Summary
This review focuses on the endocrine responses to thermal stimuli during passive heat or cold exposure, with particular reference to the relation of these responses to the changes in the body core temperature (T core). Mild to moderate hyperthermia (<1°C rise in T core) induces the release of growth hormone and prolactin (PRL). Moderate hypothermia (1°–2°C fall in T core) suppresses PRL release. A positive correlation between plasma PRL and T core suggests some role for PRL in thermoregulation. Hypothermia activates the hypothalamo-pituitary-thyroid (HPT) axis and releases thyrotropin-releasing hormone, thyroid-stimulating hormone (TSH), and thyroid hormones and increases the metabolic rate. Enhancement of extrathyroidal production of triiodothyronine (T3) from thyroxine (T4) may precede the TSH response to cold. Both severe hyperthermia and hypothermia (1°–3°C changes in T core) activate the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system, resulting in release of corticotropin-releasing factor, adrenocorticotropic hormone, cortisol, and norepinephrine. The responses in the HPT axis and the HPA axis are not apparent in humans, as they are in rats, probably owing to the larger body mass of humans. Hyperthermia stimulates the renin-angiotensin-aldosterone system and the release of arginine vasopressin (AVP) and atrial natriuretic peptide, but this might be due to nonthermal factors. Diuresis due to suppression of AVP release is induced by cold. Gonadal response to thermal stimuli is possibly suppressive. The hormonal responses induced by thermal stress are mostly dependent on the change in T core in humans; in small animals they are also dependent on the change in skin temperature.
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Matsumoto, T. et al. (2001). Endocrine Responses to Heat and Cold Stress. In: Kosaka, M., Sugahara, T., Schmidt, K.L., Simon, E. (eds) Thermotherapy for Neoplasia, Inflammation, and Pain. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67035-3_26
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