Late-stage Attentional Bias towards Food Cues Varies According to Weight Status.

The Current food environment has become increasingly obesogenic, with rates of obesity and related conditions continually rising. Advertisements for energy-dense foods are abundant and promote unhealthy eating behaviors by capitalizing on one's attentional bias towards food cues, a cognitive process resulting from the sensitization of highly reinforcing food. A heightened awareness towards food cues may promote overconsumption of energy-dense foods. The current study employed novel eye-tracking methodology to capture sustained, or late-stage, attentional bias towards food cues. Late-stage attentional bias is the aspect of attentional bias under conscious control and likely more prone to modification compared to initial/ early-stage attentional bias, which reflects automatic processes. The present study hypothesized late-stage attentional bias towards food cues is greater among individuals classified as overweight/obese than those classified as normal weight. Thirty (30) participants classified as overweight/obese (BMI ≥25) and 47 classified as normal weight (BMI <25) were assessed for late-stage attentional bias towards food cues, conceptualized as the percentage of time fixated on food cues when both food and neutral images were presented during a food-specific visual probe procedure task. Percentage of time fixated on food cues was 51.25 ± 1.27 (mean + SE) among individuals classified as overweight to obese while those classified as normal weight had a percent fixation of 47.26 ± 0.87 (P=0.03). In conclusion, individuals classified as overweight to obese have greater late-stage attentional bias towards food cues. This establishes an important factor influencing energy intake that may be modified in future clinical trials.

The Role of Dietary Protein in Body Weight Regulation among Active-Duty Military Personnel during Energy Deficit: A Systematic Review.

Active-duty military personnel are subjected to sustained periods of energy deficit during combat and training, leaving them susceptible to detrimental reductions in body weight. The importance of adequate dietary protein intake during periods of intense physical training is well established, where previous research has primarily focused on muscle protein synthesis, muscle recovery, and physical performance. Research on how protein intake may influence body weight regulation in this population is lacking; therefore, the objective of this review was to evaluate the role of dietary protein in body weight regulation among active-duty military during an energy deficit. A literature search based on fixed inclusion and exclusion criteria was performed. English language peer-reviewed journal articles from inception to 3 June 2023 were selected for extraction and quality assessment. Eight studies were identified with outcomes described narratively. The study duration ranged from eight days to six months. Protein was directly provided to participants in all studies except for one. Three studies supplied additional protein via supplementation. The Downs and Black Checklist was used to assess study quality. Five studies were classified as good, two as fair, and one as excellent. All studies reported mean weight loss following energy deficit: the most severe was 4.0 kg. Protein dose during energy deficit varied from 0.5 g/kg/day to 2.4 g/kg/day. Six studies reported mean reductions in fat mass, with the largest being 4.5 kg. Four studies reported mean reductions in fat-free mass, while two studies reported an increase. Results support the recommendation that greater than 0.8 g/kg/day is necessary to mitigate the impact of energy deficit on a decline in lean body mass, while intakes up to 1.6 g/kg/day may be preferred. However, exact recommendations cannot be inferred as the severity and duration of energy deficit varied across studies. Longer and larger investigations are needed to elucidate protein's role during energy deficit in active-duty military.

Altered motivation states for physical activity and 'appetite' for movement as compensatory mechanisms limiting the efficacy of exercise training for weight loss.

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.

Dietary Temperature's Influence on Energy Balance in Humans: Protocol for a Randomized Controlled Trial and Crossover Design.

