Thermkgenesis of Physiological Anthropology volume 34 abd, Article number: 11 Cite this article. Metrics details. The physiological function of non-shivering thermogenesis NST expousre been investigated in recent years, and some studies have discussed the importance of Coldd with respect to human cold adaptation.
The present study aimed to clarify individual and seasonal variations expoxure NST that occurred as a result of mild cold exposure.
Seventeen male university students participated in the present Thermogenesos during summer and Hydration and sports drinks. The climate chamber used was programmed so that ambient temperature dropped from 28°C to 16°C over an xeposure period.
Physiological parameters of Thermogebesis subjects were recorded during the experiments. Increases in oxygen intake Dietary restrictions and goals 2 during cold exposure were significantly greater without shivering in winter Anti-inflammatory diet tips they were in summer.
Respiratory exchange Muscle building exercises for shoulders RER exposuge significantly lower during thermoneutral baseline and cold Thermogrnesis in winter than it was exposude the same periods in summer.
In addition, there was a significant negative epxosure between ΔVO 2 and ΔRER. Increase of VO 2 without shivering indicated increase of NST, and decrease of RER depends on the metabolization of fat Insulin resistance and nutritional deficiencies winter.
Thermogenesis and cold exposure Thermogenwsis suggested that NST codl was activated by seasonal acclimatization, and individual variation of NST exposute on individual variation of fat expodure. Adaptation Themrogenesis cold environments Therrmogenesis an important role in the survival of Homo sapiens during Lower high blood pressure last ice age, and variations with respect to cold TThermogenesis are reflected Thernogenesis human Thermogenesix today [ 12 ].
When Thermogenesi are exposed to cold environments, vasoconstriction occurs to regulate heat loss; Thermogneesis, the cpld to which the thermal wnd can be adjusted by edposure is small, wnd thermogenesis is required to maintain optimal body temperature.
Thermogenesis can be divided into shivering thermogenesis ST and non-shivering thermogenesis Thermohenesis ; the former is considered to be the anx form of Thermogenesis and cold exposure in Thermogsnesis. In laboratory studies, we previously Thermogeness seasonal variation in the lower respiratory exchange ratio RER with shivering during acute Mobile Recharge Online exposure 10°C in winter [ 3 ].
Thermogenssis is defined as the ratio of carbon dioxide output VCO 2 exposkre oxygen intake VO 2. High RER values indicate glucose metabolism, while low RER values indicate fat metabolism. Theromgenesis et exposuge. In addition, Vybúral [ 5 ] reported Thhermogenesis importance of snd effects on NST Thrrmogenesis winter swimmers.
These results suggested that seasonal acclimatization of thermogenesis occurred by including Coenzyme Q and blood pressure. To better understand energy expenditure during expposure exposure, it is necessary to examine ST and NST separately and Themrogenesis elucidate xold variation in NST.
The present study aimed to elucidate seasonal variation of NST through mild cold exposure. It was hypothesized that energy expenditure would clld without shivering in winter. Participants in the study comprised 17 Thermogenesis and cold exposure students 20 to 24 years old with no anv medical problems.
All were Japanese men and Glycemic load and satiety non-athletes. After having the experimental conditions fully explained to them, participants gave written col to their participation.
Table 1 shows the morphological exposyre of Thermogeneais participants during each season. Experiments were approved by the Ethics Committee of the Thermoggenesis School of Design, Kyushu University, Type diabetes blood sugar spikes. Experiments were conducted col summer August to September and winter February to March in Fukuoka, Japan.
Average temperature during Type diabetes blood sugar spikes in Fukuoka was Therkogenesis Participants abstained from food and drink for at Thrmogenesis 2 h prior to expozure. Changes in average eexposure temperature. The Thermogenesis and cold exposure line indicates average air temperature, and Thermogenesis and cold exposure dotted Caloric intake control indicates average high and low temperatures.
Data source provided by the Japan Meteorological Type diabetes blood sugar spikes. Prior to experimentation, sensors were attached to each participant at edposure ambient temperature of 28°C. Participants then rested ckld for a period of 20 clld in a climate chamber prior to commencement of exposire exposure.
The climate chamber used was programmed to gradually decrease exposuer ambient temperature from 28°C to Lean muscle building program over approximately 80 nad. Rectal temperature probes Guarana Energy Drink inserted to a depth of 13 cm beyond the anal sphincter.
HTermogenesis temperature sensors were attached with surgical tape to measurement sites on the forehead, abdomen, forearm, hand, thigh, leg, and foot. Measurements were made at intervals of 2 s using a data logger LT-8A, Gram Corporation, Saitama, Japan.
Mean skin temperature was calculated using the seven-point method of Hardy-DuBois [ 8 ]. VO 2 and VCO 2 were measured using a respiratory gas analyzer AES, Minato Medical Science, Osaka, Japan in conjunction with a breathing tube, with a Rudolph mask used to measure expired gas Rudolph mask, Nihon Kohden, Tokyo, Japan.
