Exercise, appetite, and energy balance: The interactions between energy expenditure and intake, and the implications for weight management

This book disseminates current information pertaining to the modulatory effects of foods and other food substances on behavior and neurological pathways and, importantly, vice versa. This ranges from the neuroendocrine control of eating to the effects of life-threatening disease on eating behavior. The importance of this contribution to the scientific literature lies in the fact that food and eating are an essential component of cultural heritage but the effects of perturbations in the food/cognitive axis can be profound. The complex interrelationship between neuropsychological processing, diet, and behavioral outcome is explored within the context of the most contemporary psychobiological research in the area. This comprehensive psychobiology- and pathology-themed text examines the broad spectrum of diet, behavioral, and neuropsychological interactions from normative function to occurrences of severe and enduring psychopathological processes

Exercise, appetite control, and energy balance

Given the present worldwide epidemic of obesity, it is pertinent to ask how effective exercise could be in helping people to lose weight or to prevent weight gain. There is a widely held belief that exercise is futile for weight reduction because any energy expended in exercise is automatically compensated for by a corresponding increase in energy intake (EI). In other words, exercise elevates the intensity of hunger and drives food consumption. This “commonsense” view appears to originate in an energy-balance model of appetite control, which stipulates that energy expended will drive EI as a consequence of the regulation of energy balance. However, it is very clear that EI (food consumption or eating) is not just a biological matter. Eating does not occur solely to rectify some internal need state. Indeed, an examination of the relation between exercise and appetite control has shown a very weak coupling; most studies have demonstrated that food intake does not immediately rise after exercise, even after very high energy expenditure (EE).[1] The processes of exercise-induced EE and food consumption do not appear to be tightly linked. After exercise, there is only slow and partial compensation for the energy expended. Therefore, exercise can be very useful in helping to bring about weight loss and is even more important in preventing weight gain or weight regain. This editorial explores this issue.

The energy balance in the Ramdas layer

On calm clear nights, air at a height of a few decimetres above bare soil can be cooler than the surface by several degrees in what we shall call the Ramdas layer (Ramdas and Atmanathan, 1932). The authors have recently offered a logical explanation for such a lifted temperature minimum, together with a detailed numerical model. In this paper, we provide physical insight into the phenomenon by a detailed discussion of the energy budget in four typical cases, including one with a lifted minimum. It is shown that the net cooling rate near ground is the small difference between two dominant terms, representing respectively radiative upflux from the ground and from the air layers just above ground. The delicate energy balance that leads to the lifted minimum is upset by turbulent transport, by surface emissivity approaching unity, or by high ground cooling rates. The rapid variation of the flux emissivity of humid air is shown to dominate radiative transport near the ground.

Preliminary report on the energy balance for nonlinear oscillations

In this paper, a reliable technique for calculating angular frequencies of nonlinear oscillators is developed. The new algorithm offers a promising approach by constructing a Hamiltonian for the nonlinear oscillator. Some illustrative examples are given. (C) 2002 Published by Elsevier Science Ltd.

Prediction of FRP debonding using the global-energy-balance approach

A major research program was carried out to analyze the mechanism of FRP debonding from concrete beams using global-energy-balance approach (GEBA). The key findings are that the fracture process zone is small so there is no R-curve to consider, failure is dominated by Mode I behavior, and the theory agrees well with tests. The analyses developed in the study provide an essential tool that will enable fracture mechanics to be used to determine the load at which FRP plates will debond from concrete beams. This obviates the need for finite element (FE) analyses in situations where reliable details of the interface geometry and crack-tip stress fields are not attainable for an accurate analysis. This paper presents an overview of the GEBA analyses that is described in detail elsewhere, and explains the slightly unconventional assumptions made in the analyses, such as the revised moment-curvature model, the location of an effective centroid, the separate consideration of the FRP and the RC beam for the purposes of the analysis, the use of Mode I fracture energies and the absence of an R-curve in the fracture mechanics analysis.

Comparison of moment-curvature models for fiber-reinforced polymer plate-end debonding studies using global energy balance approach

This paper compares a number of different moment-curvature models for cracked concrete sections that contain both steel and external fiber-reinforced polymer (FRP) reinforcement. The question of whether to use a whole-section analysis or one that considers the FRP separately is discussed. Five existing and three new models are compared with test data for moment-curvature or load deflection behavior, and five models are compared with test results for plate-end debonding using a global energy balance approach (GEBA). A proposal is made for the use of one of the simplified models. The availability of a simplified model opens the way to the production of design aids so that the GEBA can be made available to practicing engineers through design guides and parametric studies. Copyright © 2014, American Concrete Institute.

The impact of whey protein isolate on energy balance regulation

Using C57BL/6J mice fed whey protein isolate (WPI) enriched high fat (HFD) or low-fat diets (LFD), this study tested the hypothesis that WPI directly impacts on adiposity by influencing lipid metabolism. WPI suppressed HFD-induced body fat and increased lean mass at 8 weeks of dietary challenge despite elevated plasma triacylglycerol (TAG) levels, suggesting reduced TAG storage. WPI reduced HFD-associated hypothalamic leptin and insulin receptor (IR) mRNA expression, and prevented HFD-associated reductions in adipose tissue IR and glucose transporter 4 expression. These effects were largely absent at 21 weeks of HFD feeding, however WPI increased lean mass and cause a trend towards decreased fat mass, with notable increased Lactobacillus and decreased Clostridium gut bacterial species. Increasing the protein to carbohydrate ratio enhanced the above effects, and shifted the gut microbiota composition away from the HFD group. Seven weeks of WPI intake with a LFD decreased insulin signalling gene expression in the adipose tissue in association with an increased fat accumulation. WPI reduced intestinal weight and length, suggesting a potential functional relationship between WPI, gastro-intestinal morphology and insulin related signalling in the adipose. Extending the study to 15 weeks, did not affect adipose fat weight, but decreased energy intake, weight gain and intestinal length. The functionality of protein sensing lysophosphatidic acid receptor 5 (LPA5) in 3T3-L1 pre-adipocytes was assessed. Over-expression of the receptor in 3T3-L1 pre-adipocytes provided a growth advantage to the cells and suppressed cellular differentiation into mature fat cells. In conclusion, the data demonstrates WPI impacts on adiposity by influencing lipid metabolism in a temporal manner, resulting possibly due to changes in lean mass, hypothalamic and adipose gene expression, gut microbiota and gastrointestinal morphology. The data also showed LPA5 is a novel candidate in regulating of preadipocyte growth and differentiation, and may mediate dietary protein effects on adipose tissue.