## 3 Results and Discussion
### Physiological/Mechanistic Interpretation of Thermoregulatory CIVC/CIVD Reactions
#### 3.2.2 A New Model for Thermoregulatory Localised CIVC/CIVD Reactions  
In the present paper, we suggest a new model for thermoregulatory localised CIVC/CIVD reactions. Figure 13 depicts the main workflow of the suggested CIVC/CIVD thermoregulatory model. The proposed model is based on the suggestion that there have to be rate-sensitive receptors, which are able to detect the changes in the heat dissipation rate (\(\dot{\mathrm{Q}}_{\mathrm{dis}}\)). This rate-sensitive mechanism, which is not yet clear, is also suggested by [PERSON] et al. (2016). It is clear from the current work and the presented results by [PERSON] et al. (2017) that the CIVC, indicated by drop in blood flow rate (\(320\pm 92\) PU), starts earlier (\(1.55\pm 21\) min), before the drop in the skin temperature. This suggests that the initial CIVC is triggered not based on skin temperature threshold, but rather on a certain threshold in the rate of heat dissipation from the skin to the surrounding environment. Under normal temperature (normothermia), the blood vessels are dilated (initial state = vasodilation), with a baseline level of vasoconstrtitive tone ([PERSON] et al., 2016). Due to the temperature difference (\(\Delta T=T_{sk}-T_{\infty}\)) between skin and the environment, which is the driving force for heat flow, there is always a certain level of negative heat flux (dissipation) from the skin to the surrounding environment. Once the step-localised cooling is applied, this results in a sudden increase in the temperature difference (\(\Delta T=18\pm 0.6\)\({}^{\circ}\)C in the first two minutes), and consequently, a sudden increase in the heat dissipation rate (\(\dot{\mathrm{Q}}_{\mathrm{dis}}=-0.15\pm 0.2\) W in the first two minutes). If this change in the heat dissipation rate is above a certain threshold, the CIVC mechanisms are activated and vasoconstriction prevailed. Then, if the heat dissipation rate reaches a constant threshold level (\(\frac{d\dot{\mathrm{Q}}_{\mathrm{dis}}}{dt}=0\)), the vasoconstriction mechanism will be interrupted and revert to vasodilation. Otherwise, the vasoconstriction state is prolonged. It should be stated here that this proposed model leaves a number of questions open for further investigation. One very important question, here, is about the nature of the rate-sensitive receptors and their working mechanism. In their work on the coding of cutaneous temperature and thermal receptors ([PERSON] et al., 2016), [PERSON] et. al. observed that the responses of cold-responding neurons peaked during the transient cooling phase and rapidly adapted to steady cold stimuli, suggesting that these neurons report temperature changes. In other word, cold-responding neurons report the relative drop in skin temperature (i.e., rate of temperature change \(\frac{dT_{sk}}{dt}\)), rather than the absolute value ([PERSON] et al., 2016). Additionally, many questions are still open regarding the nature of thermal sensation and thermal-sensory system in relation to thermoregulation ([PERSON] et al., 2016). It is possible in our case to use many of the control-system terms to describe autonomic thermoregulation reactions (CIVC/CIVD), such as the regulated (controlled) variable (finger skin temperature), sensors (skin and preoptic area of the hypothalamus), integrator/controller, and effectors or actuators (blood vessels). However, a concept such as the set point in thermoregulation, and in homeostatic regulation in general, has eluded precise identification. Determination of where such a set point is precisely located, how it is consulted, and even more fundamentally, how the precise set-point value is established has been elusive ([PERSON] et al., 2016).