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. Changes below this threshold will cause adaptive changes to maintain said range 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.
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. The former is seen as a consequence of the cold (cold fingers) while the latter is what Cold Exposure aims to manipulate.
Insulative actions are the first line of defense in thermoregulation and are metabolically cheap. These include warmth-seeking behaviour, piloerection (goose bumps), vasoconstriction to decrease subcutaneous blood flow, and changing body positions to decrease surface area. 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.
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. The accompanying increase in ATPase activity comes with an increase in substrate utilization and mitochondrial uncoupling, more subsequently more heat production.
The significance of this reactions is summed up with the quote from Cooke. 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.
Brown body fat is another reserve for non-shivering adaptive thermogenesis in adult man, although it (brown fat) is much more active in youth.
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). 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.
After muscle and fat contribute to Non-shivering Thermogenesis (NST), then shivering thermogenesis is recruited.
Shivering is defined as rapid oscillations of the body to produce kinetic heat.
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. Glycogen is primarily used rather than serum glucose.
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. This may be because of similar cellular mechanics between overfeeding and cold exposure, as both possess similar inter-individual differences although UCP1 does not seem to be suspect.
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. 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.
Studies vary depending on the degree of cold and an individual's tendency to compensate with either insulative or metabolic changes. Some results report: