Effects of exercise-rest cycles on energy balance in rats

1989 ◽  
Vol 256 (4) ◽  
pp. R886-R891 ◽  
Author(s):  
D. Richard ◽  
P. Lachance ◽  
Y. Deshaies

The present study investigated the nutritional energetics of rats exercised either intermittently or continually. Male rats were divided into three groups: a sedentary group, an intermittently trained group, and a continually trained group. Continually trained rats were exercised every day for a period of 8 wk. Over the same period, intermittently trained rats were exercised for 4 wk, each week being followed by a week of rest. Rats were trained on a rodent treadmill at a moderate intensity. Carcasses were analyzed for energy, fat, and protein contents. Brown adipose tissue (BAT) thermogenesis was assessed by measuring mitochondrial guanosine 5'-diphosphate binding. Energy intake was lower in both intermittently and continually trained rats than in sedentary animals. The weight, fat, and protein gains were, in continually trained rats, significantly lower than in sedentary animals. Similarly, intermittently trained rats had lower gains than sedentary animals, although the difference between the two groups was not as marked as the difference between sedentary and continually trained animals. Energy expenditure, which represents the difference between energy intake and energy gain, was less than sedentary controls in both intermittently and continually trained rats. The low expenditure in trained groups did not, however, relate to changes in facultative BAT thermogenesis.A low energy expenditure on components such as basal metabolic rate and obligatory diet-induced thermogenesis would most likely account for the difference in expenditure between sedentary and trained rats.(ABSTRACT TRUNCATED AT 250 WORDS)

1987 ◽  
Vol 252 (3) ◽  
pp. R617-R623 ◽  
Author(s):  
J. Arnold ◽  
D. Richard

Thermogenic response to ingestion of high-fat diet was investigated in four groups of male rats, two groups being exercise trained and two remaining sedentary. One sedentary and one trained group each received a high-fat dietary supplement in addition to the stock diet. After 35 days, body energy and protein and fat contents were determined. Results indicate that exercise reduced metabolizable energy (ME) intake by 9 and 18% in stock- and high-fat-fed trained rats, respectively. Compared with stock-fed rats, ME intake was elevated 31 and 18% in sedentary and trained high-fat-fed rats, respectively. Exercise also affected energy gains; trained rats deposited almost 60% less energy than controls. Exercise largely decreased both fat and protein contents of rats, whereas the high-fat supplement enhanced fat deposition. Energy expenditure, excluding exercise cost, was calculated on a mass-independent basis and was revealed to be similar in appropriately matched (diet) trained and sedentary rats. High-fat feeding induced increases in expenditure assumed to be due to enhanced brown adipose tissue (BAT) regulatory diet-induced thermogenesis. Conversely, exercise did not affect further the regulatory thermogenic response of BAT to stimuli originating from high-fat diet. Excluding physical activity, energy expenditure components in sum (expressed mass independently), in high-fat- and stock-fed rats, appear unaltered by exercise training.


2008 ◽  
Vol 101 (3) ◽  
pp. 408-416 ◽  
Author(s):  
Maria Maraki ◽  
Nektarios Christodoulou ◽  
Niki Aggelopoulou ◽  
Faidon Magkos ◽  
Katerina P. Skenderi ◽  
...  

A single bout of prolonged, moderate-intensity endurance exercise lowers fasting and postprandial TAG concentrations the next day. However, the TAG-lowering effect of exercise is dose-dependent and does not manifest after light exercise of low energy cost ( < 2 MJ). We aimed to investigate whether superimposing mild energy intake restriction to such exercise, in order to augment total energy deficit, potentiates the hypotriacylglycerolaemic effect. Eight healthy, sedentary, premenopausal women (age 27·1 (sem1·3) years; BMI 21·8 (sem0·9) kg/m2) performed two oral fat tolerance tests in the morning on two different occasions: once after a single bout of light exercise (100 min at 30 % of peak oxygen consumption; net energy expenditure 1·04 (sem0·01) MJ) coupled with mild energy intake restriction (1·39 (sem0·22) MJ) on the preceding day, and once after resting coupled with isoenergetic feeding on the preceding day (control). Fasting plasma TAG, TAG in the TAG-rich lipoproteins (TRL-TAG) and serum insulin concentrations were 18, 34 and 30 % lower, respectively, after exercise plus diet compared with the control trial (P < 0·05). Postprandial concentrations of plasma TAG and TRL-TAG were 19 and 27 % lower after exercise plus diet compared with the control condition (P < 0·01), whereas postprandial insulin concentrations were not different. It is concluded that a combination of light exercise along with mild hypoenergetic diet may be a practical and feasible intervention to attenuate fasting and postprandial triacylglycerolaemia, especially for people who cannot exercise for prolonged periods of time at moderate-to-high intensities, such as many sedentary individuals.