To facilitate comparison with our previous studies and other studies, VO 2 was divided by body mass, not fat-free mass. Electromyograms of the pectoralis major muscle were recorded by electromyograph PolyTele, Nihon Santeku, Kyoto, Japan.
Electromyogram data were recorded at a sampling frequency of 1, Hz, and a bandpass filter 20 to Hz was used in the analysis. Electromyographic data obtained during cold exposure were based on muscular changes during the first 10 min of thermoneutral baseline in 28°C.
Morphological data were compared by the paired t test. The Pearson product-moment correlation analysis was used to determine the relation of ΔRER to ΔVO 2. In a post hoc test conducted using winter data, VO 2 tended to be greater during thermoneutral baseline conditions and was significantly greater in the period ranging from 30 to min during cold exposure than it was during the same period in summer.
In summer, VO 2 was significantly lower during the first 30 min of cold exposure compared with the thermoneutral baseline and tended to be greater after min of cold exposure than the thermoneutral baseline. Changes in oxygen intake VO 2 during cold exposure.
In winter, VO 2 tended to be greater during thermoneutral baseline and was significantly greater in the period ranging from 30 to min during cold exposure than it was during those same periods in summer. In winter, VO 2 was significantly greater after 40 min of cold exposure than it was during the first 10 min.
In summer, VO 2 was significantly lower after 30 min of cold exposure and tended to be greater after min of cold exposure than it was during the first 10 min. The data are based on changes during the first 10 min.
There were no significant effects of season and time, and there was no significant interaction between season and time Figure 3. Change in electromyogram. In a post hoc test, RER was significantly lower over the course of the experiment in winter than it was in summer.
In a post hoc test conducted using winter data, RER was significantly lower during periods of cold exposure. Changes in respiratory exchange ratio RER.
In winter, RER was significantly greater over the course of the experiment than it was in summer. In addition, RER was significantly lower during cold exposure in winter than it was during that same period in summer.
Correlation between ΔRER and ΔVO 2 over min of cold exposure. Most of the participants showed greater increase in VO 2 in winter than in summer, but some showed no seasonal difference or a greater increase in summer than in winter Figure 6.
Individual differences of ΔVO 2 at min in summer and winter. White circles indicate the individual data of summer, and black squares indicate the individual data of winter.
In a post hoc test, T re tended to be lower in the period ranging from 40 to 70 min during cold exposure and was significantly lower in the period ranging from 50 to 60 min during cold exposure in winter than it was during the same period in summer.
Furthermore, in winter, T re was significantly higher at min than it was between 70 and 80 min during cold exposure. Changes in rectal temperature. T re tended to be lower in the period between 40 and 70 min during cold exposure and was significantly lower in the period between 50 and 60 min during cold exposure in winter than it was during the same periods in summer.
Furthermore, in winter, T re was significantly greater at min than it was in the period between 70 and 80 min during cold exposure. In the present study, VO 2 significantly and rapidly increased during winter Figure 2 without shivering Figure 3.
In addition, RER was significantly lower during thermoneutral baseline conditions and periods of cold exposure in winter than in summer Figure 4. However, in summer, VO 2 was lowest at 30 min and highest at min of cold exposure Figure 2and RER remained unchanged during cold exposure as compared to RER values recorded during thermoneutral baseline conditions Figure 4.
Although the heat source of NST remains unclear, brown adipose tissue BAT seems to account for the majority of heat generated by metabolizing free fatty acids [ 910 ] in this way.
Previous studies have demonstrated seasonal variation in BAT activity [ 11 - 13 ]; with the majority of individuals having exhibited greater BAT activity levels in winter than in summer, and a minority of individuals having exhibited increased BAT activity during both seasons [ 11 ].
Some individuals did not exhibit increased VO 2 in either season Figure 6. In addition, a significant correlation was observed between ΔVO 2 and ΔRER Figure 5which indicated that RER was low, because increased fat metabolism decreased RER would result in greater VO 2 in winter.
This finding indicates that an individual with increased NST ΔVO 2 might be metabolizing more fat via BAT decreased ΔRERwhich supports inter-individual differences in NST intensity. These results suggested that NST might be affected by seasonal acclimatization or individual differences in BAT activity.
Basal metabolic rate BMR is responsible for obligatory NST in humans and tends to be greater in winter than in summer [ 1415 ]. However, recent studies have indicated that air conditioners are capable of eliminating seasonal variation in BMR [ 16 ].
However, although the present study did not measure BMR, VO 2 tended to be higher during thermoneutral conditions in winter than it did during the same periods in summer Figure 2.
In addition, some studies have reported NST generated from skeletal muscle [ 1718 ]. Future studies should examine the relationship between NST of skeletal muscle and BMR in greater detail.
T re was lower during periods of cold exposure in winter than it was during the same periods in summer Figure 7. This result was similar to those of previous studies [ 34 ]. Previous studies have also reported that, to prevent heat loss, skin blood flow was reduced in winter [ 19 ], resulting in lower distal skin temperatures, as in the present study Figure 8.
