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Cold Exposure

The act of exposing yourself to the cold and feeling the cold and, gritting your teeth through the discomfort. It actually does appear to burn fat in an attempt to warm the body, and may carry some health benefits.

Our evidence-based analysis on cold exposure features 34 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Cold Exposure

1What is cold exposure

Cold exposure is a manipulation of thermoregulation in the extreme of reducing temperature, by changing the external temperature Cold Exposure attempts to achieve certain cellular effects which can be used towards ones goals.

Thermoregulation techniques are built around the concept of adaptive thermogenesis. The human (adult) body maintains a temperature of 98.2 +/- 0.6 °F, which translates into 36.4–37.1 °C.[1] Changes below this threshold will cause adaptive changes to maintain said range[2] and changes above this threshold will cause changes to counter the change in the opposite. As per the 'adaptive' of adaptive thermogenesis, changes are not acute and cold exposure will need to be done routinely.[3]

In regards to cold metabolism, two types of reactions occur. Insulative actions which involve redirection of blood flow away from extremities, and metabolic changes that result in an increase of the metabolic rate to produce extra heat via uncoupling reactions.[2] The former is seen as a consequence of the cold (cold fingers) while the latter is what Cold Exposure aims to manipulate.

If one method of temperature regulation is limited, the other must compensate. Thus by limiting insulative reactions, one can increase metabolic reactions.[4][5]

2Insulative actions

Insulative actions are the first line of defense in thermoregulation and are metabolically cheap.[3] These include warmth-seeking behaviour, piloerection (goose bumps), vasoconstriction to decrease subcutaneous blood flow, and changing body positions to decrease surface area.[6] Although beneficial to survival and metabolically convenient, they are opposite of the most common goals of cold exposure therapy (fat mass loss, increased metabolic rate) due to their metabolic efficiency.

After insulative reactions have been exhausted, then non-shivering adaptive thermogenesis (NST) is recruited.

3NST - Muscle response to cold exposure

Skeletal muscle appears to be a reserve for Non-shivering adaptive thermogensesis in man. In particular the reserve of potential heat comes from upregulation of Myosin ATPase activity from conversion of a 'Super-relaxed' (highly inhibited) state of myosin into an 'active' state of myosin.[7][8] The accompanying increase in ATPase activity comes with an increase in substrate utilization and mitochondrial uncoupling[9], more subsequently more heat production.[8]

The significance of this reactions is summed up with the quote from Cooke.[8] That "Shifting only 20% of myosin heads from the (Super relaxed state) into the relaxed state would increase muscle thermogenesis by approximately a factor of two, increasing whole body metabolic rate by about 16%". Information gathered initially from in vitro studies on myosin cultures and later supported with in vivo research.

4NST - Body fat response to cold exposure

Brown body fat is another reserve for non-shivering adaptive thermogenesis in adult man, although it (brown fat) is much more active in youth.[10]

Brown fat's role in heat production comes from a protein called 'Thermogenin', or Uncoupling Protein 1 (UCP1). Two other UCPs exist (2 and 3, respectively).[11] UCP1 works by disturbing the mitochondrial proton gradient used in ATP production by shuttling protons back across the inner mitochondrial membrance independent of ATP Synthase.[12][13][14]

After muscle and fat contribute to Non-shivering Thermogenesis (NST), then shivering thermogenesis is recruited.

5Shivering thermogenesis

Shivering is defined as rapid oscillations of the body to produce kinetic heat.[6]

Low-grade shivering is a physical exertion which primarily uses fatty acids as substrate. However, at higher intensities a gradual shift to carbohydrate as the primary fuel substrate is used.[15] Glycogen is primarily used rather than serum glucose.[16]

6Other interactions with Cold Exposure and Metabolic Rate

Cold exposure seems to induce a greater recompensatory thermic effect of food (TEF) upon introduciton of food, and is more significant in periods of moderate eating rather than overfeeding.[4] This may be because of similar cellular mechanics between overfeeding and cold exposure, as both possess similar inter-individual differences[17] although UCP1 does not seem to be suspect.[18]

These relations may exemplify why some animal reports have found clinically significant weight loss in drastically overfed animals exposed to near zero temperatures for a prolonged period of time.[19][20] Although these drastic results may not be applicable to humans due to a lack of B3-beta adrenergic receptor proliferance on our white adipose tissue.[21]


Studies vary depending on the degree of cold and an individual's tendency to compensate with either insulative or metabolic changes. Some results report:

  • An additional 4-6% energy expenditure when the temperature is dropped 6°C relative to comfort level. [4][22]


