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Humans are known as homeothermic endotherms. To ensure thermic balance at rest when exposed to cold, they dispose of two main thermogenic processes: shivering thermogenesis (ST) and non-shivering thermogenesis (NST). ST consists of involuntary muscle contractions and NST represents the component of Hprod that is not ST. While ST is difficult to tolerate, it is not yet known which nutrients and how much are required to stimulate NST and lower ST in the cold. Whether or not food caloric intake has an impact on the relative contribution of ST and NST to total Hprod remains to be determined. Therefore, the purpose of this thesis was 1) to quantify the effects of ingesting two quantities (1507 vs 3015 kJ) of same relative compositions on cold-induced whole-body Hprod and 2) to establish the effects of these two quantities of food on the relative contribution of ST and NST to total Hprod. Five healthy male participants were exposed to a 3h mild cold, using a liquid conditioned suit with water flowing at 15°C (COLD) or 33 °C (CON) for a total of 4 trials. Thermal, metabolic and shivering responses were measured at baseline, before and after shake ingestion. Results demonstrated that Hprod and ST intensity increased in the cold, while no significant differences were found between the ingested shakes at two different caloric equivalents. In addition, ST intensity did not change, which confirmed that NST remained the same between the two conditions. Thus, knowing that the caloric intake will not maximize the thermogenic effects in the cold (i.e. improve the comfort of the individual), is it more advantageous to bring food or additional clothing, for any activity? Clearly, more research on the exact pathways of each processes in the cold with food consumption needs to be made. To that extent, the investigation of the effect of food quality on changes in the thermogenic processes during cold exposure strikes us as a fascinating area for future research.

Human beings have been exposed to different cold conditions throughout time, and have through cold acclimation developed mechanisms to survive in these conditions. Cold acclimation can be elicited through exposure to natural cold climates, or artificially induced in a laboratory to study the body’s response to repeated cold exposures. Several studies looking at the effects of cold acclimation in humans have been conducted during the last 50 years, and have reported that cold acclimation can lead to a change in skin and core temperature, heat production and shivering. An accurate quantification of shivering thermogenesis (ST) during cold acclimation has not been done before, and most previous measurements of shivering during cold acclimation have been inaccurate and inadequate. In this study a Liquid Condition Suits (LCS) was used to elicit cold acclimation (10°C, 2hr daily, for 4 weeks) while an accurate measurement of the effect of cold acclimation on changes in muscle activity was conducted. In CHAPTER 2, results showed that four weeks of cold acclimation at 10°C did not change skin and core temperature, heat production or ST. The effects on shivering pattern and fuel selection were also analysed, but no effects of cold acclimation could be observed. These measurements were a part of a larger study, in which the effects of cold acclimation on changes in BAT were the main outcome measures. These data showed that an increase in BAT volume (45%) and activity (120%) were the only observed effects of cold acclimation. In CHAPTER 3, we set out to assess if changes in shivering from pre to post cold acclimation are associated with changes in BAT volume, and if the amount of BAT a participant possesses prior to cold acclimation can be used to predict changes in shivering intensity during cold acclimation. The interindividual variability in changes in thermal responses, heat production, shivering and BAT volume occurring between subjects during four weeks of cold acclimation was also addressed in this section.

Human beings have been exposed to different cold conditions throughout time, and have through cold acclimation developed mechanisms to survive in these conditions. Cold acclimation can be elicited through exposure to natural cold climates, or artificially induced in a laboratory to study the body’s response to repeated cold exposures. Several studies looking at the effects of cold acclimation in humans have been conducted during the last 50 years, and have reported that cold acclimation can lead to a change in skin and core temperature, heat production and shivering. An accurate quantification of shivering thermogenesis (ST) during cold acclimation has not been done before, and most previous measurements of shivering during cold acclimation have been inaccurate and inadequate. In this study a Liquid Condition Suits (LCS) was used to elicit cold acclimation (10°C, 2hr daily, for 4 weeks) while an accurate measurement of the effect of cold acclimation on changes in muscle activity was conducted. In CHAPTER 2, results showed that four weeks of cold acclimation at 10°C did not change skin and core temperature, heat production or ST. The effects on shivering pattern and fuel selection were also analysed, but no effects of cold acclimation could be observed. These measurements were a part of a larger study, in which the effects of cold acclimation on changes in BAT were the main outcome measures. These data showed that an increase in BAT volume (45%) and activity (120%) were the only observed effects of cold acclimation. In CHAPTER 3, we set out to assess if changes in shivering from pre to post cold acclimation are associated with changes in BAT volume, and if the amount of BAT a participant possesses prior to cold acclimation can be used to predict changes in shivering intensity during cold acclimation. The interindividual variability in changes in thermal responses, heat production, shivering and BAT volume occurring between subjects during four weeks of cold acclimation was also addressed in this section.

No description available.

No description available.

Brown (BAT) and white (WAT) adipose tissues are significant contributors to whole-body energy homeostasis. A disturbance in their metabolic function could result in the development of obesity and subsequent metabolic complications. The energy-sensing enzyme of the cell, AMP-activated protein kinase (AMPK), has been vastly studied in skeletal muscle and liver, but its role in BAT and WAT metabolism is elusive. We generated an inducible, adipocyte-specific knockout mouse model for the two AMPK β subunits (iβ1β2AKO) and found that iβ1β2AKO mice were intolerant to cold, and resistant to β3-adrenergic activation of BAT and browning of WAT. These defects in BAT activity were not due to the AMPK-ACC axis, but instead were due to compromised integrity of mitochondria. Mitochondrial morphology, function, and autophagy were all distorted in iβ1β2AKO mice, measured via transmission electron microscopy (TEM), respiration, and immunoblotting, respectively. These findings provide strong evidence that adipocyte AMPK regulates a fine-tuned program that responds to environmental and pharmacological inputs by maintaining mitochondrial integrity through autophagy and subsequent mitochondrial biogenesis in chronic settings. / Thesis / Master of Science (MSc) / Traditionally, there are two types of adipose tissue that appear and function differently. White adipose tissue (WAT) has evolved to store away energy in an efficient manner for later use. In contrast, brown adipose tissue (BAT) is a unique organ in mammals that has evolved over time to maintain body temperature. In essence, BAT has the ability to burn away calories as heat and is a promising therapeutic target to combat obesity and metabolic diseases such as type 2 diabetes. In our study, we have identified a potential factor that not only promotes BAT activity, but also promotes WAT to function more like BAT. By targeting this factor through drugs, there is potential to increase resting metabolic rate and fight the global epidemic of obesity.