Why Doesn't Weight Gain Blunt Appetite and Increase Movement? Nonhomeostatic Responses to Energy Surplus in Humans : Exercise and Sport Sciences Reviews

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Why Doesn't Weight Gain Blunt Appetite and Increase Movement? Nonhomeostatic Responses to Energy Surplus in Humans

Braun, Barry Ph.D., FACSM

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Exercise and Sport Sciences Reviews 38(3):p 103-104, July 2010. | DOI: 10.1097/JES.0b013e3181e37419
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The relationships between physical activity, food intake, and body weight have long been a source of interest for scientists and confusion for the lay public. Well-designed human studies suggest that the addition of regular physical activity may not cause much weight/fat loss because there is a compensatory rise in energy intake that can partially or completely offset the higher energy expenditure (4,6). The issue captured the attention of the lay public with the 2009 cover story in TIME magazine titled "Why exercise won't make you thin" (5). The central theme of the article was that exercise is ineffective for weight loss because it increases appetite and leads to higher food intake.

Although it was not pitched in those terms, students in kinesiology/physiology will recognize an example of homeostasis in which the perturbation of a system away from its habitual state invokes a physiological response that restores the initial condition. In the realm of body weight regulation, that thinking was epitomized by the "set-point theory," the operation of regulatory mechanisms that prevent deviations of body weight from a narrow range determined primarily by genetic factors. The characterization of leptin in the mid-1990s provided a convenient mechanism - a mobile system secreted from an origin (adipose tissue) sensitive to deviations in energy availability that can communicate information to a processing center (hypothalamus) capable of directing appropriate responses. Simplistically, energy deficit or surplus alters adipocyte mass, changes circulating concentrations of leptin, stimulates or inhibits various hypothalamic neuropeptides, impacts pathways (e.g., appetite, satiety, resting metabolic rate, and spontaneous activity) that raise or lower energy intake and expenditure, and restores the "appropriate" fat mass. Incorporation of insulin into this model gave rise to the idea that energy deficit lowered circulating concentrations of leptin and insulin, resulting in an "eat more, expend less" response, whereas energy surplus did exactly the opposite. This essentially homeostatic view of body weight/fat regulation is commonly depicted in physiology and nutrition textbooks.

A fly in the ointment that undercuts the tidy homeostatic story has been recognized by several people (1). Although loss of body weight generally does seem to cause the responses outlined above and regain of lost weight, the response to body weight gain is far less robust. Circulating leptin and insulin do rise in response to energy surplus/fat gain as expected, but there is little effect to lower energy intake or raise energy output. In the paper that appears in this issue of Exercise and Sport Sciences Reviews, titled "Nonhomeostatic control of human appetite and physical activity in regulation of energy balance" (2), author Katarina Borer, Ph.D., suggests a fundamental rethinking of the homeostatic view of body weight regulation. Using data from animal and human studies, she builds the case that the relationships between energy balance, putative energy-regulating hormones, appetite, and actual food intake do not conform to a homeostatic model. Although it will seem paradoxical to many kinesiologists doing physical activity studies in humans (but will be familiar to animal behaviorists), energy deficit actually increases spontaneous physical activity (food-seeking behavior) in laboratory animals, and energy surplus lowers it (reduced drive to acquire food). At the heart of the review is a summary of a recent human study by Dr. Borer's laboratory (3) in which they use a multicondition cross-over design to cleverly disentangle the relationships between energy imbalance, exercise, energy intake, putative energy-regulating hormones, and perceived appetite.

The use fulness of Dr. Borer's viewpoint lies in four messages that help to understand the complex literature and to guide future research studies.

  1. The homeostatic view of body weight regulation by physical activity and appetite is inadequate to explain either laboratory or "real-world" data.
  2. The putative energy-regulating hormones commonly measured in circulation are responsive to changes in energy balance, but perceived appetite is sensitive to recent energy intake. Therefore, it should not be surprising that hormones and appetite do not respond in parallel to interventions that alter intake and/or expenditure (7,8).
  3. Context is important - that is, food intake involves a complex set of behaviors that are sensitive to myriad social, environmental, and physiological cues.
  4. When designing studies, investigators need to be acutely aware that the specific outcomes being measured (e.g., circulating hormones vs perceived appetite vs. actual energy intake) respond to different signals, and a single intervention is unlikely to provide insight into all of them. Vertical gains in our knowledge of body weight regulation will require cleverly designed studies in which the intervention is matched with the appropriate outcome(s).

Barry Braun, Ph.D., FACSM

Department of Kinesiology

University of Massachusetts

Amherst, MA


1. Berthoud HR. Homeostatic and non-homeostatic pathways involved in the control of food intake and energy balance. Obesity 2006; 14(Suppl. 5):197S-200S.
2. Borer KT. Nonhomeostatic control of human appetite and physical activity in regulation of energy balance. Exerc. Sport Sci. Rev. 2010; 38:114-121.
3. Borer KT, Wuorinen E, Ku K, Burant C. Appetite responds to changes in meal content, whereas ghrelin, leptin, and insulin track changes in energy availability. J. Clin. Endocrinol. Metab. 2009; 94:2290-8.
4. Church TS, Martin CK, Thompson AM, Earnest CP, Mikus CR, Blair SN. Changes in weight, waist circumference and compensatory responses with different doses of exercise among sedentary, overweight postmenopausal women. PLoS One 2009; 4:e4515.
5. Cloud J. Why exercise won't make you thin. TIME Magazine. August 9, 2009. http://www.time.com/time/health/article/0,8599,1914857,00.html. Accessed May 21, 2010.
6. Donnelly JE, Hill JO, Jacobsen DJ, et al. Effects of a 16-month randomized controlled exercise trial on body weight and composition in young, overweight men and women: the Midwest Exercise Trial. Arch. Intern. Med. 2003; 163:1343-50.
7. Hagobian TA, Braun B. Physical activity and hormonal regulation of appetite: sex differences and weight control. Exerc. Sport Sci. Rev. 2010; 38:25-30.
8. Hagobian TA, Sharoff CG, Stephens BR, et al. Effects of exercise on energy-regulating hormones and appetite in men and women. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2010; 296:R233-42.
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