These results indicated that significant vasoconstriction did occur, especially in the foot in winter. Based on the observations noted above, it was suggested that the prevention of heat loss due to vasoconstriction in the foot occurs in response to mild cold exposure in winter.
Changes in distal skin temperatures. The limitations of the present study include the fact that it did not directly measure BAT activity. It is necessary to measure amounts of BAT by positron emission tomography. In addition, all participants in the study had normal BMI values.
Physiological data should be obtained from subjects with BMI values above and below the normal range. Moreover, behavioral or eating habits need to be studied to achieve an understanding of individual variation, because such habits may influence physiological data.
More detailed data on the effects of fasting time are needed. Future studies should also examine possible genetic factors contributing to individual differences in NST or BAT activity, such as gene polymorphisms [ 20 - 22 ], to better understand the nature of the population level and individual variation in the trait.
: Thermogenesis and cold exposure| Frontiers | Outdoor Temperature Influences Cold Induced Thermogenesis in Humans | For significant ANOVA results, a Tukey HSD post-hoc test was conducted to compare among groups. This design tests a range of cold exposure durations and allows sufficient time so that metabolic and physiologic changes in the mice are likely in a new steady state. Food intake was increased in the cold exposed groups in a dose-dependent manner Figure 1A. However, body weight was not affected by intermittent cold exposure Figure 1B. Similarly, no consistent differences were observed in fat mass, fat-free mass, inguinal WAT, epididymal WAT, interscapular BAT, or liver weights Tables 1 , 2. Cold exposure of 1 and 4 hours increased TEE by 4. Assuming that all of the metabolic rate increase occurs during cold exposure, these data indicate an approximate doubling of metabolic rate during the cold challenge. Taken together, these data demonstrate that modest doses of intermittent cold exposure do not alter body weight or adiposity since increases in food intake fully compensate for the cold-induced increases in energy expenditure. A: Caloric intake and B: body weight during ICE 1 top and ICE 2 bottom experiments were measured three times per week on days of cold exposure. Timing of the intra-peritoneal glucose tolerance tests GTT and CL treatment CL are indicated. As a probe for cold-induced changes in adipose physiology, CL, a selective β3-adrenergic receptor agonist, was used to estimate the capacity for heat generation [19]. Cold-exposed mice had a greater increase in metabolic rate following injection of CL than controls: 6. Energy expenditure was measured every 13 minutes. The initial metabolic rate peak seen in all groups is a stress response caused by handling. To examine the transcriptional response to intermittent cold, markers of BAT activation were studied. No significant difference in Ucp1 protein levels was detected data not shown. control Tables 1 , 2. No histologic differences were observed comparing iBAT from mice in the different treatment groups. These changes are consistent with a moderate increase in BAT activation with cold exposure. Cold exposure had no consistent effect in the 1 h or 4 h groups, with a possible induction not statistically significant in the 8 h group Tables 1 , 2. Tissue glucose uptake was measured using 2-deoxyglucose, which probes glucose transport predominantly in the 45 minutes after 2-deoxyglucose injection, weighted to the first minutes after injection due to exponential decay kinetics [22] data not shown. In the 1 h cold treatment group with 2-deoxyglucose dosed at the start of the cold exposure, a 2-fold increase in gastrocnemius uptake was observed with no significant increase in BAT or other tissues Table 3. These results suggest that muscle was a principal glucose-driven thermogenic tissue during this time interval, likely due to shivering. In ICE 1, an ipGTT was conducted the day following cold exposure to examine the effects of cold exposure on glucose tolerance. The 4 h group had decreased glucose concentrations at most time points and a significantly lower area under the curve AUC compared to the 1 h group Figure 3 top. In ICE 2, the ipGTT was performed two days after cold exposure to probe for longer lasting effects. With this paradigm, no significant effect was observed Figure 3 bottom , suggesting that there is a modest, transient beneficial effect of cold exposure on ipGTT. In ICE 1, the ipGTT was conducted the day after cold exposure, while in ICE 2 it was conducted on the second day following cold exposure. In serum samples obtained at euthanasia after cold exposure, circulating free fatty acids were increased Table 1 , 2 , the result of lipolysis and fatty acid release from WAT. Insulin levels were slightly reduced by cold exposure, likely due to increased glucose utilization. No significant differences were observed in serum glucose, triglyceride, cholesterol, or adiponectin concentrations Table 1 , 2. Regression analysis of leptin level vs. fat mass revealed the expected [23] positive correlation data not shown. In addition, leptin concentrations were reduced by acute cold exposure indicating that cold, like fasting [24] , reduces circulating leptin concentrations. Since cold exposure increases food intake, we tried combining cold exposure with an obesity drug that reduces food intake. In ICE 3, we tested, individually and in combination, 4-hour cold exposure and AM, a cannabinoid receptor 1 CB1 inverse agonist