Maximum oxygen consumption (VO_{2 max}) elicited by swimming in 20°C water or by exposure to -2.5°C in helium/oxygen (Helox) atmosphere is higher in mice selected for low (LA) than for high (HA) stress-induced analgesia (SIA) produced by swimming. However, this line difference is greater with respect to swim- than to cold-elicited VO₂. To study the possible relationship between the analgesic and thermogenic mechanisms, we acclimated HA and LA mice to a low ambient temperature (5°C) during 6 weeks, or to daily 3-min swimming in 20°C or 32°C water during 2 weeks. Next, the acclimated mice were exposed to a 15-min Helox test at -2.5°C and to a 5-min swim test at 20°C to compare VO₂ and hypothermia (T). We also measured VO₂ and T in naive HA and LA mice merely immersed for 5 min, without swimming, in 20°C water. Cold acclimation raised VO₂ and decreased T. These effects were similar in both lines in the Helox test, but smaller in the HA than in the LA line in the swim test. HA and LA mice acclimated to swimming in 20°C or in 32°C water displayed increased VO₂ and decreased T elicited by swimming, but only HA mice acclimated to 20°C swims manifested increased VO₂ and decreased T in the Helox test. We conclude that the between-line difference in VO₂ swim results from a stronger modulation of thermogenic capacities of HA mice by a swim stress-related mechanism, resulting in SIA. This is corroborated by a considerably higher VO₂ and lower T in only immersed than in freely swimming HA mice. We suggest that the predisposition to SIA observed in laboratory as well as wild animals may significantly affect both, the results of laboratory measurements of VO₂ and the interpretation of its intra- and interspecific variation.