The biology of appetite control: Do resting metabolic rate and fat-free mass drive energy intake?

The prevailing model of homeostatic appetite control envisages two major inputs; signals from adipose tissue and from peptide hormones in the gastrointestinal tract. This model is based on the presumed major influence of adipose tissue on food intake. However, recent studies have indicated that in obese people fat-free mass (FFM) is strongly positively associated with daily energy intake and with meal size. This effect has been replicated in several independent groups varying in cultural and ethnic backgrounds, and appears to be a robust phenomenon. In contrast fat mass (FM) is weakly, or mildly negatively associated with food intake in obese people. In addition resting metabolic rate (RMR), a major component of total daily energy expenditure, is also associated with food intake. This effect has been replicated in different groups and is robust. This action is consistent with the proposal that energy requirements ­ reflected in RMR (and other aspects of energy expenditure) constitute a biological drive to eat. Consistent with its storage function, FM has a strong inhibitory effect on food intake in lean subjects, but this effect appears to weaken dramatically as adipose tissue increases. This formulation can account for several features of the development and maintenance of obesity and provides an alternative, and transparent, approach to the biology of appetite control.

Appetite control and energy balance: impact of exercise.

Exercise is widely regarded as one of the most valuable components of behaviour that can influence body weight and therefore help in the prevention and management of obesity. Indeed, long-term controlled trials show a clear dose-related effect of exercise on body weight. However, there is a suspicion, particularly fuelled by media reports, that exercise serves to increase hunger and drive up food intake thereby nullifying the energy expended through activity. Not everyone performing regular exercise will lose weight and several investigations have demonstrated a huge individual variability in the response to exercise regimes. What accounts for this heterogeneous response? First, exercise (or physical activity) through the expenditure of energy will influence the energy balance equation with the potential to generate an energy deficit. However, energy expenditure also influences the control of appetite (i.e. the physiological and psychological regulatory processes underpinning feeding) and energy intake. This dynamic interaction means that the prediction of a resultant shift in energy balance, and therefore weight change, will be complicated. In changing energy intake, exercise will impact on the biological mechanisms controlling appetite. It is becoming recognized that the major influences on the expression of appetite arise from fat-free mass and fat mass, resting metabolic rate, gastric adjustment to ingested food, changes in episodic peptides including insulin, ghrelin, cholecystokinin, glucagon-like peptide-1 and tyrosine-tyrosine, as well as tonic peptides such as leptin. Moreover, there is evidence that exercise will influence all of these components that, in turn, will influence the drive to eat through the modulation of hunger (a conscious sensation reflecting a mental urge to eat) and adjustments in postprandial satiety via an interaction with food composition. The specific actions of exercise on each physiological component will vary in strength from person to person (according to individual physiological characteristics) and with the intensity and duration of exercise. Therefore, individual responses to exercise will be highly variable and difficult to predict.

The adaptive metabolic response to exercise-induced weight loss influences both energy expenditure and energy intake.

BACKGROUND/OBJECTIVES: A decline in resting energy expenditure (REE) beyond that predicted from changes in body composition has been noted following dietary-induced weight loss. However, it is unknown whether a compensatory downregulation in REE also accompanies exercise (EX)-induced weight loss, or whether this adaptive metabolic response influences energy intake (EI). SUBJECTS/METHODS: Thirty overweight and obese women (body mass index (BMI)=30.6±3.6 kg/m(2)) completed 12 weeks of supervised aerobic EX. Body composition, metabolism, EI and metabolic-related hormones were measured at baseline, week 6 and post intervention. The metabolic adaptation (MA), that is, difference between predicted and measured REE was also calculated post intervention (MApost), with REE predicted using a regression equation generated in an independent sample of 66 overweight and obese women (BMI=31.0±3.9 kg/m(2)). RESULTS: Although mean predicted and measured REE did not differ post intervention, 43% of participants experienced a greater-than-expected decline in REE (-102.9±77.5 kcal per day). MApost was associated with the change in leptin (r=0.47; P=0.04), and the change in resting fat (r=0.52; P=0.01) and carbohydrate oxidation (r=-0.44; P=0.02). Furthermore, MApost was also associated with the change in EI following EX (r=-0.44; P=0.01). CONCLUSIONS: Marked variability existed in the adaptive metabolic response to EX. Importantly, those who experienced a downregulation in REE also experienced an upregulation in EI, indicating that the adaptive metabolic response to EX influences both physiological and behavioural components of energy balance.

