Thermoneutral zone (TNZ) is defined as the range of ambient temperature (Ta) at which core temperature (Tc) regulation is achieved only by obligatory thermogenesis and sensible heat loss. Above the TNZ, (above the upper critical temperature, UCT), there is an increase of the metabolic rate because of the energy cost of the mechanisms for cooling. When environmental temperatures either exceed or fall below the TNZ, the metabolic rate increases by activation of thermoregulatory mechanisms.
When cutaneous vasodilation is unable to meet the thermal homeostatic requirements set by the POA, the SNS stimulates sweating by releasing acetylcholine which binds to muscarinic type-3 (M3) receptors expressed in the sweat glands (82). In addition, there is evidence that TRPA1 channels are required for cold-induced vasoconstriction and CIVD in paw cutaneous vasculature (77, 78), although the involvement of TRPA1 in cold sensation and thermoregulation is contentious. Furthermore, when the cold stimulus is prolonged, the cutaneous vasoconstriction abruptly stops and the vessels dilate, allowing the reperfusion of the tissue to avoid cold-induced tissue injury; a process called cold-induced vasodilation (CIVD). Cooling of the skin activates cutaneous cold thermoreceptors that initiate the vasoconstrictor response.
In rodents the effect is not so evident because they do not have a real luteal phase, but the increase of plasma progesterone concentrations during the end of proestrus and beginning of estrus may be involved in the elevated Tc levels of estrus (19) (Figure 1). Sex hormones are proposed to influence Tc by direct action on hypothalamic POA neurons. Although the mechanism(s) underlying the differences in Tc between sexes are still not well established, gonadal hormones are considered as main factors. Finally, sex-specific differences are observed in Tc levels in laboratory animals (9, 10) and in humans (6). We finally discuss how sex-dependent characteristics in thermal responses may induce metabolic differences between males and females, with a clear physiological, clinical, and therapeutic relevance.
Sex hormones play a critical role in the development of sex differences in BAT thermogenic activity (141–143). Therefore, at the usual rodent housing temperature (22 °C), BAT in female rats represents a greater proportion of total body mass, shows more hypertrophy and a more multilocular pattern of lipid droplets and exhibits higher UCP1 levels and larger and more functional BAT mitochondria. Most studies also report the influence of the ovarian cycle in the initiation of cold-induced shivering, with the set-point moving towards warmer temperatures in the luteal phase (6) (Figure 4). Sexual hormones play a central role in these sex differences, with estrogens as principal stimulators of BAT activity and WAT browning and regulators of vasomotor control, and progesterone as a thermogenic signal acting at the set-point(s) in the hypothalamus. Accordingly, cold output mechanisms will be activated at higher ambient temperatures in women than in men. The increase of Tc levels in women is a regulated process, as shown by the shifts in thermoregulatory thresholds of effector mechanisms toward the defense of this higher 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.
These results are consistent with studies of vastus lateralis muscle biopsies in which the ratio of glycolytic (phosphofructokinase, PFK) to oxidative (cytochrome oxidase) enzyme activities is significantly decreased following weight loss. Since these effects are most evident at low levels of work, i.e., those commensurate with activities of daily living, it is reasonable to infer that some of the opposition to reduced weight maintenance can be diminished by exercising at higher levels of power output 20, 24. The pre-eminence of NREE - accounting for as much of 85–90% of the decline in TEE below predicted values in weight-reduced subjects 20, 22 could be due to declines in the actual amount of physical activity performed.
The maintenance of homeothermy requires a fine regulation of food intake, heat production, heat conservation or dissipation and energy expenditure, which will heavily affect energy metabolism and energy balance. Increasing evidence has highlighted the intimate interlink between thermal and energy homeostasis. Extreme external temperatures that overwhelm the normal thermoregulatory mechanisms or, alternatively, disruptions in the normal functioning of the thermoregulatory system will produce hyperthermia or hypothermia, which may be life-threatening. Homeothermy requires a fine regulation of food intake, heat production, conservation and dissipation and energy expenditure. Thermal homeostasis is a fundamental process in mammals, which allows the maintenance of a constant internal body temperature to ensure an efficient function of cells despite changes in ambient temperature.
Muscle tissue itself is metabolically active and contributes significantly to your basal metabolic rate. One key aspect of testosterone, thermogenic or not, is its anabolic effect, meaning it helps build and preserve muscle. Let’s jump into what thermogenic testosterone really means and how it might support your wellness journey.

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