The role of exercise in thermogenesis and energy balance

1989 ◽  
Vol 67 (4) ◽  
pp. 402-409 ◽  
Author(s):  
Denis Richard ◽  
Serge Rivest
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Exercise Training ◽  
Female Rats ◽  
Male Rats ◽  
Brown Adipose ◽  
Term Energy

The role of exercise training in energy balance has been reviewed. Recent well-conducted studies showed that exercise may increase energy expenditure not only during the period of exercise itself but during the postexercise period as well. This notion of excess postexercise oxygen consumption (EPOC), which has been a controversial issue for many years, is now becoming a generally well-accepted concept, the consensus being that EPOC takes place following prolonged and strenuous exercise bouts. Besides, the role of EPOC in long-term energy balance remains to be determined. Long-term energy balance studies carried out in rats show that exercise affects energy balance by altering food intake and promoting energy expenditure. In male rats exercise causes a marked decrease in energy intake which contributes, in association with the expenditure of exercise itself, to retard lean and fat tissue growth. From the suppressed deposition of lean body mass, decreases in basal metabolic rate can be predicted in males. In female rats, exercise does not affect food intake; the lower energy gain of exercise-trained females results from the elevated expenditure rate associated with exercise itself. In both male and female rats, there is no evidence that exercise training affects energy expenditure other than during exercise itself unless the habitual feeding pattern of the rats is radically modified. The interactive effects of diet and exercise, which have to be further investigated in long-term energy balance, emerge as a promising area of research.Key words: exercise training, nutritional energetics, brown adipose tissue, diet-induced thermogenesis, body composition.

Phosphorylation of STAT3 in hypothalamic nuclei is stimulated by lower doses of leptin than are needed to inhibit food intake

2021 ◽  
Author(s):  
Ruth B.S. Harris
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Random Order ◽  
Progressive Increase ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Integrated Response

This experiment investigated which hypothalamic nuclei were activated by a dose of leptin that inhibited food intake. Food intake, energy expenditure, respiratory exchange ratio (RER) and intrascapular brown adipose tissue (IBAT) temperature were measured in male and female Sprague Dawley rats for 36 hours following an intraperitoneal injection of 0, 50, 200, 500 or 1000 mg leptin/kg with each rat tested with each dose of leptin in random order. In both males and females RER and 12 hour food intake and were inhibited only by 1000 mg leptin/kg, but there was no effect on energy expenditure or IBAT temperature. At the end of the experiment pSTAT3 immunoreactivity was measured one hour after injection of 0, 50, 500 or 1000 mg leptin/kg. In male rats the lowest dose of leptin produced a maximal activation of STAT3 in the Arc and nucleus of the solitary tract (NTS). There was no response in the dorsomedial hypothalamus but there was a progressive increase in VMH pSTAT3 with increasing doses of leptin. In female rats there was no significant change in Arc pSTAT3, NTS activation was maximal with 500 mg leptin/kg, but only the highest dose of leptin increased VMH pSTAT3. These results suggest that the VMH plays an important role in the energetic response to elevations of circulating leptin, but do not exclude the possibility that multiple nuclei provide the appropriate integrated response to hyperleptinemia.

Energy balance in exercise-trained rats acclimated at two environmental temperatures

1986 ◽  
Vol 60 (3) ◽  
pp. 1054-1059 ◽  
Author(s):  
D. Richard ◽  
J. Arnold ◽  
J. Leblanc
Keyword(s):  
Energy Balance ◽  
Energy Expenditure ◽  
Exercise Training ◽  
Energy Content ◽  
Energy Gain ◽  
Metabolizable Energy ◽  
Male Rats ◽  
Brown Adipose ◽  
Energy Gains ◽  
Environmental Temperatures