Exercise, appetite and weight management: understanding the compensatory responses in eating behaviour and how they contribute to variability in exercise-induced weight loss.

Does exercise promote weight loss? One of the key problems with studies assessing the efficacy of exercise as a method of weight management and obesity is that mean data are presented and the individual variability in response is overlooked. Recent data have highlighted the need to demonstrate and characterise the individual variability in response to exercise. Do people who exercise compensate for the increase in energy expenditure via compensatory increases in hunger and food intake? The authors address the physiological, psychological and behavioural factors potentially involved in the relationship between exercise and appetite, and identify the research questions that remain unanswered. A negative consequence of the phenomena of individual variability and compensatory responses has been the focus on those who lose little weight in response to exercise; this has been used unreasonably as evidence to suggest that exercise is a futile method of controlling weight and managing obesity. Most of the evidence suggests that exercise is useful for improving body composition and health. For example, when exercise-induced mean weight loss is <1.0 kg, significant improvements in aerobic capacity (+6.3 ml/kg/min), systolic (-6.00 mm Hg) and diastolic (-3.9 mm Hg) blood pressure, waist circumference (-3.7 cm) and positive mood still occur. However, people will vary in their responses to exercise; understanding and characterising this variability will help tailor weight loss strategies to suit individuals.

Psycho-markers of weight loss. The roles of TFEQ Disinhibition and Restraint in exercise-induced weight management.

Eating behaviour traits, namely Disinhibition and Restraint, have the potential to exert an effect on food intake and energy balance. The effectiveness of exercise as a method of weight management could be influenced by these traits. Fifty eight overweight and obese participants completed 12-weeks of supervised exercise. Each participant was prescribed supervised exercise based on an expenditure of 500 kcal/session, 5d/week for 12-weeks. Following 12-weeks of exercise there was a significant reduction in mean body weight (-3.26±3.63 kg), fat mass (FM: -3.26±2.64 kg), BMI (-1.16±1.17 kg/m(2)) and waist circumference (WC: -5.0±3.23 cm). Regression analyses revealed a higher baseline Disinhibition score was associated with a greater reduction in BMI and WC, while Internal Disinhibition was associated with a larger decrease in weight, %FM and WC. Neither baseline Restraint or Hunger were associated with any of the anthropometric markers at baseline or after 12-weeks. Furthermore, after 12-weeks of exercise, a decrease in Disinhibition and increase in Restraint were associated with a greater reduction in WC, whereas only Restraint was associated with a decrease in weight. Post-hoc analysis of the sub-factors revealed a decrease in External Disinhibition and increase in Flexible Restraint were associated with weight loss. However, an increase in Rigid Restraint was associated with a reduction in %FM and WC. These findings suggest that exercise-induced weight loss is more marked in individuals with a high level of Disinhibition. These data demonstrate the important roles that Disinhibition and Restraint play in the relationship between exercise and energy balance.

Beneficial effects of exercise: shifting the focus from body weight to other markers of health.

BACKGROUND: Exercise is widely promoted as a method of weight management, while the other health benefits are often ignored. The purpose of this study was to examine whether exercise-induced improvements in health are influenced by changes in body weight. METHODS: Fifty-eight sedentary overweight/obese men and women (BMI 31.8 (SD 4.5) kg/m(2)) participated in a 12-week supervised aerobic exercise intervention (70% heart rate max, five times a week, 500 kcal per session). Body composition, anthropometric parameters, aerobic capacity, blood pressure and acute psychological response to exercise were measured at weeks 0 and 12. RESULTS: The mean reduction in body weight was -3.3 (3.63) kg (p<0.01). However, 26 of the 58 participants failed to attain the predicted weight loss estimated from individuals' exercise-induced energy expenditure. Their mean weight loss was only -0.9 (1.8) kg (p<0.01). Despite attaining a lower-than-predicted weight reduction, these individuals experienced significant increases in aerobic capacity (6.3 (6.0) ml/kg/min; p<0.01), and a decreased systolic (-6.00 (11.5) mm Hg; p<0.05) and diastolic blood pressure (-3.9 (5.8) mm Hg; p<0.01), waist circumference (-3.7 (2.7) cm; p<0.01) and resting heart rate (-4.8 (8.9) bpm, p<0.001). In addition, these individuals experienced an acute exercise-induced increase in positive mood. CONCLUSIONS: These data demonstrate that significant and meaningful health benefits can be achieved even in the presence of lower-than-expected exercise-induced weight loss. A less successful reduction in body weight does not undermine the beneficial effects of aerobic exercise. From a public health perspective, exercise should be encouraged and the emphasis on weight loss reduced.

