Getting a kick out of thermoregulation

Leave it to our fellow Canadian physiologist William Cupples. He can even get high on thermoregulation! In the quest for reaching ever higher levels of consciousness, Cupples, a student of the 60s and 70s, undertook all kinds of manoeuvres (W. Cupples 2011, personal communication). How to reach the ultimate near-Nirvana trance? An experience no legal or less legal substance on earth can trigger? No problem, simply immerge in 10 °C cold water for an hour, then inhale 55 °C warm air for reheating. It is so good, everyone seems your friend and the sole purpose of the world is to please you. Hhmmm, that reheating-sensation might almost be worth getting shipwrecked for. Needless to mention that one of the first seminal articles authored by Cupples was on the Effect of cold water immersion and its combination with alcohol intoxication on urine flow rate of man (Cupples et al. 1980). I bet Cupples volunteered for that protocol. Scandinavia and Canada share the cold environment. As human beings, we are able to cope with relatively large ranges of ambient temperature, while, on the other hand, small changes in core body temperature will harm or kill. Thus, it does not surprise that articles in Acta Physiologica (Oxford), a journal owned by the Scandinavian Physiological Society, have substantially contributed to our understanding of thermoregulation. As physiologists, we set out to achieve a better understanding of how (i) exposure to high- and low-temperature environments affect us and are counter-acted (Rudolph et al. 2007), (ii) deviances in (core) body temperature are regulated (Hashim 2010, Nakamura 2011), and (iii) how responses to changes in ambient temperature are regulated on a molecular basis (Digel 2011). In earlier times, harsh winters were a leading cause of mortality, and this is still true today for the elderly (Wilkinson et al. 2004). Remarkably, in this study, most of the ‘usual suspects’ among the medical or socioeconomic variables tested to increase an individual's risk for hypothermic mortality were ruled out as causative. Thus, further research has been devoted to elucidating the underlying pathomechanisms. Elderly show, for example, greater increases in systolic blood pressure when exposed to even short periods of cold (Kingma et al. 2011), which was shown to be at least in part because of their lack in non-shivering thermogenesis (van Marken Lichtenbelt & Schrauwen 2011) and correlated with their impaired ability to defend their core temperature. Consistently, a higher percentage in body fat acted protectively. Hypoxia has long been thought to additionally impair temperature regulation, potentially through an effect on cutaneous vasoconstriction – another suspect recently ruled out (Simmons et al. 2011). Besides advanced age, other time spans in life show significantly altered regulatory responses to hypothermia, such as pregnancy and the postpartum period (Hartgill et al. 2011). Unfortunately, humans cannot (yet) hibernate, but we have started to apply controlled hypothermia to organs or organ systems. Mild hypothermia may be used beneficially in certain pathophysiological settings: to improve survival and limit the damage done during the resuscitation period that follows cardiac arrest, by attenuating hypoxic brain injury and improving systolic myocardial function (Schwarzl et al. 2011). Cardiovascular function, on the other hand, is strongly influenced by systemic hyperthermia, which changes vasoconstrictor responses and thus the efficiency with which baroreceptor reflexes take effect – local and systemic factors interplay in a complex network, which is not yet fully understood (Crandall & González-Alonso 2010), and in which hypohydration (Merry et al. 2010) and cerebral oxygenation (Rasmussen et al. 2010) may assume limiting roles. When we investigate mechanisms by which humans sustain what we call harsh environmental conditions, all our efforts are put into perspective by tiny beings that consist of no more than 40 000 cells each: Tardigrades (Fig. 1), or Water Bears, who populate environments that would kill any vertebrate: high-intensity radiation, being shot into the vacuum of outer space, centuries of complete dehydration and temperatures from close to absolute zero or up to 150 °C. These remarkable organisms survive by, for example, the use of specific bioprotectants and DNA repair mechanisms (Møbjerg et al. 2011) that humans, be they Scandinavian, Canadian or not, can only dream of. However, it is not only changes in ambient temperature that challenge the thermoregulatory system. Exposure to bacterial endotoxins induces fever. Interestingly, an early-in-life exposure to LPS seems to influence the adult febrile response (Saia et al. 2011). Furthermore, core body temperature and our circadian rhythms interact closely. Thus, it had been assumed that exercise, having been shown to modify circadian rhythms, does so by elevating core body temperature. However, this does not seem true, at least in poikilothermic species such as the exercising zebrafish (Egg et al. 2011). Recently, new insights have been gained on the molecular basis underlying the thermoregulatory response – some relating to all-time favourites of thermoregulation, some to surprising newcomers. Adenosine is known to be involved in metabolic and thermoregulatory control. However, Yang et al. (2010) describe a surprisingly circumscript phenotype of the adenosine A3 receptor knockout mouse, which displays changed circadian rhythms and temperature regulatory responses. Weber & Campbell (2011) have reviewed the current state-of-the art on the temperature dependence of the cooperative Hb-O2 interaction: How can oxygen be efficiently unloaded in the working muscle, but, at the same time, be utilized by heat and/or cold-tolerant species in changing environments? Variable species-specific effectors answer this problem, which all serve the common purpose to reduce temperature dependence of the Hb-O2 interaction. Thermosensation is one of the main functions of the transient receptor potential vanilloid (TRPV) channels (Moran et al. 2011 (Baylie & Brayden 2011). Interestingly, TRPV 1-4 do not mainly seem to be involved in thermoregulation, but rather in thermal hyperalgesia (TRPV1), noxious heat sensation (TRPV2/3) and general peripheral thermosensation (TRPV4). Vascular innervation regulates arterial tone, and, as such, is critically involved in thermoregulation. Storkebaum & Carmeliet (2011) describe a novel role of the vascular endothelial growth factor system within the vascular neuroeffector junctions and its potential relevance for local and systemic defects of thermoregulation or thermally triggered pathologies such as Raynaud's phenomenon. Articles in Acta Physiologica have, as is true for many other topics, considerably advanced our understanding of thermoregulation. However, knowing more often implies the realization of how much we still need to learn. PBP is contemplating on copying Cupples and coworkers’ protocol on cold water immersion and its combination with alcohol intoxication.

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