The common frog (Rana temporaria) spends the coldest months of each year overwintering in ice-covered ponds where temperatures can vary from 0.5 to 4.0 degrees C. Over the course of a winter season, the animals enter progressively into a state of metabolic @entity308 that relies almost exclusively on aerobic production of @entity855 . However, if aerobic metabolism is threatened, for example by @entity519 , decreases in the animal's metabolic rate can reach upwards of 75% compared with the 50% decrease seen during normoxia. Under these conditions, the major proportion of the overall reduction in whole-animal metabolic rate can be accounted for by metabolic suppression of the skeletal muscle (which makes up approximately 40% of body mass). Little is known about the properties of mitochondria during prolonged periods of metabolic @entity308 , so we have examined several aspects of mitochondrial metabolism in the skeletal muscle of frogs over periods of hibernation of up to 4 months. Mitochondria isolated from the skeletal muscle of frogs hibernating in @entity519 water show a considerable reorganisation of function compared with those isolated from normoxic submerged animals at the same temperature (3 degrees C). Both the active (state 3) and resting (state 4) respiration rates of mitochondria decrease during @entity519 , but not normoxic, hibernation. In addition, the affinity of mitochondria for @entity26 increases during periods of acute @entity519 stress during normoxic hibernation as well as during long-term hibernation in @entity519 water. The decrease in mitochondrial state 4 respiration rates during @entity519 hibernation evidently occurs through a reduction in electron-transport chain activity, not through a lowered proton conductance of the mitochondrial inner membrane. The reduced aerobic capacity of frog skeletal muscle during @entity519 hibernation is accompanied by lowered activities of key enzymes of mitochondrial metabolism caused by changes in the intrinsic properties of the mitochondria. In the absence of @entity26 , the mitochondrial F(1)F(o)- @entity4430 (the @entity855 synthase) begins to run backwards as it actively pumps protons from the matrix in an attempt to maintain the mitochondrial membrane potential. At this time, the @entity855 synthase functions as an @entity4430 to preserve a certain proton-motive force. Frogs limit @entity855 wastage during @entity519 by a profound inhibition of the @entity855 synthase. Taken together, our studies show that protonmotive force is lowered aerobically by restricting electron supply and during @entity519 by restricting mitochondrial @entity4430 activity.

Adaptive plasticity of skeletal muscle energetics in hibernating frogs: mitochondrial proton leak during metabolic XXXX .

@entity4430 :: ('1769', 'Gene') :: ['ATPase'] @entity308 :: ('MESH:D003866', 'Disease') :: ['depression'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity519 :: ('MESH:D000860', 'Disease') :: ['increasingly hypoxic conditions', 'anoxia', 'hypoxic'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity308 :: (MESH:D003866,Disease) :: ['depression']
