Influence of thermal balance on cold-induced vasodilation

Abstract

We examined the effect of thermal balance perturbation on cold-induced vasodilation through a dynamic A-B-A-B design applying heat (condition A) and cold (condition B) to the body's core, while the hand is exposed to a stable cold stimulus. Fifteen healthy adults (8 men, 7 women) volunteered. Applications of heat and cold were achieved through water immersions in two tanks maintained at 42 and 12°C water temperature, respectively, in an A-B-A-B fashion. Throughout the experiment, the participants' right hand up to the ulnar styloid process was placed inside a temperature-controlled box set at 0°C air temperature. Results demonstrated that cold-induced vasodilation occurred only during condition B and at times when body heat content was decreasing but rectal temperature had not yet dropped to baseline levels. Following the occurrence of all cold-induced vasodilation events, rectal temperature was reduced, and the phenomenon ceased when rectal temperature fell below baseline. Heart rate variability data obtained before and during cold-induced vasodilation demonstrated a shift of autonomic interaction toward parasympathetic dominance, which, however, was attributed to a sympathetic withdrawal. Receiver operating characteristics curve analyses demonstrated that the cold-induced vasodilation onset cutoff points for rectal temperature change and finger temperature were 0.62 and 16.76°C, respectively. It is concluded that cold-induced vasodilation is a centrally originating phenomenon caused by sympathetic vasoconstrictor withdrawal. It is dependent on excess heat, and it may be triggered by excess heat with the purpose of preserving thermal balance.finger blood flow; thermoregulation COLD-INDUCED VASODILATION (CIVD) is a counterintuitive acute increase in local cutaneous blood flow occurring in humans and other homoeotherms exposed to cold (11), first identified in 1930 (35). The emergence of CIVD has been described as nonsystematic, and, hence, its function(s) as well as its causative agent(s) remain unexplainable (10,11,40). We recently proposed that CIVD is a thermoregulatory mechanism triggered by increased mean body temperature (19). 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).Our primary objective in this experiment...

On the origins of cold-induced vasodilation

“…We have reported a sympathetic withdrawal during CIVD (Flouris and Cheung 2009b) in line with the evidence that CIVD is attributed to an interruption of adrenergic neurotransmission (Johnson et al 1986). Given that sympathetic activity is generally inversely associated with core temperature (Sawasaki et al 2001), Daanen and Layden derived that ''…the sympathetic activity must have been continuously increasing during the cooling period'' which led them to the conclusion that CIVD in our study ''…was of peripheral rather than central origin''.…”

Enhancement of the finger cold-induced vasodilation response with exercise training

“…In particular, there are findings supporting the hypothesis that local paralysis of vasoconstrictory tone is the primary mechanism of CIVD (Daanen 2003), whereas others suggest a central component caused by sympathetic vasoconstrictor withdrawal (Flouris and Cheung 2009;Flouris et al 2008).…”

Thermometry and calorimetry assessment of sweat response during exercise in the heat

“…A flexible thermistor (MA-100, Thermometrics, Edison, NJ, USA) was inserted in the participants' ear canal and was used as an index of tympanic temperature using a previously described procedure (Flouris and Cheung 2009). Values for rectal and tympanic temperature were recorded throughout the thermal protocol at 8-s intervals using a data logger (Smartreader 8 Plus, ACR, Vancouver, Canada) interfaced with a computer to allow for their continuous monitoring by the investigators.…”

“…This is noteworthy because it may lead to erroneous conclusions with regards to the control of sweat secretion. The probability of this scenario can be examined by investigating sweat rate responses during simultaneous minute-by-minute measurements of the individual heat balance components by whole-body partitional calorimetry (Vallerand et al 1992a, b;Flouris and Cheung 2009). Hence, our objective in this experiment was to characterise sweat rate responses in a hot environment during rest and subsequent increasing levels of exercise in relation to thermometrically (i.e., rectal, tympanic, mean skin and mean body temperatures) and calorimetrically derived (i.e., change in body heat storage) thermal parameters.…”