Peripheral vasoconstriction and reduced blood flow to extremities, such as the tail and paws in rodents and hands and feet in human, is an efficient mechanism to reduce heat loss in cold environments (66). Mammals also increase or decrease food consumption and locomotor activity to maintain thermal balance in cold and warm environments, respectively (3, 69, 70). The preference of females for warmer ambient temperatures might also be due to central mechanisms controlling whole body thermal homeostasis, i.e., sex-dependent control of the temperature set point(s) in the brain. Sex differences in sensitivity to cold and warm temperatures exist in rodents as well as in humans. In contrast, cold and heat nociceptors convey noxious temperatures and mostly do not adapt (37). Thus, it was shown that in lightly dressed women, metabolic heat production increases when air temperature decreases below 31 °C, while in men the LCT was found at 28.5 °C (32).
Nevertheless, while humans can maintain a constant Tc across the range of temperatures which are considered as the TNZ (between the LCT and UCT) (Figure 3), Tc rises in mice, especially over 30 °C (24, 25), with a circadian variation. Women present lower levels of basal metabolic rate (BMR) than men (a reduction of about a 23%) (13, 33), even at a given body mass, although the difference is much smaller (about 3%) (33). In contrast, females have more fat content than males (both whole body and subcutaneous), which increases insulation. The increase in heat production required to balance heat lost is inversely proportional to environmental temperature (Figure 3).
During repeated sauna exposure, a strong relationship was also noted between body mass loss, body surface area and heart rate response in healthy adult males (Boraczyński et al., 2018). Stable levels of body water (approximately 60% of body mass in adult men) and stable body temperature are required for healthy circulation and many physiological processes (Mayer & Bar-Or, 1994; Sawka, 1992). A positive correlation between body temperature and PRL secretion was reported by Christensen, Jørgensen, Møller, Møller, and Orskov (1985), whereas Lammintausta et al. (1976) observed a significant decrease in sodium excretion from the body during and after heat exposure in the sauna. These hormones include cortisol (COR), testosterone (TES) and dehydroepiandrosterone sulfate (DHEA-S). The group of hormones that regulate physiological processes during thermal stress involves steroid hormones that are fat-soluble and can easily cross cell membranes.
In the current study, COR levels decreased during repeated hot and cold treatment, which contradicts the results reported by Kauppinen et al. (1989) who observed an increase in COR concentrations during combined sauna treatment, in particular with ice-water immersion. Serum COR levels decreased significantly, whereas a significant increase in TES was not observed during repeated thermal stress and cold water immersion. Serum COR, TES, and GH22kD levels increased after high-intensity exercise, but further changes in hormone concentrations were not observed at the end of the sauna session (Rissanen et al., 2019). The aim of this study was to analyze the basic responses of the endocrine system in young healthy men with moderate and high levels of PA, who were exposed to heat during four 12-min sessions in a Finnish sauna. There is a general scarcity of published studies investigating the impact of thermal stress on hormonal changes in men with different physical activity (PA) levels who are regular sauna users.
BAT burns calories by activating mitochondria, your cells’ energy powerhouses, which release energy as heat instead of storing it. Testosterone-treated cells had lower lipolytic activity and increased expression of antilipolytic receptors alpha 2A-AR. We report that the expression of each AR subtype gene was distinctively regulated by NE and sex hormones in brown adipocytes. Therefore, the effect of testosterone, 17 beta-estradiol, progesterone, and norepinephrine (NE) on adrenergic receptor (AR) gene expression (alpha 2A-, beta 1-, -, and beta 3-AR) and lipolytic activity was investigated in differentiated brown adipocytes in culture.
Podstawski et al. (2013) demonstrated that a visit to the sauna can be a stressful experience for people who are rarely subjected to heat therapy. Regular sauna bathing may alleviate and prevent the risk of both acute and chronic diseases (Laukkanen et al., 2019). Each sauna session was followed by a 6-min cool-down break during which the participants were immersed in cold water (10−11°C) for 1 min. Mice overexpressing the melanocortin 4 receptor (MC4R) antagonists agouti signaling protein (ASP) or agouti-related peptide (AgRP) 86- as well as rodents and humans with hypomorphic mutations in MC4R 87, disruptions of POMC gene expression 88, 89 or of proproneuropeptide (e.g., POMC, pro-ACTH, pro-TRH) processing by prohormone convertases 90, 91 - are obese. Thus, decreased circulating leptin concentrations as a result of reduced fat mass has the net effect of stimulating food intake 1. Leptin is an adipocyte derived molecule that circulates in weight-stable individuals in direct proportion to fat mass 79. However, after a few months on a high fat diet, these changes are no longer evident 74, 75, indicating that resistance to sustained increased adiposity is less sustained than resistance to decreased adiposity 69.
This indicates that the increased appetite and lipogenesis compensate for the increase in energy expenditure. One might even be able to induce the effects of TH selectively, activating thermogenesis, for example, without concomitantly stimulating appetite and lipogenesis, which counteract the energy dissipation caused by TH. UCP-null mice apparently do not show hypothermia at room temperature, and their sensitivity to cold was revealed by the challenge of exposing them at 5°C (11). However, the extent to which FT participates in maintaining body temperature at room temperature (about 22°C) has not been defined. As mentioned above, one can argue that the half-a-degree-lower core temperature of the α1TR-deficient mouse (16) is due to a reduced FT caused by a limiting α1TR-dependent factor in the NE signaling pathway. While the lizard will rapidly equilibrate its body temperature with the ambient, the mouse will remain homeothermic and without activating FT, since by definition is at thermoneutrality temperature.
Contrarily, mice deficient in TRPM8 (the main cold sensor) develop obesity when housed at mild temperatures, exhibiting diurnal hyperphagia, reduced lipid utilization (70) and an altered circadian physiology (14). Furthermore, the study of the metabolic effects of cold ambient temperatures, including the activation of cold thermosensors is an emerging field with great physiological and medical interest. In contrast, during long-term cold exposures, the rise in food intake is insufficient to compensate for the increased metabolic output (169, 178, 179), resulting in a progressive reduction of fat mass. In contrast, in the last decades, humans have greatly increased the time spent indoors, with a widespread access to central heating and air conditioning and higher expectations of thermal comfort.

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