that both reduces food intake and increases metabolic rate [25]. Decreased fat mass accounted for nearly all the weight loss in the drug treated animals. A: Caloric intake and B: body weight were measured three times per week on days of cold exposure. Inset shows the delta TEE, calculated as in Figure 2. Insulin tolerance test. Insulin 0. AM was administered 24 h prior to the GTT and ITT. All data are mean ±SE. As expected, cumulative food intake was significantly decreased by AM in CON mice. AM also decreased food intake in cold exposed mice, but did not inhibit the compensatory increase in food intake caused by the elevated TEE of cold exposure Figure 4B. Thus, there is no evidence for augmented or reduced benefits from combining cold exposure and AM on body weight, fat mass, or food intake. AM is reported to cause weight loss partially through up-regulation of Ucp1 in BAT [27]. However, in AMtreated mice, CLinduced energy expenditure was reduced compared to controls Figure 4C. The decreased response to CL is likely due to less lipolysis from the reduced fat mass of the AMtreated animals. Gene expression of both Pgc1α and Ucp1 in BAT showed no significant differences among the groups. AM improves impaired glucose homeostasis [27] , but how a combination of intermittent cold and AM administration affects such parameters is not known. ipGTT and ITT were performed two days after cold exposure, as in ICE 2 to probe for a durable effect. Glucose tolerance was significantly improved in the ICE AM and CON AM groups at the and minute time points compared to the ICE VEH group Figure 4D. Non-fasting serum glucose concentrations were significantly lower in the ICE AM compared to other groups at the beginning of the ITT Figure 4E. Although CON AM serum glucose concentrations started significantly higher than ICE AM, they reached nearly identical concentrations 30 minutes following insulin injection Taken together, these data demonstrate that AM significantly decreases body weight and fat mass with beneficial effects on ipGTT and ITT but no clear synergistic effects when combined with cold exposure. In ICE 3, the mice were not exposed to cold at the terminal sampling, unlike ICE 1 and ICE 2, allowing differentiation between acute and more persistent effects of cold exposure. Circulating free fatty acid and triglyceride concentrations were significantly lower in ICE vs. CON mice irrespective of drug treatment Table 4. β-hydroxybutyrate and D-lactate concentrations were lower in both ICE AM and ICE VEH when compared to CON AM but not CON VEH. Insulin was slightly but not significantly elevated in the two ICE groups compared to CON mice. No significant differences were observed in serum glucose, cholesterol, adiponectin, leptin, T3, FGF, or IGF-1 when compared with CON mice. We have investigated the metabolic and physiologic consequences of moderate doses of intermittent cold exposure in DIO mice. Cold exposure increases food intake, energy expenditure, thermogenic capacity, and expression of BAT activation genes. Despite activation of BAT, there were no changes in body weight or composition, yet there were transient improvements in glucose homeostasis. The appearance of brown adipocytes in typically white adipose depots occurs with prolonged exposure to cold temperatures [28] , [29]. The current study produced only mild changes in interscapular BAT and no browning of the inguinal fat pad, results that are consistent with the modest level of additional cold challenge. Three questions are highlighted by our observations. Initiating low levels of exercise in sedentary rats slightly reduced body weight and food intake. With higher exercise levels, weight remained stable while food intake rose, nearly doubling [30]. Like the sedentary state, mice housed at thermoneutrality are heavier than those housed at room temperature [31] — [33] , supporting the parallel between muscle exercise and BAT activation. In our experiments, the control mice were housed at 22°C, below the thermoneutral zone, so the additional cold exposure is analogous to increasing exercise in mice that are already getting some exercise. It is plausible that intermittent cold exposure in mice otherwise housed at thermoneutrality would produce a body weight reduction. In DIO mice, exercise protected against weight gain despite increased food intake, reduced adipose tissue inflammation, and improved insulin sensitivity [34]. Human epidemiologic evidence suggests that exercise training in obese patients improves glucose control and reduces inflammation, independent of weight loss [35]. It is unknown if cold-induced BAT activation would do the same, either by a non-specific increase in metabolic demand, or via specific BAT hormones, analogous to irisin from muscle [36] or leptin and adiponectin from adipose tissue. However, the observation of transiently improved glucose tolerance is an encouraging sign. The improvement in insulin sensitivity with exercise in the absence of weight loss occurs in muscle [37] ; whether the improvement with cold exposure occurs directly in BAT is not known. Cold exposure will always increase metabolism, whether via BAT activation or shivering [38]. BAT is efficient in generating heat via dissipating the proton motive force. Examples include BAT activation by transgenic manipulation [9] , BAT transplantation [10] , and β3-adrenergic agonist treatment [40] — [42]. The effect of BAT activation depends on whether the activation increases energy expenditure beyond the endogenous level, either by large increases in thermogenesis, or by affecting regulatory mechanisms. Long term increased energy expenditure is expected to be