Large Increase In Metabolic Rate Research Articles

The energetic cost of mounting an immune response for Pallas's long-tongued bat (Glossophaga soricina).

The acute phase response (APR) is the first line of defense of the vertebrate immune system against pathogens. Mounting an immune response is believed to be energetically costly but direct measures of metabolic rate during immune challenges contradict this assumption. The energetic cost of APR for birds is higher than for rodents, suggesting that this response is less expensive for mammals. However, the particularly large increase in metabolic rate after APR activation for a piscivorous bat (Myotis vivesi) suggests that immune response might be unusually costly for bats. Here we quantified the energetic cost and body mass change associated with APR for the nectarivorous Pallas’s long-tongued bat (Glossophaga soricina). Activation of the APR resulted in a short-term decrease in body mass and an increase in resting metabolic rate (RMR) with a total energy cost of only 2% of the total energy expenditure estimated for G. soricina. This increase in RMR was far from the large increase measured for piscivorous bats; rather, it was similar to the highest values reported for birds. Overall, our results suggest that the costs of APR for bats may vary interspecifically. Measurement of the energy cost of vertebrate immune response is limited to a few species and further work is warranted to evaluate its significance for an animal’s energy budget.

Respiration, thermogenesis, and thermoregulation of Victoria cruziana flowers

The flowers of Victoria cruziana bloom over two consecutive nights, during which time they dramatically increase their metabolic rate (MR) to raise their internal temperature by 7–10°C above air temperature. To investigate the metabolic cost of thermogenesis in V. cruziana and determine the role of ambient temperature and developmental phase on floral temperature, flowers growing in an outdoor pond were measured in situ by placing them within a temperature-controlled, flow-through respirometry chamber. The flower’s metabolic rate and temperature were recorded simultaneously over the 40h of their two-night flowering cycle. During this time, flowers were exposed to either a normal (cool nights, warm days) or an inverted (cool days, warm nights) thermal regime. V. cruziana flowers exposed to normal daily temperature variation showed a large increase in MR on the first evening that declined steadily over the subsequent days. Exposure to experimentally-manipulated cooler daytime temperatures did not stimulate flowers to increase their MR, indicating a lack of thermoregulatory capacity. However, rewarming a cooled flower on the second evening caused a large increase in MR, but not in temperature. This increase appeared to arise due to the delayed consumption of energy reserves that would otherwise have been used over the course of the preceding day, coupled with a more open, and less insulated, floral chamber. The pattern of thermogenesis shown by V. cruziana is unlike that of its closest relative, V. amazonica, which shows large increases in MR and temperature over both nights of flowering.

Highlights from the Literature

Highlights from the Literature

Transient peripheral warming accompanies the hypoxic metabolic response in the golden-mantled ground squirrel

The hypoxic metabolic response of mammals involves a reversible metabolic suppression, possibly brought about by a reduction in the body temperature set-point. In the present study we tested the hypothesis that this is accompanied by a transient increase in heat loss that facilitates the decline in body temperature and metabolic rate. Peripheral heat distribution was assessed using infrared thermography to measure the surface temperatures of the golden-mantled ground squirrel at three different ambient temperatures (10, 22 and 30 degrees C). During early hypoxic exposure, surface temperatures increased dramatically in the feet, ears and nose, and this increase was more dramatic and prolonged at 22 degrees C than at the other two temperatures. These increases were associated with a fall in metabolic rate. Following this initial increase, surface temperatures decreased back to control values, and at 10 degrees C, the surface temperatures of the eyes and body decreased below normoxic levels. Subsequent normoxic recovery was not accompanied by transient changes in surface temperatures, despite large increases in metabolic rate associated with post-hypoxic shivering and thermogenesis. The temporal changes in surface temperature suggest that peripheral blood flow is initially increased during hypoxia, shifting heat away from the core to the periphery and thus facilitating cooling. These results are consistent with the hypothesis that hypoxia leads to a regulated fall in body temperature.

