This article describes the interplay among energy intake, energy expenditure, and body energy stores and illustrates how an understanding of energy balance can help us develop strategies to reduce obesity. First, reducing obesity requires modifying both energy intake and energy expenditure, not simply focusing on either alone. Food restriction alone will not be effective in reducing obesity if human physiology is biased toward achieving energy balance at a high energy flux (ie, at a high level of energy intake and expenditure). In previous environments, a high energy flux was achieved with a high level of physical activity, but in today's sedentary environment, it is increasingly achieved through weight gain. Matching energy intake to a high level of energy expenditure will likely be more feasible for most people than restricting food intake to meet a low level of energy expenditure. Second, from an energy balance point of view, we are likely to be more successful in preventing excessive weight gain than in treating obesity. The reason is that the energy balance system shows stronger opposition to weight loss than to weight gain. Although large behavior changes are needed to produce and maintain reductions in body weight, small behavior changes may be sufficient to prevent excessive weight gain. The concept of energy balance combined with an understanding of how the body achieves balance may be a useful framework for developing strategies to reduce obesity rates.

Obesity is often considered to be a result of either excessive food intake or insufficient physical activity. There is a great debate about which behavior deserves the most responsibility, but this approach has not yet produced effective or innovative solutions. We believe that obesity can best be viewed in terms of energy balance. The first law of thermodynamics states that body weight cannot change if, over a …

Energy Balance and Obesity

The Merriam-Webster dictionary defines hunger as (1) a craving for food, and (2) any strong craving. Appetite is defined as the natural desire for satisfying some want or need, as of food. Other definitions have introduced emphasis on this or that component. Carlson,’ for example, has defined hunger as “a more or less uncomfortable feeling of pressure and pain referred to the region of the stomach”; Grossman and Stein: in an excellent article on hunger feelings following insulin and their persistence after vagotomy, have distinguished between the sensation of being “hungry all over” and epigastric pangs. Other authors have emphasized differences in psychic associations, as well as in intensity, between appetite and hunger. All these considerations should make it clear that hunger and appetite are generally understood to be sensations or feelings that, as such, are not properly amenable to regulation. The sensory meaning has been so generally accepted that, desirable though it may be to reject it, as suggested by Doctor Hollander, it seems a little late in the day to do so. It is even diflicult to record the appearance of these sensations and, a fortiori, their intensity, except through a behavioristic approach. As all of us have known empirically since childhood and as can be clearly evidenced in the laboratory, a multiplicity of factors, emotions, urges, environmental temperature, necessity for exercise, will interfere to modify the tendency to partake of food. Often, the course of action in time of these factors is complex: acute exposure to cold will inhibit tendency to eat in a first phase, yet increase it later. When dealing with a problem which can be attacked only behavioristically and which depends on a multiplicity of variables, the only systematic approach that I know of is the statistical method of Skinner, who studied the frequency or probability of responses to this or that stimulus. With the collaboration of Anliker, an experimental psychologist versed in the “Skinner box” techniques (as well as in electronics and recording techniques), we have recently embarked on the study of the probability of response to exposure to food and on the frequency of work for food of normal mice, as well as of littermates with the hereditary obese hyperglycemic syndrome, goldthioglucose obesity, and hypothalamic obesity. This study will enable us, we hope, to obtain analysis of correlations of response to various physiologic stimuli, as well as an exploration of how much conditioning can be introduced in these responses. Results, however, are too preliminary to warrant a report a t this date. Even then, of course, they will not deal with a regulation, but only with a pattern of feeding.

Regulation of energy intake and the body weight: the glucostatic theory and the lipostatic hypothesis.