BACKGROUND: According to the first law of thermodynamics, energy cannot be created or destroyed in an isolated system. Water has a characteristically high heat capacity, indicating that the temperature of ingested fluids and meals could contribute to energy homeostasis. Citing the underlying molecular mechanisms, we present a novel hypothesis that states that the temperature of one's food and drink contributes to energy balance and plays a role in the development of obesity. We provide strong associations with certain molecular mechanisms that are activated by heat and correlate them with obesity and a hypothetical trial that could test this hypothesis. We conclude that if meal or drink temperature proves to contribute to energy homeostasis, then depending on its contribution and scale, future clinical trials should attempt to adjust this effect when analyzing data. In addition, previous research and established relationships of disease states with dietary patterns, energy intake, and food component intakes should be revisited. We understand the common assumption that thermal energy in food is absorbed by the body during digestion and dissipated as heat into the environment, not contributing to the energy balance. We challenge this assumption herein, including a proposed study design that would test our hypothesis. OBJECTIVE: This paper hypothesizes that the temperature of ingested foods or fluids influences energy homeostasis through the expression of heat shock proteins (HSPs), especially HSP-70 and HSP-90, which are expressed to a greater extent in obesity and are known to cause deficits in glucose metabolism. METHODS: We provide preliminary evidence supporting our hypothesis that greater dietary temperatures disproportionally induce activation of both intracellular and extracellular HSPs and that these HSPs influence energy balance and contribute to obesity. RESULTS: This trial protocol has not been initiated and funding has not been sought at the time of this publication. CONCLUSIONS: To date, no clinical trials are available regarding the potential effects of meal and fluid temperature on weight status or its confounding effects in data analysis. A potential mechanism is proposed as a basis by which higher temperatures of foods and beverages might influence energy balance via HSP expression. On the basis of the evidence supporting our hypothesis, we propose a clinical trial that will further elucidate these mechanisms. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): PRR1-10.2196/42846.

Characterizing motor impulsivity of individuals classified as overweight to obese.

Deficits in the impulse control system are an important predictor of energy intake and body weight. Adults classified as overweight to obese may possess these deficits as a general behavioral trait or they may be food-specific. The present study assessed motor impulsivity (ability to suppress a pre-potent response) when presented with food and neutral (non-food) cues, testing if deficits in motor impulsivity is specific to food cues or a general trait among participants classified as overweight to obese. The proportion of inhibitory failures to no-go targets following food cues (10.8%) was significantly greater than the proportion of inhibitory failures to no-go targets following neutral cues (1.9%, p â€‹< â€‹0.001). These differences remained when covering for sex and hunger. This indicates deficits in food-specific impulse control (as opposed to general impulse control) are present in those classified as overweight to obese. Understanding the specific aspect of impulse control that is present in this population is needed for the development of future impulse control training interventions that seek to change eating behaviors as a means for weight control.

Dietary adaptation for weight loss maintenance at Yale (DAWLY): Protocol and predictions for a randomized controlled trial.

Background: Current therapies for obesity treatment are effective at producing short-term weight loss, but weight loss maintenance remains a significant challenge. Here we investigate the impact of pre-intervention dietary fat intake on the efficacy of a dietary supplement to support weight loss maintenance. Preclinical work demonstrates that a vagal afferent pathway critical for sensing dietary lipids is blunted by a high-fat diet (HFD), resulting in a reduced preference for a low-fat emulsion and severe blunting of the dopamine (DA) response to the gastric infusion of lipids. Infusion of the gut lipid messenger oleoylethanolamide (OEA), which is also depleted by HFD, immediately reverses this DA blunting and restores preference for the low-fat emulsion. Studies of OEA supplementation for weight loss in humans have had limited success. Given the strong effect of HFD on this pathway, we designed a study to test whether the efficacy of OEA as a weight loss treatment is related to pre-intervention habitual intake of dietary fat. Methods/Design: We employed a randomized, double-blind, placebo-controlled trial in which 100 adults with overweight/obesity (OW/OB) were randomized to receive either OEA or placebo daily for 16 months. Following a baseline evaluation of diet, metabolic health, adiposity, and brain response to a palatable an energy dense food, participants in both groups underwent a 4-month behavioral weight loss intervention (LEARN®) followed by a 1-year maintenance period. The study aims are to (1) determine if pre-intervention dietary fat intake moderates the ability of OEA to improve weight loss and weight loss maintenance after a gold standard behavioral weight loss treatment; (2) identify biomarkers that predict outcome and optimize a stratification strategy; and (3) test a model underlying OEA's effectiveness. Discussion: Focusing on interventions that target the gut-brain axis is supported by mounting evidence for the role of gut-brain signaling in food choice and the modulation of this circuit by diet. If successful, this work will provide support for targeting the gut-brain pathway for weight loss maintenance using a precision medicine approach that is easy and inexpensive to implement. Clinical Trial Registration: [www.ClinicalTrials.gov], identifier [NCT04614233].

The influence of active video game play upon physical activity and screen-based activities in sedentary children.

