A. Taylor","doi":"10.1080/23328940.2016.1176102","DOIUrl":"https://doi.org/10.1080/23328940.2016.1176102","url":null,"abstract":"ABSTRACT Aim: Static muscle activation elicits intensity-dependent, non-thermal sweating that is presumably controlled by feedforward (central command) mechanisms. However, it is currently unknown how the size of the recruited muscle mass interacts with that mechanism. To investigate the possible muscle-size dependency of that non-thermal sweating, the recruitment of two muscle groups of significantly different size was investigated in individuals within whom steady-state thermal sweating had been established and clamped. Methods: Fourteen passively heated subjects (climate chamber and water-perfusion garment) performed 60-s, static handgrip and knee-extension activations at 30% and 50% of maximal voluntary force, plus a handgrip at 40% intensity (143.4 N) and a third knee extension at the same absolute force. Local sweating from four body segments (averaged to represent whole-body sudomotor activity), three deep-body and eight skin temperatures, heart rates and perceptions of physical effort were measured continuously, and analyzed over the final 30 s of exercise. Results: In the presence of thermal clamping and low-level, steady-state sweating, static muscle activation resulted in exercise-intensity dependent changes in the whole-body sudomotor response during these handgrip and knee-extension actions (P < 0.05). However, there was no evidence of a dependency on the size of the recruited muscle mass (P > 0.05), yet both dependencies were apparent for heart rate, and partially evident for the sensations of physical effort. Conclusion: These observations represent the first evidence that exercise-related sudomotor feedforward is not influenced by the size of the activated muscle mass, but is instead primarily dictated by the intensity of the exercise itself.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"97 1","pages":"252 - 261"},"PeriodicalIF":0.0,"publicationDate":"2016-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79206954","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: 10.1080/23328940.2016.1179380
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":"134 1","pages":"240 - 251"},"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":"13 1","pages":"197 - 198"},"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":"40 1","pages":"557 - 566"},"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}
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