During hibernation and daily torpor, metabolic rate (MR) can be maximally r
educed to only 1 or 12%, respectively, of the minimum euthermic levels. The
physiological mechanisms causing these metabolic reductions remain unclear
and are under debate. Earlier observations based on high ratio of (MReuthe
rmia/MRhibernation) and high corresponding Q(10) values (>3), suggest tempe
rature-independent mechanisms such as tissue acidification through retentio
n of respiratory CO2 may be involved in actively inhibiting metabolism beyo
nd the effect of low body temperature (Tb) alone. This, however, has been c
hallenged due to inherent problems in defining the proper MReuthermia For c
omparison and the proper execution of Q(10) calculation. The proposition th
at a reduced thermoconductance during torpor could account for the reduced
metabolism and that the (Tb-Ta) gradient ultimately determines the level of
metabolism during torpor have also been challenged. Since the thermoregula
tory set-point (Tset) is progressively lowered during entry into torpor and
remains low during torpor, and hibernators and daily heterotherms are capa
ble of strong thermogenic efforts even at low Tb the prevailing level of MR
during torpor likely reflects the thermogenic magnitude (or its suppressio
n) of the error signal (Thypo-Tset) and the Arrhenius effect on MR. To date
, however, no direct evidence hits been provided to argue Fur or against an
y of the above conjectures. We have proposed a different experimental appro
ach which could allow direct comparison of minimum MR at the same Tb during
hibernation and induced hypothermia. This hopefully will resolve if active
inhibition of MR is indeed a state-dependent characteristic of torpor and
hibernation.