The effect of body temperature on the hunting response of the middle finger skin temperature

Abstract

The relationship between body temperature and the hunting response (intermittent supply of warm blood to cold exposed extremities) was quantified for nine subjects by immersing one hand in 8 degree C water while their body was either warm, cool or comfortable. Core and skin temperatures were manipulated by exposing the subjects to different ambient temperatures (30, 22, or 15 degrees C), by adjusting their clothing insulation (moderate, light, or none), and by drinking beverages at different temperatures (43, 37 and 0 degrees C). The middle finger temperature (Tfi) response was recorded, together with ear canal (Tear), rectal (Tre), and mean skin temperature (Tsk). The induced mean Tear changes were -0.34 (0.08) and +0.29 (0.03) degrees C following consumption of the cold and hot beverage, respectively. Tsk ranged from 26.7 to 34.5 degrees C during the tests. In the warm environment after a hot drink, the initial finger temperature (T(fi,base)) was 35.3 (0.4) degrees C, the minimum finger temperature during immersion (T(fi,min)) was 11.3 (0.5) degrees C, and 2.6 (0.4) hunting waves occurred in the 30-min immersion period. In the neutral condition (thermoneutral room and beverage) T(fi,base) was 32.1 (1.0) degrees C, T(fi,min) was 9.6 (0.3) degrees C, and 1.6 (0.2) waves occurred. In the cold environment after a cold drink, these values were 19.3 (0.9) degrees C, 8.7 (0.2) degrees C, and 0.8 (0.2) waves, respectively. A colder body induced a decrease in the magnitude and frequency of the hunting response. The total heat transferred from the hand to the water, as estimated by the area under the middle finger temperature curve, was also dependent upon the induced increase or decrease in Tear and Tsk. We conclude that the characteristics of the hunting temperature response curve of the finger are in part determined by core temperature and Tsk. Both T(fi,min) and the maximal finger temperature during immersion were higher when the core temperature was elevated; Tsk seemed to be an important determinant of the onset time of the cold-induced vasodilation response.

Influence of thermal balance on cold-induced vasodilation

“…Although our finding was based on finger temperature and not on actual blood flow data, it is supported by observations of a central component to CIVD (8,34,37,41,42,46). Furthermore, thermal balance has been shown to influence CIVD in a way that whole body cooling results in delayed CIVD onset (14,17,30,46), whereas increased thermogenesis (44) or body heat content (14) result in accelerated CIVD response.The difficulty to hitherto elucidate the CIVD response may be partly attributable to the currently incomplete understanding of its neurophysiological mechanisms. These mechanisms can be explored by monitoring heart rate variability (HRV) during CIVD because the cardiovascular adaptations to thermal stimuli are the result of a simultaneous activation of the peripheral vascular and cardiac efferent branches of the autonomic nervous system (36).…”

“…Although our finding was based on finger temperature and not on actual blood flow data, it is supported by observations of a central component to CIVD (8,34,37,41,42,46). Furthermore, thermal balance has been shown to influence CIVD in a way that whole body cooling results in delayed CIVD onset (14,17,30,46), whereas increased thermogenesis (44) or body heat content (14) result in accelerated CIVD response.…”

“…Ergo, according to the deductive reasoning rule of transposition (7), since the presence of CIVD implies excess heat in a cold environment, it can be inferred that CIVD will not occur in circumstances in which excess heat is not present in a cold environment. Additional support for this notion is provided by previous investigations in different mammalian models, suggesting a correspondence between oscillations in peripheral temperature/blood flow during cold exposures and body (8,11,13,14,17,24,30,34,37,41,42,44,46) or ambient temperature (33,45). It is also generally agreed that there is a central component in CIVD, given that normothermic and/or centrally warm homoeotherms demonstrate accelerated CIVD responses (14,44), while those that are centrally cold reveal CIVDs of delayed onset and lesser magnitude (14,17,30,46).…”

“…The literature contains two previous studies that investigated the influence of altered thermal balance on CIVD, both showing that body heat content exerts a potent influence on CIVD (14,43). These studies suggested that mean skin temperature and T re serve as inputs for the vasomotor center in the central nervous system that determines the finger vasomotor status by modifying the sympathetic output to the peripheral nerves (14).…”

“…These studies suggested that mean skin temperature and T re serve as inputs for the vasomotor center in the central nervous system that determines the finger vasomotor status by modifying the sympathetic output to the peripheral nerves (14). Based on this hypothesis, sympathetic output increases and peripheral vasoconstriction occurs when the core and the skin are cool, while CIVD appears to be superimposed on the general vascular status of the peripheral blood vessels (14). Our results are in contrast to this hypothesis, since the HRV data obtained before and during CIVD demonstrated a shift of autonomic interaction toward parasympathetic dominance.…”