  1. ^ Normal oral, rectal, tympanic and axillary body temperature in adult men and women: a systematic literature review.
  2. ^ a b van Marken Lichtenbelt WD, Daanen HA. Cold-induced metabolism. Curr Opin Clin Nutr Metab Care. (2003)
  3. ^ a b Cannon B, Nedergaard J. Nonshivering thermogenesis and its adequate measurement in metabolic studies. J Exp Biol. (2011)
  4. ^ a b c van Marken Lichtenbelt WD, et al. Individual variation in body temperature and energy expenditure in response to mild cold. Am J Physiol Endocrinol Metab. (2002)
  5. ^ Wijers SL, Saris WH, van Marken Lichtenbelt WD. Cold-induced adaptive thermogenesis in lean and obese. Obesity (Silver Spring). (2010)
  6. ^ a b Makinen TM. Different types of cold adaptation in humans. Front Biosci (Schol Ed). (2010)
  7. ^ Stewart MA, et al. Myosin ATP turnover rate is a mechanism involved in thermogenesis in resting skeletal muscle fibers. Proc Natl Acad Sci U S A. (2010)
  8. ^ a b c Cooke R. The role of the myosin ATPase activity in adaptive thermogenesis by skeletal muscle. Biophys Rev. (2011)
  9. ^ Wijers SL, et al. Human skeletal muscle mitochondrial uncoupling is associated with cold induced adaptive thermogenesis. PLoS One. (2008)
  10. ^ Cypess AM, Kahn CR. The role and importance of brown adipose tissue in energy homeostasis. Curr Opin Pediatr. (2010)
  11. ^ Enerbäck S. Brown adipose tissue in humans. Int J Obes (Lond). (2010)
  12. ^ Palou A, et al. The uncoupling protein, thermogenin. Int J Biochem Cell Biol. (1998)
  13. ^ Jia JJ, et al. The polymorphisms of UCP1 genes associated with fat metabolism, obesity and diabetes. Mol Biol Rep. (2010)
  14. ^ Jia JJ, et al. The polymorphisms of UCP2 and UCP3 genes associated with fat metabolism, obesity and diabetes. Obes Rev. (2009)
  15. ^ Haman F, et al. Metabolic requirements of shivering humans. Front Biosci (Schol Ed). (2010)
  16. ^ Weber JM, Haman F. Fuel selection in shivering humans. Acta Physiol Scand. (2005)
  17. ^ Wijers SL, Saris WH, van Marken Lichtenbelt WD. Individual thermogenic responses to mild cold and overfeeding are closely related. J Clin Endocrinol Metab. (2007)
  18. ^ Anunciado-Koza R, et al. Inactivation of UCP1 and the glycerol phosphate cycle synergistically increases energy expenditure to resist diet-induced obesity. J Biol Chem. (2008)
  19. ^ Nikonova L, et al. Mesoderm-specific transcript is associated with fat mass expansion in response to a positive energy balance. FASEB J. (2008)
  20. ^ Guerra C, et al. Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity. J Clin Invest. (1998)
  21. ^ Kozak LP. Brown fat and the myth of diet-induced thermogenesis. Cell Metab. (2010)
  22. ^ Dauncey MJ. Influence of mild cold on 24 h energy expenditure, resting metabolism and diet-induced thermogenesis. Br J Nutr. (1981)
  23. Grimaldi D, et al. Evidence of a diurnal thermogenic handicap in obesity. Chronobiol Int. (2015)
  24. Johnson F, et al. Could increased time spent in a thermal comfort zone contribute to population increases in obesity?. Obes Rev. (2011)
  25. Gilbert SS, et al. Thermoregulation as a sleep signalling system. Sleep Med Rev. (2004)
  26. Cannon B, Nedergaard J. Metabolic consequences of the presence or absence of the thermogenic capacity of brown adipose tissue in mice (and probably in humans). Int J Obes (Lond). (2010)
  27. van Marken Lichtenbelt WD, et al. Cold-activated brown adipose tissue in healthy men. N Engl J Med. (2009)
  28. van der Lans AA, et al. Cold acclimation recruits human brown fat and increases nonshivering thermogenesis. J Clin Invest. (2013)
  29. Saito M, et al. High incidence of metabolically active brown adipose tissue in healthy adult humans: effects of cold exposure and adiposity. Diabetes. (2009)
  30. Bernhard MC, et al. Warm Ambient Temperature Decreases Food Intake in a Simulated Office Setting: A Pilot Randomized Controlled Trial. Front Nutr. (2015)
  31. Rowe EA, Rolls BJ. Effects of environmental temperature on dietary obesity and growth in rats. Physiol Behav. (1982)
  32. Cannon B, Nedergaard J. Thermogenesis challenges the adipostat hypothesis for body-weight control. Proc Nutr Soc. (2009)
  33. Schellen L, et al. Differences between young adults and elderly in thermal comfort, productivity, and thermal physiology in response to a moderate temperature drift and a steady-state condition. Indoor Air. (2010)
  34. Warwick PM, Busby R. Influence of mild cold on 24 h energy expenditure in 'normally' clothed adults. Br J Nutr. (1990)