2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson’s disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.


1998 ◽  
Vol 274 (3) ◽  
pp. E510-E515 ◽  
Author(s):  
Labros S. Sidossis ◽  
Robert R. Wolfe ◽  
Andrew R. Coggan

We have recently shown that increased carbohydrate flux decreases fat oxidation during exercise by inhibition of fatty acid entry into the mitochondria. Because endurance training reduces the rate of carbohydrate flux during exercise, we hypothesized that training increases fat oxidation by relieving this inhibition. To test this hypothesis, five sedentary and five endurance-trained men exercised on a cycle ergometer at an oxygen consumption (V˙o 2) of ∼2.0 l/min, representing 80 and 40% peakV˙o 2, respectively. [1-13C]oleate and [1-14C]octanoate, long- and medium-chain fatty acids, respectively, were infused for the duration of the studies. Carbohydrate oxidation was significantly higher in the sedentary group (196 ± 9 vs. 102 ± 17 μmol ⋅ kg−1 ⋅ min−1, P < 0.05). Oleate oxidation was higher in the trained group (3.8 ± 0.6 vs. 1.9 ± 0.3 μmol ⋅ kg−1 ⋅ min−1, P < 0.05), whereas octanoate oxidation was not different between the two groups. The percentage of oleate that was taken up by tissues and oxidized was higher in the trained group (76 ± 7 vs. 58 ± 3%, P < 0.05). However, the percentage of octanoate taken up and oxidized was not different (82 ± 3 vs. 85 ± 4%, not significant). Because octanoate, unlike oleate, can freely diffuse across the mitochondrial membrane, the present results suggest that the difference in fatty acid oxidation between trained and untrained individuals may be due to enhanced fatty acid entry into the mitochondria.


2017 ◽  
Vol 313 (4) ◽  
pp. R357-R371 ◽  
Author(s):  
Zachary S. Roberts ◽  
Tami Wolden-Hanson ◽  
Miles E. Matsen ◽  
Vitaly Ryu ◽  
Cheryl H. Vaughan ◽  
...  

Oxytocin (OT) administration elicits weight loss in diet-induced obese (DIO) rodents, nonhuman primates, and humans by reducing energy intake and increasing energy expenditure. Although the neurocircuitry underlying these effects remains uncertain, OT neurons in the paraventricular nucleus are positioned to control both energy intake and sympathetic nervous system outflow to interscapular brown adipose tissue (BAT) through projections to the hindbrain nucleus of the solitary tract and spinal cord. The current work was undertaken to examine whether central OT increases BAT thermogenesis, whether this effect involves hindbrain OT receptors (OTRs), and whether such effects are associated with sustained weight loss following chronic administration. To assess OT-elicited changes in BAT thermogenesis, we measured the effects of intracerebroventricular administration of OT on interscapular BAT temperature in rats and mice. Because fourth ventricular (4V) infusion targets hindbrain OTRs, whereas third ventricular (3V) administration targets both forebrain and hindbrain OTRs, we compared responses to OT following chronic 3V infusion in DIO rats and mice and chronic 4V infusion in DIO rats. We report that chronic 4V infusion of OT into two distinct rat models recapitulates the effects of 3V OT to ameliorate DIO by reducing fat mass. While reduced food intake contributes to this effect, our finding that 4V OT also increases BAT thermogenesis suggests that increased energy expenditure may contribute as well. Collectively, these findings support the hypothesis that, in DIO rats, OT action in the hindbrain evokes sustained weight loss by reducing energy intake and increasing BAT thermogenesis.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 623-623
Author(s):  
Luiz Dos Anjos ◽  
Bruna Silva ◽  
Vivian Wahrlich

