Recovering body temperature from acute cold stress is associated with delayed proinflammatory cytokine production in vivo

A poor outcome of whole-body hypothermia often results from a late complication, rather than from acute effects of hypothermia. A low body (cell) temperature or the increase in the concentrations of the stress hormones cortisol, epinephrine, and norepinephrine in response to acute cold stress have been proposed as potent proinflammatory cytokine suppressant. In the current study, we tested the hypothesis that the recovery of body temperature from a whole-body intermittent cold-water immersion (CWI, at 13-14 degrees C for a total 170 min) is associated with a delayed response of proinflammatory cytokines in young healthy men. Our results revealed a delay in the increase in the proinflammatory interleukin 6 and interleukin 1 beta cytokines after the CWI, which paralleled the changes in cortisol, epinephrine, norepinephrine, and body temperature. CWI decreased tumor necrosis factor alpha (TNF-alpha) immediately and 1 h after the CWI. Although TNF-alpha had recovered to the preimmersion level at 2 h after CWI, its natural circadian cycle kinetics was disrupted until 12 h after the CWI. Furthermore, we showed that CWI strongly modified the white blood cell counts, with changes reaching a peak between 1 and 2 h after the CWI.

Automated summary

Whole-body hypothermia can lead to delayed changes in proinflammatory cytokines and white blood cell counts, which parallel fluctuations in cortisol, epinephrine, norepinephrine, and body temperature.