BACKGROUND: Few children meet physical activity recommendations, partly due to the prevalence of screen-based sedentary activities. Active video game (AVG) play produces light to moderate physical activity. Yet, providing children access to AVG does not increase physical activity, possibly because children who play AVG may also tend towards sedentary screen-based activities. How multiple days of AVG play influences children's choice of other activities is not yet known. PURPOSE: To examine how AVG influences children's physical activity, sedentary screen-based activities, and other alternative activities. METHODS: Sedentary children (N = 49) played AVG 3 times/week and sedentary video games (SVG) ad libitum for 6 weeks, followed by 4 weeks of ad libitum play of both AVG and SVG. Participants wore an activity monitor for 7 days and completed a 24-hour activity recall on 4 randomly selected days at baseline, week 6, and week 10. RESULTS: AVG play increased during the intervention (p < 0.01). Light activity and SVG play both decreased baseline to 10 weeks (p = 0.006) and 6 to 10 weeks (p = 0.017). Non-SVG sedentary behavior increased from baseline to 10 weeks (p = 0.005) and 6 to 10 weeks (p = 0.007). Changes over time were not observed in physical activity, or recall-measured active play, social activities, other hobbies, television or computer/phone use. CONCLUSION: AVG play did not change children's objectively-measured physical activity or subjectively measured active play. SVG time was substituted with other sedentary behaviors. AVG did not increase time engaged in SVG or screen-based devices.

Reactive Oxygen Species (ROS) and Antioxidants as Immunomodulators in Exercise: Implications for Heme Oxygenase and Bilirubin.

Exercise is commonly prescribed as a lifestyle treatment for chronic metabolic diseases as it functions as an insulin sensitizer, cardio-protectant, and essential lifestyle tool for effective weight maintenance. Exercise boosts the production of reactive oxygen species (ROS) and subsequent transient oxidative damage, which also upregulates counterbalancing endogenous antioxidants to protect from ROS-induced damage and inflammation. Exercise elevates heme oxygenase-1 (HO-1) and biliverdin reductase A (BVRA) expression as built-in protective mechanisms, which produce the most potent antioxidant, bilirubin. Together, these mitigate inflammation and adiposity. Moderately raising plasma bilirubin protects in two ways: (1) via its antioxidant capacity to reduce ROS and inflammation, and (2) its newly defined function as a hormone that activates the nuclear receptor transcription factor PPARα. It is now understood that increasing plasma bilirubin can also drive metabolic adaptions, which improve deleterious outcomes of weight gain and obesity, such as inflammation, type II diabetes, and cardiovascular diseases. The main objective of this review is to describe the function of bilirubin as an antioxidant and metabolic hormone and how the HO-1-BVRA-bilirubin-PPARα axis influences inflammation, metabolic function and interacts with exercise to improve outcomes of weight management.

Exercise increases attentional bias towards food cues in individuals classified as overweight to obese.

BACKGROUND: The obesity epidemic continues to be a major public health concern. Although exercise is the most common weight loss recommendation, weight loss outcomes from an exercise program are often suboptimal. The human body compensates for a large percentage of the energy expended through exercise to maintain energy homeostasis and body weight. Increases in energy intake appear to be the most impactful compensatory behavior. Research on the mechanisms driving this behavior has not been fully elucidated. PURPOSE: To determine if exercise influences the attentional processing towards food cues (attentional bias) and inhibitory control for food cues among individuals classified as overweight to obese who do not exercise. METHODS: Thirty adults classified as overweight to obese participated in a counterbalanced, crossover trial featuring two assessment visits on separate days separated by at least one week. Attentional bias and inhibitory control towards food cues was assessed prior to and after a bout of exercise where participants expended 500 kcal (one assessment visit) and before and after a 60 min bout of watching television (second assessment visit). Attentional bias was conceptualized as the percentage of time fixated on food cues when both food and neutral (non-food) cues were presented during a food-specific dot-probe task. Inhibitory control, specifically motor impulsivity, was assessed as percentage of inhibitory failures during a food-specific Go/NoGo task. RESULTS: A significant condition by time effect was observed for attentional bias towards food cues, independent of hunger, whereas attentional bias towards food cues was increased pre-post exercise but not after watching TV. Inhibitory control was not affected by exercise or related to attentional bias for food cues. CONCLUSIONS: An acute bout of exercise increased attentional bias for food cues, pointing to a mechanism that may contribute to the weight loss resistance observed with exercise. Future trials are needed to evaluate attentional bias towards food cues over a longitudinal exercise intervention.

Cutting edge concepts: Does bilirubin enhance exercise performance?

