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 degrees 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 degrees 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 degrees 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.