Exposure of an animal to stressful stimuli, perceived by the animal as a threatening, emergency condition, elicits a transient decrease of pain sensitivity, which often affects thermoregulatory mechanisms in the threatened organism. We studied the interaction between emergency and thermoregulatory components of swim stress in developing swim stress-induced analgesia (SSIA). The subjects were mice selectively bred for high analgesia (HA) induced by swimming in 20 degrees C water, and displaying profound swim hypothermia. The mice were acclimated to one of the following conditions: (1) ambient cold (5 degrees C, mimicking the thermal component of swim stress); (2) daily 3-min swimming at 32 degrees C (mimicking the emergency, emotional in nature, component of swim stress), or (3) daily swimming at 20 degrees C (a combination of both emergency and thermal component of swim stress). Following each of the procedures the analgesia induced by swimming in 20 degrees C water and by acute exposure to -2.5 degrees C in helium/oxygen (Helox) atmosphere was measured. Analgesia was also assessed in a group of naive mice immersed in 20 degrees C shallow water with the purpose of eliminating the emergency condition, but assuring the animal's contact with the cold water environment. Cold acclimation markedly attenuated Helox-induced analgesia (HIA) without affecting SSIA, whereas repeated swims attenuated SSIA without affecting HIA. The results suggest that hypothermia is the only stimulus eliciting HIA, while the emergency condition of swimming is essential for inducing SSIA. The significantly lower magnitude of SSIA in mice acclimated to repeated swims in 20 degrees C than in 32 degrees C water suggests that SSIA develops due to an interaction between the emergency and hypothermic components of swim stress. This is further supported by a greater hypothermia and greater analgesia in freely swimming than in immersed naive mice.