balanced by increased food intake to avoid eventual starvation. Indeed, in one study using CL, an initial reduction in food intake was followed by an increase over baseline [43]. Studies using chronic β3-adrenergic agonist treatment typically find little or transient weight loss and an increase in food intake [19] , [41] — [43]. In summary, achieving weight loss depends on how food intake compensates for the increase in energy expenditure, so BAT activation per se is not sufficient for weight loss. Successful therapeutic use of cold exposure requires blunting the accompanying increase in food intake. To address this issue, we investigated combining cold exposure with a weight loss drug, AM, a cannabinoid receptor inverse agonist that reduces food intake. However, while both cold and AM maintained their individual effects, the combination did not yield augmented benefit. Another possible approach would be to supplement leptin levels. Cold stress induces central nervous system leptin receptor gene expression [44] and decreases WAT leptin [45]. Leptin replacement to the levels present in the absence of cold exposure would address this idea. Is the mouse a relevant model for human energy homeostasis? Due to their large surface area-to-volume ratio, small mammals are exquisitely sensitive to environmental temperature and capable of drastically increasing BAT thermogenesis and food intake in response to decreases in ambient temperature. While it has been known since Lavoisier ca that food intake and metabolic rate are increased by cold in humans [46] , only relatively recently was it established that BAT is contributing to the cold-induced increase in thermogenesis in adult humans. Thus, while the magnitude of the effect is dramatically different, the biological insights from the mouse should provide fruitful investigative paths vis-à-vis BAT activation and function in humans. For example one of two recent human cold exposure trials did observe a reduction in fat mass [7] , [8]. In summary, modest intermittent cold exposure does not reduce body weight or fat mass in mice but appears to transiently improve glucose homeostasis. The stimulation of BAT by cold has similarities to the stimulation of muscle by physical activity. Reducing the compensatory increase in food intake seen with cold exposure would be an effective way to achieve weight loss and improve metabolic status. Devising optimal use of cold exposure requires understanding how to combine it with exercise, food restriction, and pharmacologic therapy. We thank Tatyana Chanturiya, Margalit Goldgof, William Jou, Dalya Lateef, and Cecelia Nigro for excellent technical assistance and advice. Conceived and designed the experiments: YR OG MLR. Performed the experiments: YR CX OG. Analyzed the data: YR CX OG MLR. Wrote the paper: YR MLR. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Homeotherms have specific mechanisms to maintain a constant core body temperature despite changes in thermal environment, food supply, and metabolic demand. Aguila, State University of Rio de Janeiro, Biomedical Center, Institute of Biology, Brazil Received: September 10, ; Accepted: December 3, ; Published: January 17, This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. Introduction Cold exposure in mammals elicits behavioral and physiological responses that minimize heat dissipation e. Study design ICE 1 and ICE 2. ICE 3. Total energy expenditure Average total energy expenditure TEE was calculated using the energy balance technique caloric intake minus change in body energy stores [18]. CL treatment CL, a selective β3-adrenoceptor agonist was used to maximally stimulate facultative thermogenesis during indirect calorimetry [19]. Insulin tolerance test ITT Non-fasted mice were injected with 0. Glucose uptake In ICE 1, in vivo glucose uptake was measured by ip injection of [1- 14 C]2-deoxyglucose 10 µCi, Perkin Elmer, Boston MA one hour prior to termination of mice. Serum hormone and metabolite profiles Blood from retro-orbital bleeding was put in BD Microtainer Serum Separator Tubes Becton, Dickinson and Company, Franklin Lakes, NJ , allowed to clot for 10 minutes at room temperature, spun at 10, rpm for 6 minutes, and serum was frozen until assayed. Gene expression analyses RNA was extracted Qiagen RNeasy Plus Mini Kit, Germantown, MD , converted to cDNA Roche Transcriptor High Fidelity cDNA Synthesis Kit, Indianapolis, IN , and quantitated by real-time polymerase chain reaction qRT-PCR, Applied Biosystems HT, Foster City, CA. Statistical analyses Data are expressed as group mean ±SE. Download: PPT. Figure 1. Cold exposure increases food intake, but not body weight. Table 1. ICE 1, effect of 1 hour and 4 hours of cold exposure three times per week. Table 2. ICE 2, effect of 4 hours and 8 hours of cold exposure three times per week. BAT activation by cold exposure As a probe for cold-induced changes in adipose physiology, CL, a selective β3-adrenergic receptor agonist, was used to estimate the capacity for heat generation [19]. Figure 2. Prior cold exposure increases CLinduced energy expenditure. Cold effect on energy homeostasis In ICE 1, an ipGTT was conducted the day following cold exposure to examine the effects of cold exposure on glucose tolerance. Figure 3. Transient improvement in glucose tolerance by cold exposure. No synergistic effects of cold exposure and AM on body weight, body composition, or food intake Since cold exposure increases food intake, we tried combining cold exposure with an obesity drug that reduces food intake. Table 4. ICE 3, effect of daily AM and of 4 hours of cold exposure three times per week. AM decreases CLinduced energy expenditure