scholarly journals An hourglass mechanism controls torpor bout length in hibernating garden dormice

2021 ◽  
Author(s):  
Thomas Ruf ◽  
Kristina Gasch ◽  
Gabrielle Stalder ◽  
Hanno Gerritsmann ◽  
Sylvain Giroud
Keyword(s):  
Oxygen Consumption ◽  
Cellular Damage ◽  
Torpor Bout ◽  
Bout Length ◽  
Garden Dormouse ◽  
Rate Of Oxygen Consumption ◽  
Metabolic Imbalance ◽  
Eliomys Quercinus ◽  
Periodic Arousals ◽  
Torpor Bouts

Hibernating mammals drastically lower their rate of oxygen consumption and body temperature (Tb) for up to several weeks, but regularly rewarm and stay euthermic for brief periods (< 30 h). It has been hypothesized that these periodic arousals are driven by the development of a metabolic imbalance during torpor, that is, the accumulation or the depletion of metabolites or the accrual of cellular damage that can be eliminated only in the euthermic state. We obtained oxygen consumption (as a proxy of metabolic rate) and Tb at 7-minute intervals over entire torpor-arousal cycles in the garden dormouse (Eliomys quercinus). Torpor bout duration was highly dependent on mean oxygen consumption during the torpor bout. Oxygen consumption during torpor, in turn, was elevated by Tb, which fluctuated only slightly in dormice kept at∼3-8°C. This corresponds to a well-known effect of higher Tb on shortening torpor bout lengths in hibernators. Arousal duration was independent from prior torpor length, but arousal mean oxygen consumption increased with prior torpor Tb. These results, particularly the effect of torpor oxygen consumption on torpor bout length, point to an hourglass mechanism of torpor control, i.e., the correction of a metabolic imbalance during arousal. This conclusion is in line with previous comparative studies providing evidence for significant interspecific inverse relationships between the duration of torpor bouts and metabolism in torpor. Thus, a simple hourglass mechanism is sufficient to explain torpor/arousal cycles, without the need to involve non-temperature-compensated circadian rhythms.

Hibernation in the Eastern Pygmy Possum, Cercartetus-Nanus (Marsupialia, Burramyidae)

1993 ◽  
Vol 41 (1) ◽  
pp. 67 ◽  
Author(s):  
F Geiser
Keyword(s):  
Oxygen Consumption ◽  
Body Temperature ◽  
Metabolic Rate ◽  
Air Temperature ◽  
The Body ◽  
Daily Torpor ◽  
Rate Of Oxygen Consumption ◽  
The Mean ◽  
Cercartetus Nanus ◽  
Torpor Bouts

The pattern of torpor was examined in the eastern pygmy possum, Cercartetus nanus (21 g). Animals displayed torpor regularly in the laboratory, and the occurrence of torpor increased with decreasing air temperature (T(a)). At high T(a) (18-degrees-C) animals usually exhibited daily torpor, but torpor bouts of up to 2 days were observed occasionally. The duration of torpor bouts lengthened with a lowering of T(a) and the mean bout duration at T(a) = 5-degrees-C was 17.0 +/- 2.5 days. The minimum metabolic rate (measured as rate of oxygen consumption) of torpid individuals was 0.018 +/- 0.003 mL O2 g-1 h-1, which is less than 2% of the basal metabolic rate. The body temperature (T(b)) Of torpid animals fell to a minimum of 1.3 +/- 0.4-degrees-C. These results clearly demonstrate that Cercartetus nanus is a deep hibernator.

scholarly journals Remnant kidney oxygen consumption: hypermetabolism or hyperbole?

1992 ◽  
Vol 3 (2) ◽  
pp. 151-156
Author(s):  
R M Culpepper ◽  
A C Schoolwerth
Keyword(s):  
Oxygen Consumption ◽  
Free Radicals ◽  
Renal Mass ◽  
Tissue Injury ◽  
Reactive Species ◽  
Cellular Damage ◽  
Oxygen Reactive Species ◽  
Rate Of Oxygen Consumption ◽  
The Face ◽  
Remnant Kidney

On the basis of observations in surgically created remnant kidneys of rat and dog, a novel hypothesis for progressive injury in the setting of reduced renal mass has been put forth. Both rat and dog remnant kidneys exhibit significant hypertrophy that is accompanied by an increased rate of oxygen consumption (QO2) per remaining nephron but not per gram of tissue. This putative "hypermetabolism" is seen in the face of progressive scarring of the tubulointerstitial compartment of the remnant kidney, and interventions that reduce QO2 in these models have been associated with reduced tissue injury in previous studies. The proposed pathway by which an increase in QO2 leads to cellular damage is via the production of oxygen-reactive species or free radicals. In this article, the available data upon which this "hypermetabolism" hypothesis is based are reviewed and the constructs within which these data have been analyzed are examined. From these considerations, a set of questions not yet answered that may serve to direct more fruitful query into this intriguing problem

scholarly journals Recovery heat in muscular contraction without lactic acid formation

1931 ◽  
Vol 108 (757) ◽  
pp. 279-301 ◽  
Keyword(s):  
Acetic Acid ◽  
Oxygen Consumption ◽  
Lactic Acid ◽  
Muscular Contraction ◽  
Acid Formation ◽  
Anaerobic Conditions ◽  
Spontaneous Breakdown ◽  
Rate Of Oxygen Consumption ◽  
Resting Muscle

In a comparison of muscles poisoned with mono-iodo-acetic acid (IAA) in the presence and in the absence of oxygen respectively, Lundsgaard (1930) found:- (1) That the spontaneous breakdown of phosphagen in poisoned resting muscle is much more rapid under anaerobic conditions. (2) That the onset of the characteristic contracture produced by IAA is accompanied always by an increase in the rate of oxygen consumption.