The present study was carried out to investigate the effects of exercise training on energy balance in male rats acclimated at two different environmental temperatures. Sedimentary and exercised rats were housed and trained at either 24 or 4 degrees C, with the training program consisting of running on a motor-driven treadmill within their respective environments. After 45 days, energy, protein, and fat contents of rats were determined together with the energy content of food and feces. The results show that metabolizable energy intake was reduced by 10% in exercise-trained groups. Substantial differences in energy gains were observed between sedentary and trained rats; sedentary rats showed almost three times more energy gain than trained rats. Carcass analysis revealed the energy gain differences to be mainly due to varied amounts of fat deposition. Energy expenditure (kJ) excluding the cost of exercise training was corrected for metabolic body size (BW 0.75), which in turn showed no significant differences between trained rats and their respective sedentary controls. The present results suggested that exercise training in rats leads to neither increase nor decrease in energy expenditure through components additional to physical activity. The present results also indicated that brown adipose tissue thermogenesis, as assessed through mitochondrial guanosine 5′-diphosphate binding, was not significantly modified by exercise training, regardless of the temperature at which the rats were housed and trained.

Effects of exercise training on energy balance of ovariectomized rats

1987 ◽  
Vol 253 (5) ◽  
pp. R740-R745 ◽  
Author(s):  
D. Richard ◽  
L. Rochon ◽  
Y. Deshaies ◽  
R. Denis
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Exercise Training ◽  
Treated Group ◽  
Energy Gain ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Estradiol Treatment ◽  
Brown Adipose

The purpose of the present study was to investigate both the respective and interactive roles of exercise training and ovarian hormones on the regulation of energy balance. Female rats were divided into sedentary and exercise-trained groups. Each group thus formed was further divided into a sham-operated group, an ovariectomized group, or ovariectomized estradiol-treated group. Rats were exercise trained on a rodent motor-driven treadmill. After 33 days of treatment, rats were killed and the energy contents of carcasses, feces, and food were determined. Brown adipose tissue (BAT) thermogenesis was assessed through mitochondrial GDP binding. The results show that ovariectomy led to increases in food intake, body weight, and protein gains, whereas estradiol treatment abolished these effects. The results also show that exercise training reduced fat gain. Exercise training interacted with ovariectomy on energy gain; in sedentary rats ovariectomy enhanced the energy gain, an effect that disappeared in exercise-trained rats. However, exercise training was found to alter neither body weight and protein gains nor energy intake. Ovariectomy did not affect energy expenditure when the results are expressed in relative terms (kJ.kg body wt-0.67.day-1). Similarly, exercise training did not modify energy expenditure (kJ.kg body wt-0.67.day-1) once the cost of the training program was subtracted. BAT mitochondrial GDP binding was not affected by any of the experimental treatments. The present results therefore suggest that neither ovariectomy nor exercise training affect energy expenditure through regulatory forms of BAT-mediated thermogenesis.

scholarly journals Role of Ventromedial Hypothalamus in Sucrose-Induced Obesity on Metabolic Parameters

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Metabolic Parameters ◽  
Male Rats ◽  
Significant Weight Gain ◽  
The Metabolic Syndrome

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.

scholarly journals The role of RFamide peptides in feeding

2007 ◽  
Vol 192 (1) ◽  
pp. 3-15 ◽  
Author(s):  
David A Bechtold ◽  
Simon M Luckman
Keyword(s):  
Biological Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Feeding Behaviour ◽  
Animal Kingdom ◽  
Primary Function

In the three decades since FMRFamide was isolated from the clam Macrocallista nimbosa, the list of RFamide peptides has been steadily growing. These peptides occur widely across the animal kingdom, including five groups of RFamide peptides identified in mammals. Although there is tremendous diversity in structure and biological activity in the RFamides, the involvement of these peptides in the regulation of energy balance and feeding behaviour appears consistently through evolution. Even so, questions remain as to whether feeding-related actions represent a primary function of the RFamides, especially within mammals. However, as we will discuss here, the study of RFamide function is rapidly expanding and with it so is our understanding of how these peptides can influence food intake directly as well as related aspects of feeding behaviour and energy expenditure.