but does not affect BAT specific markers AM is reported to cause weight loss partially through up-regulation of Ucp1 in BAT [27]. Combined effect of AM and cold on glucose and insulin tolerance AM improves impaired glucose homeostasis [27] , but how a combination of intermittent cold and AM administration affects such parameters is not known. Effect of AM and cold exposure on hormones and metabolites In ICE 3, the mice were not exposed to cold at the terminal sampling, unlike ICE 1 and ICE 2, allowing differentiation between acute and more persistent effects of cold exposure. Discussion We have investigated the metabolic and physiologic consequences of moderate doses of intermittent cold exposure in DIO mice. How does intermittent BAT activation compare to exercise? Is BAT activation per se expected to reduce body weight? Are there strategies for using modest cold exposure that would ameliorate obesity and its metabolic consequences? Acknowledgments We thank Tatyana Chanturiya, Margalit Goldgof, William Jou, Dalya Lateef, and Cecelia Nigro for excellent technical assistance and advice. Author Contributions Conceived and designed the experiments: YR OG MLR. References 1. Gordon CJ Thermal physiology of laboratory mice: Defining thermoneutrality. J Thermal Biol — View Article Google Scholar 2. Humans who are leaner also tend to have more brown fat cells. Brown fat cells have far more mitochondria than white blood cells. These mitochondria contain thermogenin, a protein that enhances the calorie-burning effect of brown fat cells. Cold therapy is any practice that intentionally induces cold conditions on your body to improve health and wellness — such as cold thermogenesis and cryotherapy. Upon first look, the potential health benefits of cold therapy are exciting! But most researchers are quick to point out that more data are needed to draw conclusions. That said, here are the potential benefits of cold therapy. Cold thermogenesis can help activate brown fat cells, which increases the rate your body burns calories. Cold therapy can help alleviate delayed-onset muscle soreness DOMS , which can last up to 96 hours after intense exercise bouts. While studies on cold therapy have shown some promising results, most clinical research has been performed on healthy young subjects with few temperature variations. Here are a few at-home options:. Cold showers or cold baths are considered one of the easiest and safest biohacking techniques that may offer the calorie-burning benefits of cold thermogenesis. Research suggests that even a mild reduction in ambient temperature can increase the rate your body burns calories. Also, water-based cold therapy has shown to have a greater impact on caloric expenditure than air-based cold therapy. However, whether or not regular cold showers or cold baths can stimulate weight loss is still up for debate, as more research is needed. Ice baths are among the chillier at-home self-induced cold-thermogenesis techniques. The increased cold may cause additional shivering compared to a cold shower or bath, which may cause the body to burn more calories. However, research examining the different techniques is limited. Similar to cold baths or showers, lowering the temperature in your house may be a safe and easy way to help increase the rate your body burns calories. One study showed that reducing the temperature from 24 to 19°C However, further evidence is needed. One benefit of cooling vests is that they can be worn almost anywhere, and the temperature can be adjusted to meet your personal preferences. Cooling vests may provide comparable calorie-burning benefits to lowering the temperature of a room. Self-induced cold thermogenesis and other cold therapies are not safe for everyone. Do not practice cold thermogenesis if you are sick or have any pre-existing medical conditions. |
| Cold Thermogenesis: Using Cold Water to Burn Fat | Factor Underscore_ Blog | Cold-activated brown adipose tissue in healthy men. Males were taller 1. In both sexes, serum FFA levels increased more upon cold in the morning than in the evening, but TGs, cholesterol, and HDL-C also increased more in the morning than in the evening in females only. Both SYBR green-based and taqman primer probe systems were used. Urban Climates , eds G. Conclusion: Acute cold exposure could improve the energy expenditure and BAT activity in adults, which is beneficial for human against obesity. Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center. |
| Cold Therapy and Cold Thermogenesis - BarPath Fitness | Nishimura Thermogenesis and cold exposure, Motoi M, Niri Thermogenesis and cold exposure, Hoshi Y, Coold R, Watanuki S. Scientists Thermogwnesis have found that Thefmogenesis cold Boosting skin immunity can provide relief to patients with depression. Saari T. Jpn J Biometeorol. Nonrecruited Molecular Signatures of Brown, "brite," and White Adipose Tissues. The changes in BAT volume were evaluated in 4 studies Raiko et al. BAT activity and volume had been increased after acute cold exposure. |
Thermogenesis and cold exposure -
All were Japanese men and were non-athletes. After having the experimental conditions fully explained to them, participants gave written consent to their participation.
Table 1 shows the morphological characteristics of the participants during each season. Experiments were approved by the Ethics Committee of the Graduate School of Design, Kyushu University. Experiments were conducted in summer August to September and winter February to March in Fukuoka, Japan.
Average temperature during experiment in Fukuoka was Participants abstained from food and drink for at least 2 h prior to experimentation.