Proximal tubule dysfunction in cystine-loaded tubules: effect of phosphate and metabolic substrates

1996 ◽  
Vol 271 (3) ◽  
pp. F717-F722
Author(s):  
G. Bajaj ◽  
M. Baum
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Tricarboxylic Acid Cycle ◽  
Dimethyl Ester ◽  
Proximal Tubules ◽  
Intracellular Atp ◽  
Metabolic Substrates ◽  
Rate Of Oxygen Consumption ◽  
Intracellular Phosphate

Intracellular cystine loading by use of cystine dimethyl ester (CDME) results in a generalized inhibition in proximal tubule transport due, in part, to a decrease in intracellular ATP. The present study examined the importance of phosphate and metabolic substrates in the proximal tubule dysfunction produced by cystine loading. Proximal tubule intracellular phosphorus was 1.8 +/- 0.1 in control tubules and 1.1 +/- 0.1 nmol/mg protein in proximal tubules incubated in vitro with CDME P < 0.001). Infusion of sodium phosphate in rabbits and subsequent incubation of proximal tubules with a high-phosphate medium attenuated the decrease in proximal tubule respiration and prevented the decrease in intracellular ATP with cystine loading. Tricarboxylic acid cycle intermediates have been shown to preserve oxidative metabolism in phosphate-depleted proximal tubules. In proximal tubules incubated with either 1 mM valerate or butyrate, there was a 42 and 34% reduction (both P < 0.05) in the rate of oxygen consumption with cystine loading. However, tubules incubated with 1 mM succinate or citrate had only a 13 and 14% P = NS) reduction in the rate of oxygen consumption, respectively. These data are consistent with a limitation of intracellular phosphate in the pathogenesis of the proximal tubule dysfunction with cystine loading.

Viability and respiratory activity ofPseudomonas syringaecells starved in buffer

1995 ◽  
Vol 41 (4-5) ◽  
pp. 372-377 ◽  
Author(s):  
João P. S. Cabral
Keyword(s):  
Oxygen Consumption ◽  
Electron Transport ◽  
Pseudomonas Syringae ◽  
Respiratory Activity ◽  
Bacterial Cells ◽  
Intact Cells ◽  
Rate Of Oxygen Consumption ◽  
Metabolic Activities ◽  
Different Levels ◽  
Number Of Cells

Pseudomonas syringae cells starved in buffer released orcinol-reactive molecules and materials that absorbed ultraviolet light. The number of cells culturable in nutrient medium decreased more rapidly than the number of intact particles determined by microscopy. The results suggested that starvation resulted in the lysis of an increasing number of cells, and that a fraction of the intact particles were not culturable. Starvation also resulted in a decrease in the rate of oxygen consumption with acetate, glycerol, and succinate, but at different levels. Whereas the respiration of acetate and glycerol decreased concomitantly with culturability, the respiration of succinate decreased to levels similar to the concentration of intact cells, suggesting that all intact particles respired the succinate, but only the culturable cells respired the acetate and glycerol. The results suggest that measuring the activity of the electron-transport system can overestimate the viability of starved bacterial cells, and that complex metabolic activities such as the respiration of acetate and glycerol are probably better suited for the evaluation of this parameter.Key words: Pseudomonas syringae, starvation, culturability, viability, respiration.

scholarly journals EFFECTS OF AZIDE AND CHLORETONE ON THE SODIUM AND POTASSIUM CONTENTS AND THE RESPIRATION OF FROG SCIATIC NERVES

1958 ◽  
Vol 41 (5) ◽  
pp. 959-988 ◽  
Author(s):  
W. P. Hurlbut
Keyword(s):  
Oxygen Consumption ◽  
Respiratory Depression ◽  
Conduction Block ◽  
Slow Conduction ◽  
Ionic Distribution ◽  
Rate Of Oxygen Consumption ◽  
Sciatic Nerves ◽  
Time Courses ◽  
Sodium And Potassium

Azide (0.2 to 5.0 mM) and chloretone (2.0 to 15.0 mM) reversibly inhibited 20 to 90 per cent of the resting respiration of frog sciatic nerves, and caused a loss of potassium and a gain of sodium in this tissue. The changes in ionic contents that developed after 5 or 10 hours were roughly correlated with the degree of respiratory depression, but the time courses of these changes were different with the two reagents. In azide these changes appeared to begin immediately, while in chloretone, at concentrations between 3.0 and 5.0 mM, the ionic shifts developed after a delay of several hours. Fifteen millimolar chloretone produced immediate changes in ionic contents several times greater than those produced by anoxia. The changes in ionic distribution produced in 5 hours by anoxia, 5.0 mM azide, or 5.0 mM chloretone were at least partially reversible; those produced by 15.0 mM chloretone were irreversible. With the exception of 15.0 mM chloretone the ionic shifts produced by these reagents may be due primarily to the depression of the respiration, although there are indications that azide acts, in addition, by another pathway. Concentrations of azide or chloretone that depressed the resting rate of oxygen consumption more than 50 per cent produced a slow conduction block, while 15.0 mM chloretone blocked conduction within 15 minutes.

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