AUTHOR=Flack Kyle D. , Stults-Kolehmainen Matthew A. , Creasy Seth A. , Khullar Saumya , Boullosa Daniel , Catenacci Victoria A. , King Neil TITLE=Altered motivation states for physical activity and ‘appetite’ for movement as compensatory mechanisms limiting the efficacy of exercise training for weight loss JOURNAL=Frontiers in Psychology VOLUME=14 YEAR=2023 URL=https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2023.1098394 DOI=10.3389/fpsyg.2023.1098394 ISSN=1664-1078 ABSTRACT=

Weight loss is a major motive for engaging in exercise, despite substantial evidence that exercise training results in compensatory responses that inhibit significant weight loss. According to the Laws of Thermodynamics and the CICO (Calories in, Calories out) model, increased exercise-induced energy expenditure (EE), in the absence of any compensatory increase in energy intake, should result in an energy deficit leading to reductions of body mass. However, the expected negative energy balance is met with both volitional and non-volitional (metabolic and behavioral) compensatory responses. A commonly reported compensatory response to exercise is increased food intake (i.e., Calories in) due to increased hunger, increased desire for certain foods, and/or changes in health beliefs. On the other side of the CICO model, exercise training can instigate compensatory reductions in EE that resist the maintenance of an energy deficit. This may be due to decreases in non-exercise activity thermogenesis (NEAT), increases in sedentary behavior, or alterations in sleep. Related to this EE compensation, the motivational states associated with the desire to be active tend to be overlooked when considering compensatory changes in non-exercise activity. For example, exercise-induced alterations in the wanting of physical activity could be a mechanism promoting compensatory reductions in EE. Thus, one’s desires, urges or cravings for movement–also known as “motivation states” or “appetence for activity”-are thought to be proximal instigators of movement. Motivation states for activity may be influenced by genetic, metabolic, and psychological drives for activity (and inactivity), and such states are susceptible to fatigue-or reward-induced responses, which may account for reductions in NEAT in response to exercise training. Further, although the current data are limited, recent investigations have demonstrated that motivation states for physical activity are dampened by exercise and increase after periods of sedentarism. Collectively, this evidence points to additional compensatory mechanisms, associated with motivational states, by which impositions in exercise-induced changes in energy balance may be met with resistance, thus resulting in attenuated weight loss.