Exercise performance is dependent on many factors, such as muscular strength and endurance, cardiovascular capacity, liver health, and metabolic flexibility. Recent studies show that plasma levels of bilirubin, which has classically been viewed as a liver dysfunction biomarker, are elevated by exercise training and that elite athletes may have significantly higher levels. Other studies have shown higher plasma bilirubin levels in athletes and active individuals compared to general, sedentary populations. The reason for these adaptions is unclear, but it could be related to bilirubin's antioxidant properties in response to a large number of reactive oxygen species (ROS) that originates from mitochondria during exercise. However, the mechanisms of these are unknown. Current research has re-defined bilirubin as a metabolic hormone that interacts with nuclear receptors to drive gene transcription, which reduces body weight. Bilirubin has been shown to reduce adiposity and improve the cardiovascular system, which might be related to the adaption of bilirubin increasing during exercise. No studies have directly tested if elevating bilirubin levels can influence athletic performance. However, based on the mechanisms proposed in the present review, this seems plausible and an area to consider for future studies. Here, we discuss the importance of bilirubin and exercise and how the combination might improve metabolic health outcomes and possibly athletic performance.

Fat and Carbohydrate Interact to Potentiate Food Reward in Healthy Weight but Not in Overweight or Obesity.

Prior work suggests that actual, but not estimated, energy density drives the reinforcing value of food and that energy from fat and carbohydrate can interact to potentiate reward. Here we sought to replicate these findings in an American sample and to determine if the effects are influenced by body mass index (BMI). Thirty participants with healthy weight (HW; BMI 21.92 ± 1.77; M ± SD) and 30 participants with overweight/obesity (OW/OB; BMI 29.42 ± 4.44) rated pictures of common American snacks in 120-kcal portions for liking, familiarity, frequency of consumption, expected satiety, healthiness, energy content, energy density, and price. Participants then completed an auction task where they bid for the opportunity to consume each food. Snacks contained either primarily carbohydrate, primarily fat, or roughly equal portions of fat and carbohydrate (combo). Replicating prior work, we found that participants with HW bid the most for combo foods in linear mixed model analyses. This effect was not observed among individuals with OW/OB. Additionally, in contrast with previous reports, our linear regression analyses revealed a negative relationship between the actual energy density of the snacks and bid amount that was mediated by food price. Our findings support altered macronutrient reinforcement in obesity and highlight potential influences of the food environment on the regulation of food reward.

Incentive sensitization for exercise reinforcement to increase exercise behaviors.

Individuals can be sensitized to the reinforcing effects of exercise, although it is unknown if this process increases habitual exercise behavior. Sedentary men and women (body mass index: 25-35 kg/m2, N = 52) participated in a 12-week aerobic exercise intervention. Exercise reinforcement was determined by how much work was performed for exercise relative to a sedentary alternative in a progressive ratio schedule task. Habitual physical activity was assessed via accelerometry. Post-intervention increases in exercise reinforcement predicted increases in physical activity bouts among those who expended over 2000 kcal per week in exercise and who compensated for less than 50 percent of their exercise energy expenditure.

Development of MacroPics: A novel food picture set to dissociate the effects of carbohydrate and fat on eating behaviors.

Emerging evidence suggests that fat and carbohydrate interact to potentiate the reward value of food (DiFeliceantonio et al., 2018). The primary goal of the current study was to develop a novel picture set to facilitate research into the effects of macronutrient composition on food choice and eating behavior. Toward this aim, we developed "MacroPics." In Experiment 1, we photographed 120-kcal portions of 60 snack foods falling into one of the three macronutrient categories: (1) mostly carbohydrate, (2) mostly fat, or (3) a combination of fat and carbohydrate. Sixty-one participants rated the images for liking, familiarity, frequency of consumption, healthiness, estimated energy content (in kcal), and expected satiation. A subset of these images consisting of 36 items was then selected in an iterative process to minimize differences in ratings between the macronutrient categories while simultaneously ensuring similar within-category variability on a number of food characteristics (e.g., energy density, portion size, retail price) and visual properties (e.g., color, complexity, visual area). In Experiment 2, an independent sample of 67 participants rated the pictures of the final 36-item MacroPics. Both experiments reveal similar participant ratings across categories for item liking, familiarity, frequency, healthiness, and estimated energy content. Protein content was higher in the fat compared to the carbohydrate and combination categories, leading to higher ratings of estimated satiety and energy density for fatty foods. Item and macronutrient category characteristics of the final MacroPics set are reported.

