The best research is hypothesis-driven. Occasionally, the techniques necess
ary for investigators to address their hypotheses are readily available; mo
re often, they are not. A consequence is that investigators usually need to
acquire, adapt, or develop appropriate methodology. This has certainly bee
n the case in thermoregulatory research. A major advance in thermoregulator
y studies was the recognition that core temperature often provides little i
nformation about central regulation. In contrast, much has been learned by
specifically quantifying response thresholds (triggering core temperatures)
, gains (incremental intensity increases with further core-temperature devi
ation), and maximum response intensities. Critical to this effort was metho
dology for quantifying responses under clinical conditions, and development
of practical models that compensate for the typical simultaneous changes i
n core and skin temperatures. These studies led to the recognition that ane
sthetics profoundly inhibit thermoregulatory control, but do so in a specif
ic fashion: they increase warm-defense thresholds while simultaneously decr
easing cold-response thresholds. The results is a 10- to 20-fold increase i
n the interthreshold range (temperatures not triggering thermoregulatory de
fenses). New methods were also required to fully quantify changes in body h
eat content and, especially, distribution of heat within body tissues. Amon
g the most important has been a technique whereby roughly 20 needle thermoc
ouples are inserted in the arms and legs. The resulting temperature distrib
ution is then fit to a fourth-order radial regression and integrated over v
olume. Studies using these methods have demonstrated that an internal redis
tribution of body heat is the primary cause of core hypothermia in most sur
gical patients.