Increased blood oxygen affinity during digestion in the snake Python molurus.

Many snakes exhibit large increases in metabolic rate during digestion that place extensive demands on efficient oxygen transport. In the present study, we describe blood oxygen affinity following three weeks of fasting and 48 h after feeding in the Burmese python (Python molurus). We also report simultaneous measurements of arterial blood gases and haematological parameters. Arterial blood was obtained from chronically implanted catheters, and blood oxygen-dissociation curves were constructed from oxygen content measurements at known oxygen partial pressure (P(O(2))) values at 2% and 5% CO(2). Arterial pH remained constant at approximately 7.6 after feeding, but digestion was associated with an approximately 6 mmol l(-1) increase in [HCO(3)(-)], while CO(2) partial pressure (P(CO(2))) increased from 2.21+/-0.13 kPa in fasted animals to 2.89+/-0.17 kPa at 48 h after feeding. Blood oxygen affinity in vivo was predicted on the basis of pH in vivo and the blood oxygen-dissociation curves obtained in vitro. The blood oxygen affinity in vivo increased during digestion, with P(50) values decreasing from 4.58+/-0.11 kPa to 3.53+/-0.24 kPa. This increase was associated with a significant decrease in the red blood cell [NTP]/[Hb(4)] ratio (relationship between the concentrations of organic phosphates and total haemoglobin) and a significant decrease in mean cellular haemoglobin content, which is indicative of swelling of the red blood cells. Our data for blood oxygen affinity and arterial oxygen levels, together with previously published values of oxygen uptake and blood flows, allow for a quantitative evaluation of oxygen transport during digestion. This analysis shows that a large part of the increased metabolism during digestion is supported by an increased venous extraction, while arterial P(O(2)) (Pa(O(2))) and haemoglobin saturation do not vary with digestive status. Thus, we predict that venous P(O(2)) (Pv(O(2))) is reduced from a fasting value of 5.2 kPa to 1.6 kPa during digestion.

Cue-induced changes in basal local cerebral glucose utilization 13 days after morphine sensitization in the Fischer 344 rat: relevance for drug craving

The present experiment tested the hypothesis that some persistent neural adaptation develops during the course of repeated sensitizing doses of morphine administered to rats. A sub-hypothesis was that this imprint would be of greater magnitude in the presence of morphine-conditioned cues. In order to test these hypotheses basal local cerebral metabolic rates for glucose (LCMR glu) were determined 13 days after the last of four 10-mg/kg doses of morphine administered in 36 h to Fischer 344 male rats. LCMR glu was determined using the 2-deoxy- d-[1- 14C]glucose method (2-DG). Half of the rats, the conditioned group, were placed in the 2-DG chamber after each injection and half, the nonconditioned group, were placed in a neutral environment. A control group received only saline in lieu of morphine. All metabolic rates were determined in a nondrugged state. The major finding was large increases in metabolic rate throughout the forebrain in the sensitized rats. This was especially so in the conditioned group, 46 out of 93 areas examined had significant increases while in the nonconditioned group it was 25 out of 93. Both the core and shell of the nucleus accumbens showed significant elevations in metabolic rates in the presence of morphine cues but only the shell in the absence of the cues. There were no significant decreases in basal metabolic activity in any of the brain regions evaluated in either experimental group. The present finding suggests that changes in the brains of these morphine-sensitized rats may model the altered brain states responsible for drug craving in human drug addicts.

Peroxisome proliferators as adjuvants for the reverse-electron-transport therapy of obesity: an explanation for the large increase in metabolic rate of MEDICA 16-treated rats