Glucocorticoids and insulin: reciprocal signals for energy balance

1995 ◽  
Vol 268 (1) ◽  
pp. R142-R149 ◽  
Author(s):  
A. M. Strack ◽  
R. J. Sebastian ◽  
M. W. Schwartz ◽  
M. F. Dallman
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Diabetic Rats ◽  
Energy Gain ◽  
Energy Stores ◽  
The Central Nervous System ◽  
Streptozotocin Induced Diabetes ◽  
Term Energy

Signals that regulate long-term energy balance have been difficult to identify. Increasingly strong evidence indicates that insulin, acting on the central nervous system in part through its effect on neuropeptide Y (NPY), inhibits food intake. We hypothesized that corticosteroids and insulin might serve as interacting, reciprocal signals for energy balance, acting on energy acquisition, in part through their effects on hypothalamic NPY, as well as on energy stores. Because glucocorticoids also stimulate insulin secretion, their role is normally obscured. Glucocorticoids and insulin were clamped in adrenalectomized rats with steroid replacement and streptozotocin-induced diabetes. Glucocorticoids stimulated and insulin inhibited NPY mRNA and food intake. Glucocorticoids inhibited and insulin increased energy gain as determined by the change in body weight. When adrenalectomized diabetic rats were treated, corticosterone stimulated and insulin inhibited food intake, and, respectively, inhibited and increased overall energy gain. More than 50% of the variance was explained by regression analysis of the two hormones on food intake and body weight. Thus glucocorticoids and insulin are major, antagonistic, long-term regulators of energy balance. The effects of corticosterone and insulin on food intake may be mediated, in part, through regulation of hypothalamic NPY synthesis and secretion.

Insulin and metabolic efficiency in rats. II. Effects of NE and cold exposure

1986 ◽  
Vol 251 (6) ◽  
pp. R1118-R1125
Author(s):  
T. J. Bartness ◽  
C. J. Billington ◽  
A. S. Levine ◽  
J. E. Morley ◽  
N. E. Rowland ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Expenditure ◽  
Cold Exposure ◽  
Diabetic Rats ◽  
Metabolic Efficiency ◽  
Maximal Energy ◽  
Brown Adipose

The role of insulin in metabolic efficiency (ME, i.e., efficiency of body wt gain) was examined under conditions of maximal energy expenditure in control and diabetic rats. Long-lasting insulin was administered using a protocol that did not affect food intake and increased ME in both groups. Half the animals were injected chronically with norepinephrine (NE). NE alone in controls decreased body weight and ME and increased brown adipose tissue (BAT) growth, thermogenic potential [cytochrome c oxidase activity (COA)], and lipoprotein lipases (LPL) activity; however, in diabetics, body weight, ME, and food intake all decreased and only BAT LPL activity and DNA content increased. The combination of NE and insulin increased BAT protein and COA in diabetics; in controls, all BAT measures were further increased and ME was intermediate to that of either treatment alone. Cold exposure decreased body weight and ME, increased food intake and qualitatively produced similar increases in BAT growth, COA, and LPL activity in both controls and diabetics. In diabetics, combined cold exposure and insulin did not affect the increase in BAT growth or LPL activity resulting from either treatment alone, but in controls this combination decreased BAT growth and COA. It is concluded that, even under conditions of maximal energy expenditure, both extremes of basal insulin status result in decreased BAT growth and thermogenic potential, but have opposite effects on ME.

Effects of ovarian hormones on energy balance and brown adipose tissue thermogenesis

1986 ◽  
Vol 250 (2) ◽  
pp. R245-R249 ◽  
Author(s):  
D. Richard
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Energy Intake ◽  
Ovarian Hormones ◽  
Ovariectomized Rats ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

This study was carried out to investigate the nutritional energetics of ovariectomized rats with or without ovarian hormone replacement. Rats were divided into five groups: 1) sham operated, 2) ovariectomized, 3) ovariectomized and treated with progesterone, 4) ovariectomized and treated with estradiol, or 5) ovariectomized and treated with estradiol and progesterone. After 36 days of treatment, energy contents of all five groups were determined together with energy content of food and feces. Brown adipose tissue thermogenesis was assessed through mitochondrial GDP binding assay. Results show that ovariectomy leads to a 16% increase in metabolizable energy intake. This increase was accompanied by a twofold increase in body energy gain. Progesterone did not further affect energy intake and gain in ovariectomized rats. However, increases in both food intake and energy gain were prevented by the estradiol replacement therapy. There was no difference in energy expenditure between sham-operated and ovariectomized rats in the absence of estradiol. In estradiol-treated animals, energy expenditure (kJ.kg body wt-0.75 . day-1) showed a slight increase. There was no difference in protein content of interscapular brown adipose tissue between all five groups. GDP binding was slightly reduced in ovariectomized estradiol-treated rats. It is concluded from this study that ovarian hormones produce their effects on energy balance mainly by altering food intake.