Abstract Objectives To assess different methods of estimating energy balance (EB) and its components in a sample of older people (age ≥ 60 years) living in a tropical city in Brazil. Methods EB was calculated in 85 older individuals (69 women) as the difference between energy intake (EI), obtained by three 24-hour dietary recalls on nonconsecutive days, and total daily energy expenditure (TDEE) estimated by 24-hour physical activity recalls (24hPAR, subjective method) and accelerometry (ACC, objective method) on the same days. Basal metabolic rate (BMR) was estimated by a validated local predictive equations derived from a sample of healthy adults from the same city and by international equations (Schofield). Resting energy expenditure (MET) was also estimated by local predictive equation and the conventional value of 3.5 mL.kg−1.min−1. Anthropometry and % body fat (DXA) assessment was also obtained. Results Mean (SD) age was 69.0 (5.5) years with a mean BMI of 26.7 (4.4) kg.m−2 and %BF of 39.4 (7.9). BMR from locally-derived equations (1050.7 ± 188.7 kcal.day−1) was significantly lower than BMR estimated by the Schofield's equation (1286.5 ± 145.3 kcal.day−1). Likewise, predicted MET was significantly lower than the conventional value. Despite the high prevalence of overweight (66% with BMI ≥ 25 kg.m−2), EB was always negative for the 24hPAR method (−863.5 ± 799.5 kcal.day−1) but positive (252.1 ± 726.6 kcal.day−1) with the ACC method when MET was calculated with population-specific equations. EB estimated by ACC was also negative (−122.7 ± 781.0 kcal.day−1) using the conventional MET value. Conclusions The findings of this study indicate that EB is negative when the subjective method of TDEE estimation is used but becomes positive with the objective method. It is also evident that BMR and MET equations derived from samples of the population of interest may help improve the final estimates of TDEE and EB in older adults. Funding Sources CNPq (310,461/2016–20 and 485,168/2011–1) and FAPERJ (E-26/111.496/2011; E-26/202.514/2018; E-26/203.068/2017).


1988 ◽  
Vol 66 (10) ◽  
pp. 1297-1302 ◽  
Author(s):  
Denis Richard ◽  
Pierre Boily ◽  
Marie-Claude Dufresne ◽  
Martin Lecompte

The present study was aimed at studying energy balance in mice fed a high-fat diet. Albino mice were divided into three groups. One group had free access to the stock diet, whereas the two other groups consumed a high-fat diet. One of the high-fat fed groups was fed ad libitum, whereas the other was offered a restricted amount of the same diet so that its energy intake was comparable to the group of mice given the stock diet. Energy balance measurements, which included indirect calorimetry and carcass analysis, were performed. Brown adipose tissue (BAT) properties were also investigated. The results show that gains in both body weight and fat were higher in mice that had free access to high-fat diet than in mice fed the stock diet. In animals given a restricted amount of the high-fat diet, fat gain increased, whereas protein gain was reduced in comparison with animals fed the stock diet. Unrestricted access to the high-fat diet led to an increase in both energy intake and energy gain. As revealed by both slaughter and indirect calorimetry techniques energy expenditure was, in high-fat fed mice, 40% higher than in animals fed either stock or a restricted amount of high-fat diet. Nadolol was shown to suppress a large part of the elevated metabolic rate seen in mice fed an unrestricted high-fat diet. In those mice, BAT mitochondrial GDP binding was also increased. In summary, the present results confirm that adaptive diet-induced thermogenesis (DIT) develops in mice made hyperphagic by an energy-dense palatable diet. The present study provides further evidence that adaptive DIT is mediated by the sympathetic nervous system and involves BAT. Finally, it appears that the extent to which adaptive DIT develops is related to the degree of hyperphagia.


Author(s):  
I. Sadaf Farooqi

Body weight is determined by an interaction between genetic, environmental, and psychosocial factors acting through the physiological mediators of energy intake and expenditure (1). By definition, obesity results from an imbalance between energy intake and energy expenditure and in any individual, excessive caloric intake or low energy expenditure, or both, may explain the development of obesity. A third factor, nutrient partitioning, a term reflecting the propensity to store excess energy as fat rather than lean tissue, may contribute.


Sign in / Sign up

Export Citation Format

Share Document