The efficacy of reverse-electron-transport therapy of obesity should be promoted by agents which up-regulate hepatocyte enzymes that are potentially rate-limiting for mitochondrial fatty acid oxidation and electron shuttles. Peroxisome proliferator drugs, including the fibrates used to treat hyperlipidemia, may be useful in this regard, as they induce malic enzyme, the mitochondrial glycerol-3-phosphate dehydrogenase, and carnitine palmitoyl transferase I in rodent hepatocytes. An agent of this class, MEDICA 16, has the additional property of potently inhibiting both citrate lyase and acetyl-CoA carboxylase. As a result, me thyl-substituted di a ca rboxylic acids (MEDICA) 16 can be expected to disinhibit hepatic fatty acid oxidation while up-regulating electron shuttle mechanisms, and thus should stimulate reverse electron transport. This may explain the remarkable 40% increase in basal metabolic rate observed in normal rats ingesting MEDICA 16 – an effect not associated with any compensatory increase in food intake. Relative to controls, the MEDICA 16-treated rats achieved a 50% reduction in body fat and a modest increase in lean mass, such that weight and growth were not changed. In other rodent strains, MEDICA 16 has prevented obesity diabetes and atherogenesis. However, whether MEDICA 16 and other peroxisome proliferator drugs will have clinical utility in reverse-electron-transport therapy may hinge on their ability to induce key enzymes inhuman hepatocytes; cell culture studies to evaluate this are required.

Ventilation and oxygen extraction in the little penguin ( Eudyptula minor), at different temperatures in air and water

Oxygen consumption, (V̇ O2), carbon dioxide production (V̇ CO2) and ventilation were measured in little penguins ( Eudyptula minor) in air and water over a range of ambient temperatures. Barometrically measured minimum ventilation was very low (112 ± 23 ml·min −1 over the range 15–20°C, n=9), principally due to a lower than predicted respiratory frequency (f) (6.9±1.1 min −1). This low ventilation resulted in a very high oxygen extraction (E O2) and low air convection requirement ( V̇i/V̇ O 2 ). Despite large increases in metabolic rate in birds in cold water, V̇ i/V̇ O 2 and hence E O 2 did not vary in non-heat exposed penguins over a range of air and water temperatures. Mean extraction was 53.2±10.8% (n=82) corresponding to an air convection requirement of 1.13±2.5L·L −1. Above thermoneutrality there was a dramatic increase in ventilation and fall in E O2 resulting from increases in both f and tidal volume ( Vt). Eng-expired gases were measuerd at thermoneutrality and during heat exposure. At thermoneutrality Fe CO 2 ′ was 0.074±0.005, and Fe O 2 ′ 0.115±0.009. During heat exposure end expired gases approached atmospheric levels.

Normal muscle energy metabolism.

In all cells, ATP plays a central role in providing a chemical form of potential energy which is enzymatically converted through specific coupling mechanisms into useful work of the cell, e.g. macromolecular synthesis, osmotic, electrical and mechanical work. Striated muscle cells, and skeletal muscle cells in particular, are excellent preparations for studies of the regulation of this energy production and utilization. The reason is that, in contrast with other cells which operate under steady physiological states, the metabolic rate of muscle cells can be increased ten- to fifty-fold above the basal rate by stimulating the muscle to mechanical activity. This large increase in metabolic rate allows exploration of non-steady state energy perturbations, which gives important insight into general aspects of metabolic regulation.KeywordsOxygen Consumption RateCreatine PhosphateStriate Muscle CellATPase RateContractile PhaseThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Quantitative observations on thermal and metabolic responses to cold of workers using vibrating tools.

Quantitative observations on thermal and metabolic responses of 32 patients exposed to moderate cold of vibration hazards due to using chain saw were performed. In this study, many cases showed trends of both in increase of metabolic rate and decrease of mean skin temperatures. The ratio of 60 min mean value of the increase of metabolic rate/decrease of mean skin temperature is 3.5 +/- 2.60. Twenty-two patients (68.8%) indicated the value larger than 3. There are many with markedly large increase in metabolic rate in those who affected Raynaud's phenomenon. It can be suggested that many of the patients with the vibration hazards indicate an decrease of the cold tolerance ot the moderate cold exposure.

