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EDITORIAL
HIGHLIGHTED TOPICS
A Physiological Systems Approach to Human and Mammalian Thermoregulation
In addition to this incertitude on the neural mechanisms underlying the whole body maintenance of core temperature, the mechanisms underlying the thermogenic and thermolytic responses that act to return core temperature toward its set point or null zone also remain unresolved. In these aforementioned areas, this Highlighted Topics series examines the regulation of body temperature from physiological systems approach in nine mini-reviews appearing in three issues of the Journal. In this April issue are reviews of whole body neural models of temperature regulation, and in the May issue will be reviews of mechanisms underpinning thermoeffector responses, including cutaneous vascular, eccrine sweating, and shivering responses. The final issue in June will give reviews of the influence of changes in body temperature on ventilation in large and small mammals. The detailed content of each mini-review in the series is described in the following paragraphs.
In this April issue, three mini-reviews address the set-point and null-zone neuronal models of temperature regulation in mammals. First Dr. Michel Cabanac describes Dr. H. T. Hammel's set-point model of temperature regulation and defends the general application of the set-point model to other physiological states, including fever with an elevated set point and anapyrexia with a lowered set point. Next, the potential neuronal basis of Hammel's set-point model is discussed in the mini-review by Dr. Jack A. Boulant. The tenants of Hammel's original set-point model are suggested to be supported by recent electrophysiological and morphological data where hypothalamic warm-sensitive neurons act to integrate ascending information from cutaneous thermoreceptors and that temperature-insensitive neurons in the hypothalamus provide the basis of the set-point temperature in Hammel's model. As well, recordings and morphology of excitatory postsynaptic potential (EPSP)-driven neurons in the preoptic area and in the anterior hypothalamus (PO/AH) are presented and suggested to fulfill the role of the efferent neurons in Hammel's model. In the third and final mini-review in the April issue, Dr. John Bligh outlines his theory of the null-zone model of homeothermy. His model is based on the interplay of two variables with different responses coefficients, rather than on a comparison of a variable to a constant or set point. A reciprocal cross inhibition between both a cold sensor to heat production effector pathway and a warm sensor to heat loss effector pathway is the second main component of his model, and the outcome of the model is the defense of a null zone of core temperatures. This alternative view on maintenance of core temperature also suggests temperature-insensitive neurons in the hypothalamus, thought to provide a stable reference signal for a set-point model of temperature regulation, may be neurons totally unrelated to maintenance of body temperature or homeothermy. In this light, the null-zone model accounts for the inherent variability of the sensor and effector responses for the maintenance of a stable core temperature.
In the May issue, the focus of the series will shift from integrative whole body neural models of temperature regulation to mini-reviews focused on thermoeffector responses. Dr. Dean L. Kellogg Jr., will summarize the systemic and local mechanisms underlying cutaneous vasodilatation and vasoconstriction in humans. The known mechanisms by which sympathetic cholinergic nerves mediate active vasodilatation and sympathetic noradrenergic nerves mediate cutaneous active vasoconstriction will be reviewed as will the candidate cotransmitters for these active responses. The mini-review will also present a summary of the vasodilatation and vasoconstriction responses due to changes in local tissue temperatures in human skin and will conclude with suggestions for future studies. These suggested areas of future investigation include 1) resolving the cotransmitter systems responsible for both active cutaneous vasodilatation and vasoconstriction; 2) identifying the neurotransmitter(s) that are released with skin warming and cause local hyperemia; and 3) resolving the nonneural mechanisms underlying vascular responses with prolonged local cooling of skin.
In the second mini-review in the May issue, Dr. Francois Haman will focus on mechanisms underlying variations in thermogenesis during long-term shivering and how this relates to survival in cold environments. In this context, both the influences of the substrate oxidation profile and fiber type recruitment will be examined for their affect on thermogenesis. It will be demonstrated that it is still unclear how variations in carbohydrate and lipid substrate oxidation rates contribute to variations in this heat production, although increases in shivering thermogenesis do appear plausible with glycogen supercompensation of skeletal muscle. Additionally, with an increased recruitment of type II fibers that are specialized for carbohydrate oxidation, it will be shown this is another potential avenue to help increase cold exposure survival as a consequence of shivering thermogenesis. Future directions in this area of thermoregulation research will be suggested to focus on strategies to improve shivering thermogenesis and on identifying what limits shivering endurance in hypothermic humans.