scholarly journals Indirect calorimetry in laboratory mice and rats: principles, practical considerations, interpretation and perspectives

2012 ◽  
Vol 303 (5) ◽  
pp. R459-R476 ◽  
Author(s):  
Patrick C. Even ◽  
Nachiket A. Nadkarni
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Indirect Calorimetry ◽  
Very High Frequency ◽  
Metabolic Challenge ◽  
The Common ◽  
Free Feeding ◽  
Basal Energy Expenditure

In this article, we review some fundamentals of indirect calorimetry in mice and rats, and open the discussion on several debated aspects of the configuration and tuning of indirect calorimeters. On the particularly contested issue of adjustment of energy expenditure values for body size and body composition, we discuss several of the most used methods and their results when tested on a previously published set of data. We conclude that neither body weight (BW), exponents of BW, nor lean body mass (LBM) are sufficient. The best method involves fitting both LBM and fat mass (FM) as independent variables; for low sample sizes, the model LBM + 0.2 FM can be very effective. We also question the common calorimetry design that consists of measuring respiratory exchanges under free-feeding conditions in several cages simultaneously. This imposes large intervals between measures, and generally limits data analysis to mean 24 h or day-night values of energy expenditure. These are then generally compared with energy intake. However, we consider that, among other limitations, the measurements of V̇o2, V̇co2, and food intake are not precise enough to allow calculation of energy balance in the small 2–5% range that can induce significant long-term alterations of energy balance. In contrast, we suggest that it is necessary to work under conditions in which temperature is set at thermoneutrality, food intake totally controlled, activity precisely measured, and data acquisition performed at very high frequency to give access to the part of the respiratory exchanges that are due to activity. In these conditions, it is possible to quantify basal energy expenditure, energy expenditure associated with muscular work, and response to feeding or to any other metabolic challenge. This reveals defects in the control of energy metabolism that cannot be observed from measurements of total energy expenditure in free feeding individuals.

Effects of corticotropin-releasing factor on energy balance in rats are sex dependent

1989 ◽  
Vol 257 (6) ◽  
pp. R1417-R1422 ◽  
Author(s):  
S. Rivest ◽  
Y. Deshaies ◽  
D. Richard
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Serum Testosterone ◽  
Corticotropin Releasing Factor ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Significant Difference

The purpose of this study was to investigate the effects of a chronic intracerebroventricular administration of corticotropin-releasing factor (CRF) on energy balance of male and female rats. One week after their delivery to the laboratory, both male and female rats were divided into two groups. One group in each sex was treated with human/rat CRF, while another group was infused with the vehicle. Chronic administration of CRF was accomplished by means of miniosmotic pumps connected to a cannula that was stereotaxically directed into the third ventricle. Food intake and body weight were measured each day during the study. After 14 days of treatment, the rats were killed by decapitation. Energy, fat, and protein contents of the carcasses were quantified. Serum testosterone and estradiol were assayed in males and females, respectively. Administration of CRF significantly reduced body weight gain and food intake in male rats. No significant difference in those variables was observed between female rats treated with CRF and their controls infused with saline. Similarly, metabolizable energy intake and body energy gain were reduced in male rats infused with CRF, whereas no difference was observed between female animals treated with CRF and those infused with saline. In male rats, body fat and body protein contents were lower in CRF-treated than in saline-infused rats. In female rats, CRF did not affect body composition. Serum testosterone in male rats and serum estradiol in female animals were reduced after chronic infusion of CRF.(ABSTRACT TRUNCATED AT 250 WORDS)

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