Individual variability following 12 weeks of supervised exercise: identification and characterization of compensation for exercise-induced weight loss.

OBJECTIVE: To identify and characterize the individual variability in compensation for exercise-induced changes in energy expenditure (EE). DESIGN: Twelve-week exercise intervention. SUBJECTS: Thirty-five overweight and obese sedentary men and women (body mass index, 31.8+/-4.1 kg m(-2); age, 39.6+/-11.0 years) were prescribed exercise five times per week for 12 weeks under supervised conditions. MEASUREMENTS: Body weight, body composition, resting metabolic rate (RMR), total daily energy intake (EI) and subjective appetite sensations were measured at weeks 0 and 12. RESULTS: When all subjects' data were pooled, the mean reduction in body weight (3.7+/-3.6 kg) was significant (P<0.0001) and as predicted, which suggested no compensation for the increase in EE. However, further examination revealed a large individual variability in weight change (-14.7 to +1.7 kg). Subjects were identified as compensators (C) or noncompensators (NC) based on their actual weight loss (mean NC=6.3+/-3.2 kg and C=1.5+/- 2.5 kg) relative to their predicted weight loss. C and NC were characterized by their different metabolic and behavioural compensatory responses. Moderate changes in RMR occurred in C (-69.2+/-268.7 kcal day(-1)) and NC (14.2+/-242.7 kcal day(-1)). EI and average daily subjective hunger increased by 268.2+/-455.4 kcal day(-1) and 6.9+/-11.4 mm day(-1) in C, whereas EI decreased by 130+/-485 kcal day(-1) and there was no change in subjective appetite (0.4+/-9.6 mm day(-1)) in NC. CONCLUSION: These results demonstrate that expressing the exercise-induced change in body weight as a group mean conceals the large inter-individual variability in body weight and compensatory responses. Individuals who experience a lower than predicted weight loss are compensating for the increase in EE.

Lipid composition and chemotaxonomy of Pseudomonas putrefaciens (Alteromonas putrefaciens).

The major polar lipids in cells of Pseudomonas putrefaciens NCIB 10472 grown on nutrient agar were phosphatidylethanolamine, phoisphatidylglycerol, a glucosyldiacylglycerol, a glucuronosyldiacylglycerol and an ornithine amide lipid. An additional phospholipid, tentatively identified as acyl phosphatidylglycerol or bis-phosphatidic acid, was a trace component of the wall lipids from broth cultures, which lacked the glycolipids and the ornithine amide lipid. The wall lipids from broth cultures of three further strains of P. putrefaciens (NCIB 10471, NCIB 11156 and NCTC 10737) contained all of the above lipids, and in two cases (strains NCIB 10471 and NCIB 11156) had an unusually high content of free fatty acid. Fatty acid compositions of the extractable lipids were qualitatively similar for all four strains: the major components were iso-pentadecanoic acid, pentadecanoic acid, a cis-heptadecenoic acid and a cis-hexadecenoic acid. Anteiso fatty acids were minor components in strain NCIB 10472. Lipid mixtures in which the ornithine amide lipid was present also contained small amounts of beta-hydroxy fatty acids: in strain NCIB 10472 the major ones were the straight-chain and iso-branched C16 acids. Lipopolysaccharides from all four strains had similar, complex fatty acid compositions. The major non-hydroxy acids were the straight-chain and iso-branched C13 acids. beta-Hydroxy acids common to all strains included the straight-chain C11, C12, C13, C14 and C15 acids, together with branched-chain C13 and C15 acids probably belonging to the iso series. The lipopolysaccharide from strains NCIB 10472 also contained C12 and C14 hydroxy acids of the same series, and small amounts of C13 and C15 beta-hydroxy acids probably belonging to the anteiso series. The close resemblance in both polar lipid and fatty acid compositions between strains of P. putrefaciens and Pseudomonas rubescens is further evidence that these species are synonymous. Significant differences between the lipids and fatty acids of P. putrefaciens and those reported for a strain of Alteromonas haloplanktis do not harmonize with a proposal to transfer the former organism to the genus Alteromonas.