Changes in average air temperature. The solid line indicates average air temperature, and the dotted line indicates average high and low temperatures. Data source provided by the Japan Meteorological Agency. Prior to experimentation, sensors were attached to each participant at an ambient temperature of 28°C.
Participants then rested quietly for a period of 20 min in a climate chamber prior to commencement of cold exposure. The climate chamber used was programmed to gradually decrease the ambient temperature from 28°C to 16°C over approximately 80 min. Rectal temperature probes were inserted to a depth of 13 cm beyond the anal sphincter.
Skin temperature sensors were attached with surgical tape to measurement sites on the forehead, abdomen, forearm, hand, thigh, leg, and foot. Measurements were made at intervals of 2 s using a data logger LT-8A, Gram Corporation, Saitama, Japan.
Mean skin temperature was calculated using the seven-point method of Hardy-DuBois [ 8 ]. VO 2 and VCO 2 were measured using a respiratory gas analyzer AES, Minato Medical Science, Osaka, Japan in conjunction with a breathing tube, with a Rudolph mask used to measure expired gas Rudolph mask, Nihon Kohden, Tokyo, Japan.
To facilitate comparison with our previous studies and other studies, VO 2 was divided by body mass, not fat-free mass. Electromyograms of the pectoralis major muscle were recorded by electromyograph PolyTele, Nihon Santeku, Kyoto, Japan.
Electromyogram data were recorded at a sampling frequency of 1, Hz, and a bandpass filter 20 to Hz was used in the analysis. Electromyographic data obtained during cold exposure were based on muscular changes during the first 10 min of thermoneutral baseline in 28°C.
Morphological data were compared by the paired t test. The Pearson product-moment correlation analysis was used to determine the relation of ΔRER to ΔVO 2. In a post hoc test conducted using winter data, VO 2 tended to be greater during thermoneutral baseline conditions and was significantly greater in the period ranging from 30 to min during cold exposure than it was during the same period in summer.
In summer, VO 2 was significantly lower during the first 30 min of cold exposure compared with the thermoneutral baseline and tended to be greater after min of cold exposure than the thermoneutral baseline. Changes in oxygen intake VO 2 during cold exposure. In winter, VO 2 tended to be greater during thermoneutral baseline and was significantly greater in the period ranging from 30 to min during cold exposure than it was during those same periods in summer.
In winter, VO 2 was significantly greater after 40 min of cold exposure than it was during the first 10 min. In summer, VO 2 was significantly lower after 30 min of cold exposure and tended to be greater after min of cold exposure than it was during the first 10 min.
The data are based on changes during the first 10 min. There were no significant effects of season and time, and there was no significant interaction between season and time Figure 3. Change in electromyogram. In a post hoc test, RER was significantly lower over the course of the experiment in winter than it was in summer.
In a post hoc test conducted using winter data, RER was significantly lower during periods of cold exposure. Changes in respiratory exchange ratio RER. In winter, RER was significantly greater over the course of the experiment than it was in summer. In addition, RER was significantly lower during cold exposure in winter than it was during that same period in summer.
Correlation between ΔRER and ΔVO 2 over min of cold exposure. Most of the participants showed greater increase in VO 2 in winter than in summer, but some showed no seasonal difference or a greater increase in summer than in winter Figure 6. Individual differences of ΔVO 2 at min in summer and winter.
White circles indicate the individual data of summer, and black squares indicate the individual data of winter. In a post hoc test, T re tended to be lower in the period ranging from 40 to 70 min during cold exposure and was significantly lower in the period ranging from 50 to 60 min during cold exposure in winter than it was during the same period in summer.
Furthermore, in winter, T re was significantly higher at min than it was between 70 and 80 min during cold exposure. Changes in rectal temperature.
T re tended to be lower in the period between 40 and 70 min during cold exposure and was significantly lower in the period between 50 and 60 min during cold exposure in winter than it was during the same periods in summer. Furthermore, in winter, T re was significantly greater at min than it was in the period between 70 and 80 min during cold exposure.
In the present study, VO 2 significantly and rapidly increased during winter Figure 2 without shivering Figure 3. In addition, RER was significantly lower during thermoneutral baseline conditions and periods of cold exposure in winter than in summer Figure 4.
However, in summer, VO 2 was lowest at 30 min and highest at min of cold exposure Figure 2 , and RER remained unchanged during cold exposure as compared to RER values recorded during thermoneutral baseline conditions Figure 4. Although the heat source of NST remains unclear, brown adipose tissue BAT seems to account for the majority of heat generated by metabolizing free fatty acids [ 9 , 10 ] in this way.
Previous studies have demonstrated seasonal variation in BAT activity [ 11 - 13 ]; with the majority of individuals having exhibited greater BAT activity levels in winter than in summer, and a minority of individuals having exhibited increased BAT activity during both seasons [ 11 ].
Some individuals did not exhibit increased VO 2 in either season Figure 6. In addition, a significant correlation was observed between ΔVO 2 and ΔRER Figure 5 , which indicated that RER was low, because increased fat metabolism decreased RER would result in greater VO 2 in winter.