Adaptive changes in the calorigenic effect of catecholamines: Role of changes in the adenyl cyclase system and of changes in the mitochondria

1. The adaptation responsible for a four-fold increase in the magnitude of the calorigenic response to catecholamines has been studied in the cold-acclimated rat which serves as a model in which the magnitude of the response can be varied by varying the acclimation temperature. 2. It is not possible to attribute the enhanced calorigenic response to noradrenaline to an increase in the noradrenaline-stimulated adenyl cyclase (the receptor system for noradrenaline) in either brown adipose tissue or skeletal muscle, the principal tissues in which the response occurs, because no increase in the activity of the noradrenaline-stimulated adenyl cyclase occurs in either tissue in cold-acclimated rats in association with the enhanced response to noradrenaline. 3. A transient increase in the total (fluoride-stimulated) adenyl cyclase occurs in brown adipose tissue during the first week of acclimation to cold. The increase takes place in the absence of protein synthesis and is thought to be due to an alteration of the properties of the plasma membrane as a consequence of the intense cold-induced sympathetic stimulation of this tissue. Transient increases in both total (fluoride-stimulated) and catecholamine-stimulated adenyl cyclase have been observed in skeletal muscle during the first week of acclimation to cold, apparently in association with shivering, but are no longer present when acclimation has fully developed. 4. The mitochondria of both red and white skeletal muscle of cold-acclimated rats are shown to be increased in number but decreased in size. The total mitochondrial mass per gram of muscle is not altered (no change in mitochondrial protein or cytochrome oxidase per gram of tissue) but the mitochondria are smaller (less protein and cytochrome oxidase per mitochondrion) and more numerous (more mitochondria per gram of muscle). Mitochondria isolated from the muscle of cold-acclimated rats have normal ADP/O and respiratory control ratios and an increased rate of state 3 and state 4 respiration. The morphologically altered mitochondria thus appear to have normal coupling and control mechanisms yet to differ metabolically in some respect. 5. The turnover of some, but not all, proteins of the skeletal muscle mitochondria and the brown adipose tissue mitochondria is accelerated in the cold-acclimated rat. The morphological alteration appears thus to be associated with an altered metabolism of mitochondrial proteins. 6. Inhibition of mitochondrial protein synthesis by oxytetracycline prevents the change in mitochondrial morphology (the appearance of the smaller and more numerous mitochondria) in muscle during acclimation to cold and causes its reversal if it has already taken place. It also prevents the proliferation of mitochondria in brown adipose tissue and reverses it if it has already occurred. Mitochondrial protein synthesis is therefore necessary for the development and the maintenance of the altered mitochondrial morphology in both skeletal muscle and brown adipose tissue of the cold-acclimated rat. The treatment with oxytetracycline also prevents the development of the enhanced calorigenic response to noradrenaline during acclimation to cold and reverses it if it has already developed. When cold-acclimated rats undergo deacclimation the increased number of mitochondria in muscle diminishes as does the enhancement of the calorigenic response to noradrenaline. It is concluded that the enhancement of the calorigenic response to noradrenaline is closely associated with the alteration of the mitochondria of muscle and brown adipose tissue. 7. Removal of about one third of the total brown adipose tissue showed that this tissue could not be a major site of the enhanced calorigenic response to noradrenaline in cold-acclimated rats. However, the interscapular brown adipose tissue exerted an influence on the capacity of other tissues, presumably skeletal muscle, to maintain an enhanced calorigenic response to noradrenaline. An endocrine function of interscapular brown adipose tissue has been proposed. 8. The detailed biochemical mechanism of the calorigenic response to noradrenaline remains a mystery. However, the four-fold enhancement of the response in cold-acclimated rats is shown to be associated with an alteration in muscle mitochondria which requires mitochondrial protein synthesis and an increased turnover of some mitochondrial proteins. Moreover, it is influenced in an unknown way by the brown adipose tissue. The alteration in function of these altered mitochondria is not revealed by conventional measurements of metabolic functions. The way in which the altered mitochondria permit the muscle to respond to noradrenaline with such a large increase in metabolic rate is still unknown. It is hoped that the observations reported here will provide some clues to its mechanism.