In contrast to the preceding mini-review on thermoffector response in cold environments, the third mini-review in the May issue by Drs. Manabu Shibasaki, Thad E. Wilson, and Craig G. Crandall will focus on the thermal and non-thermal factors influencing eccrine sweating in warm environments. This mini-review will highlight that, although it is well established that afferent input for this thermolytic response is from combinations of skin and core temperatures and that the efferent pathway for eccrine sweating is via cholinergic sudomotor nerves and muscarinic receptors, several nonthermal modulators of eccrine sweating need to be considered to fully understand this heat loss response. To this end the review will extend to examine the influences of changes in fluid volumes and plasma osmolarity on eccrine sweating rates. In the condition of decreased plasma volume, the potential interplay between baroreceptor unloading will also be summarized to indicate a controversy remains as to the potential influence of these pressure receptors on eccrine sweating. Additional nonthermal factors that influence eccrine sweating will also be presented, including exercise and central command or "muscle metaboreceptors," heat acclimation, and microgravity exposure. Future directions of research will be suggested to include examining how exercise during bed rest and microgravity exposure act to preserve eccrine sweating and other thermoregulatory responses.
The final issue of the series in June will commence with a mini-review by Drs. Avijit Datta and Michael J. Tipton on the "cold-shock" response evident with cold-water immersion. This response, they will indicate, is comprised of an initial gasp, hypertension, and a subsequent hyperventilation. Each of these two preceding ventilation components of the cold-shock response increase the risk of drowning, are elicited by rapid skin cooling, and are of a strength great enough to override conscious or other autonomic respiratory controls of ventilation. They will indicate that after a cold-shock response, the combination of the reestablishment of respiratory rhythm after apnea, hypoxemia, and coincident sympathetic nervous plus cyclic vagal stimulation appear to act as an arrhythmogenic trigger. The potential clinical implications of this dangerous physiological state will the be discussed in relation to sudden death during immersion, underwater birth, and sleep apnea.
In the second mini-review of the June issue, Dr. David Robertshaw will discuss the mechanisms of the panting response that appears to be most evident and effective for cooling in small hyperthermic mammals, many of whom do not sweat. Respiratory evaporative heat loss from the upper airways cools the venous drainage from the nasal epithelium, and, through a countercurrent heat exchange, this lowers the temperature of the cranium's arterial blood supply, giving a selective brain cooling (SBC). In larger hyperthermic mammals that lack both a carotid rete and the cranial anatomy typical of small panting species, a drop of cranial below thoracic temperatures is also evident, suggesting that SBC may be a widely evidenced response. The function of SBC will be suggested to act as an important water conservation mechanism through a negative feedback loop whereby brain cooling reduces evaporative heat loss to help conserve body water. It will also be indicated during high stress responses, such as typical in a fight or flight response, that SBC may be abandoned potentially to ensure maximal respiratory evaporative heat loss.
In the final mini-review in the June issue, I will examine the influences of elevations in body temperatures on ventilation in mammals in the absence of panting. It is not evident for these mammals, especially for humans whose main heat loss is through surface evaporation of eccrine sweat, how body temperature induces this increase in ventilation nor why this response is evident. It will be shown the potential mechanisms underlying this thermal response are either a multiplicative, positive interaction of resting modulators of ventilation including arterial pH and partial pressures of CO2 and O2 and body temperature and/or a direct additive effect of body temperature on ventilation. A rationale will be presented for the existence of temperature-induced elevations and temperature-induced suppressions of ventilation in nonpanting mammals. Finally it will be suggested that future studies are needed to unravel the influence of different modulators of ventilation in nonpanting hyperthermic mammals.
The mini-reviews in this Highlighted Topic series can only be viewed as a sampling of the excellent systems-level research on temperature regulation in mammals. As a first goal, it is hoped that this series will help to stimulate both new and continued physiological systems level research to help resolve the existing problems identified in these mini-reviews. In addition, because it appears inevitable the molecular biology (4) and integrative physiological systems-level approaches to the study of temperature regulation will eventually merge, a second goal is that this series will act as a starting point to foster new collaborations between these two groups of physiologists.
School of Kinesiology
Simon Fraser University
Burnaby, British Columbia, Canada
e-mail: matt{at}sfu.ca
REFERENCES
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