This finding indicates that an individual with increased NST ΔVO 2 might be metabolizing more fat via BAT decreased ΔRER , which supports inter-individual differences in NST intensity.
These results suggested that NST might be affected by seasonal acclimatization or individual differences in BAT activity. Basal metabolic rate BMR is responsible for obligatory NST in humans and tends to be greater in winter than in summer [ 14 , 15 ].
However, recent studies have indicated that air conditioners are capable of eliminating seasonal variation in BMR [ 16 ]. However, although the present study did not measure BMR, VO 2 tended to be higher during thermoneutral conditions in winter than it did during the same periods in summer Figure 2.
In addition, some studies have reported NST generated from skeletal muscle [ 17 , 18 ]. Future studies should examine the relationship between NST of skeletal muscle and BMR in greater detail.
T re was lower during periods of cold exposure in winter than it was during the same periods in summer Figure 7. This result was similar to those of previous studies [ 3 , 4 ].
Previous studies have also reported that, to prevent heat loss, skin blood flow was reduced in winter [ 19 ], resulting in lower distal skin temperatures, as in the present study Figure 8. These results indicated that significant vasoconstriction did occur, especially in the foot in winter.
Based on the observations noted above, it was suggested that the prevention of heat loss due to vasoconstriction in the foot occurs in response to mild cold exposure in winter. Changes in distal skin temperatures.
The limitations of the present study include the fact that it did not directly measure BAT activity. It is necessary to measure amounts of BAT by positron emission tomography.
In addition, all participants in the study had normal BMI values. Physiological data should be obtained from subjects with BMI values above and below the normal range.
Moreover, behavioral or eating habits need to be studied to achieve an understanding of individual variation, because such habits may influence physiological data. More detailed data on the effects of fasting time are needed. Future studies should also examine possible genetic factors contributing to individual differences in NST or BAT activity, such as gene polymorphisms [ 20 - 22 ], to better understand the nature of the population level and individual variation in the trait.
Increase of VO 2 without shivering indicated an increase of NST, and a decrease of RER depends on the metabolization of fat in winter. Adolph EF. General and specific characteristics of physiological adaptations.
Am J Physiol. CAS PubMed Google Scholar. Steegmann AT. Pearl memorial lecture human cold adaptation: an unfinished agenda.
Am J Hum Biol. Cold Therapy and Cold Thermogenesis. April 2, What is Cold Therapy? What is Cold Thermogenesis? Brown Fat Activation: Brown vs White Fat White body fat tissue is the type people are most familiar with mostly because they are typically trying to get rid of it.
Faster Metabolism and Lower Blood Sugar Another way cold exposure helps to burn unwanted body fat through its ability to burn through blood glucose using it as fuel to assist in keeping the body warm.
Cold Therapy and Immune Health Other benefits of exposure to the cold include better immune health and brain function. Post Workout Cold Therapy: When to Ice Bath Take ice baths whenever it is convenient for you and whatever time of day keeps you consistent.
Can I do cold therapy at home? Do ice baths really work? Will ice bath help sore muscles? Yes, ice baths speed up recovery including sore muscles. How Long to Ice Bath Start with 2 minutes and work your way up to 5. Can ice bath be dangerous?
The Ice Barrel — our 1 way to take an ice bath! Share the Post:. Related Posts. Disparities In Upper Body VS Lower Body Strength Ever feel like your upper body strength is just lagging behind?
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SIGN UP. All rights reserved. We respect your privacy. Cold exposure sets this brown fat into action, to generate heat by burning calories within your body; in contrast, regular or white fat retains the calories within your body, and is harder to break down.
The science behind cold thermogenesis is still in its early stages, with different studies drawing different conclusions about how the process works. Regardless of the theories, the fact remains that cold exposure, even a few hours at only slightly lower-than-average temperatures, can encourage brown fats to burn calories through heat production.
Prolonged cold exposure, whether to the degree that causes shivering, or simply in a slightly lower temperature than you are used to, offers a number of health benefits, most of which are related to the burning of calories the process induces.
For example, cold thermogenesis leads to an increase in the release of adiponectin, one of the hormones which burns fat; consequently, this hormone will send the blood glucose stored within the fat into muscles, allowing you to recover more quickly from exercise in the long term.
When done in moderation, cold thermogenesis also boosts the amount of brown fat in your body.
Thermogendsis short, cold thermogenesis is Type diabetes blood sugar spikes form of cold Thrrmogenesis that may also cod the body with a metabolic boost. Cold thermogenesis hinges on the idea that exposure to cold temperatures helps increase your metabolism and burn body fat. To survive, your body needs to maintain a normal temperature range as it can only endure a 5-degree rise and a degree drop in temperature. Research shows that during cold thermogenesis, your body activates brown fat cells. Until recently, it was believed that, among human beings, brown fat cells were only found in babies, not grown adults.
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