Voluntary physical activity and exercise training can favorably influence brain plasticity by facilitating neurogenerative, neuroadaptive, and neuroprotective processes. At least some of the processes are mediated by neurotrophic factors. Motor skill training and regular exercise enhance executive functions of cognition and some types of learning, including motor learning in the spinal cord. These adaptations in the central nervous system have implications for the prevention and treatment of obesity, cancer, depression, the decline in cognition associated with aging, and neurological disorders such as Parkinson's disease, Alzheimer's dementia, ischemic stroke, and head and spinal cord injury. Chronic voluntary physical activity also attenuates neural responses to stress in brain circuits responsible for regulating peripheral sympathetic activity, suggesting constraint on sympathetic responses to stress that could plausibly contribute to reductions in clinical disorders such as hypertension, heart failure, oxidative stress, and suppression of immunity. Mechanisms explaining these adaptations are not as yet known, but metabolic and neurochemical pathways among skeletal muscle, the spinal cord, and the brain offer plausible, testable mechanisms that might help explain effects of physical activity and exercise on the central nervous system.

/pdf/neurobiology-of-exercise-1kklto9two.pdf

Neurobiology of exercise.

Background Obesity is a major health problem due, in part, to physical inactivity. The amount of activity needed to prevent weight gain is unknown. Objective To determine the effects of different amounts and intensities of exercise training. Design Randomized controlled trial (February 1999–July 2002). Setting and Participants Sedentary, overweight men and women (aged 40-65 years) with mild to moderate dyslipidemia were recruited from Durham, NC, and surrounding communities. Interventions Eight-month exercise program with 3 groups: (1) high amount/vigorous intensity (calorically equivalent to approximately 20 miles [32.0 km] of jogging per week at 65%-80% peak oxygen consumption); (2) low amount/vigorous intensity (equivalent to approximately 12 miles [19.2 km] of jogging per week at 65%-80%), and (3) low amount/moderate intensity (equivalent to approximately 12 miles [19.2 km] of walking per week at 40%-55%). Subjects were counseled not to change their diet and were encouraged to maintain body weight. Main Outcome Measures Body weight, body composition (via skinfolds), and waist circumference. Results Of 302 subjects screened, 182 met criteria and were randomized and 120 completed the study. There was a significant ( P Conclusions In nondieting, overweight subjects, the controls gained weight, both low-amount exercise groups lost weight and fat, and the high-amount group lost more of each in a dose-response manner. These findings strongly suggest that, absent changes in diet, a higher amount of activity is necessary for weight maintenance and that the positive caloric imbalance observed in the overweight controls is small and can be reversed by a modest amount of exercise. Most individuals can accomplish this by walking 30 minutes every day.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/216495/ioi30059.pdf

Effects of the Amount of Exercise on Body Weight, Body Composition, and Measures of Central Obesity STRRIDE—A Randomized Controlled Study

Dietary obesity in adult rats: Similarities to hypothalamic and human obesity syndromes

I T IS GENERALLY assumed that the relationship of food intake to exercise is one of direct proportionality above the basal level corresponding to inactivity. It is the purpose of the first part of this article to show that such a concept is an oversimplification at variance with the facts. Similarly, it is usually assumed that following exercise an obese animal or person will increase food intake in direct proportion, whatever the intake prior to exercise or the energy expended in exercise. It has been shown (I) that in the hereditary obese hyperglycemic syndrome (2, 3), a decrease in voluntary activity (to less than 2 % of the normal in adult animals) is an essential aspect of the etiology of the obesity; this lack of activity was shown to precede the development of the obesity and is not simply a result of the overweight (I). When obese mice also carry the waltzing gene and are in nearly constant rotary movement in their cages, their weight rarely exceeds 40 gm instead of twice that value. In another report (4) it has been demonstrated that mice made obese by goldthioglucose injection (2) will lose weight if given the opportunity to practice unrestricted exercise. It is the purpose of the second part of this paper to show that the development of hereditary obesity in mice can be considerably slowed down by forcing these animals to exercise.

N. B. Marshall

Papers

Exercise, Food Intake and Body Weight in Normal Rats and Genetically Obese Adult Mice