Exercise for Weight Loss: Further Evaluating Energy Compensation with Exercise.

PURPOSE: This study assessed how individuals compensate for energy expended during a 12-wk aerobic exercise intervention, elucidating potential mechanisms and the role exercise dose plays in the compensatory response. PARTICIPANTS AND DESIGN: Three-arm, randomized controlled trial among sedentary adults age 18 to 40 yr, body mass index of 25 to 35. Groups included six exercise sessions per week, two sessions per week, and sedentary control. METHODS: Rate of exercise energy expenditure was calculated from a graded exercise test averaged across five heart rate zones. Energy compensation was calculated as the difference between expected weight loss (based on exercise energy expenditure) and changes in fat and fat-free mass (DXA). Resting energy expenditure was assessed via indirect calorimetry and concentrations of acylated ghrelin, leptin, insulin, and Glucagon-like peptide 1 (GLP-1) were assessed fasting and postprandial (six timepoints over 2 h). RESULTS: The 6-d·wk group expended more energy (2753.5 kcal) and exercised longer (320.5 min) per week than the 2-d·wk group (1490.7 kcal, 1888.8 min, P < 0.05), resulting in greater fat loss compared with the 2-d or control groups (P < 0.05). Exercise groups did not differ in the % or total kcal compensated. Greater decreases in area under the curve (AUC) for acylated ghrelin predicted greater fat loss, regardless of group, energy expended per week, exercise duration, or exercise intensity. Changes in leptin AUC was the only independent predictor for energy compensation, with a greater decrease in leptin AUC predicting less energy compensation. Exercise frequency, energy expended, duration, or intensity did not influence energy compensation. CONCLUSIONS: Leptin is an important factor in successful weight loss through exercise, with greater postprandial decreases promoting less compensation. Greater amounts of exercise do not influence the compensatory response to an exercise-induced energy deficit.

The consequences of exercise-induced weight loss on food reinforcement. A randomized controlled trial.

BACKGROUND: Obesity remains a primary threat to the health of most Americans, with over 66% considered overweight or obese with a body mass index (BMI) of 25 kg/m2 or greater. A common treatment option many believe to be effective, and therefore turn to, is exercise. However, the amount of weight loss from exercise training is often disappointingly less than expected with greater amounts of exercise not always promoting greater weight loss. Increases in energy intake have been prescribed as the primary reason for this lack of weight loss success with exercise. Research has mostly focused on alterations in hormonal mediators of appetite (e.g.: ghrelin, peptide YY, GLP-1, pancreatic polypeptide, and leptin) that may increase hunger and/or reduce satiety to promote greater energy intake with exercise training. A less understood mechanism that may be working to increase energy intake with exercise is reward-driven feeding, a strong predictor of energy intake and weight status but rarely analyzed in the context of exercise. DESIGN: Sedentary men and women (BMI: 25-35 kg/m2, N = 52) were randomized into parallel aerobic exercise training groups partaking in either two or six exercise sessions/week, or sedentary control for 12 weeks. METHODS: The reinforcing value of food was measured by an operant responding progressive ratio schedule task (the behavioral choice task) to determine how much work participants were willing to perform for access to a healthy food option relative to a less healthy food option before and after the exercise intervention. Body composition and resting energy expenditure were assessed via DXA and indirect calorimetry, respectively, at baseline and post testing. RESULTS: Changes in fat-free mass predicted the change in total amount of operant responding for food (healthy and unhealthy). There were no correlations between changes in the reinforcing value of one type of food (healthy vs unhealthy) to changes in body composition. CONCLUSION: In support of previous work, reductions in fat-free mass resulting from an aerobic exercise intervention aimed at weight loss plays an important role in energy balance regulation by increasing operant responding for food.

Increasing the Reinforcing Value of Exercise in Overweight Adults.

Objectives: This study determined whether a moderate- or high-dose exercise program increases exercise reinforcement. Increasing the relative reinforcing value of exercise (RRVexercise; i.e., incentive sensitization of exercise) may increase the usual physical activity (PA) participation. Preference and/or tolerance for the intensity of exercise was also assessed. Design: Sedentary men and women (body mass index, BMI: 25-35 kg/m2) were randomized into parallel exercise training groups expending either 300 (n = 18) or 600 (n = 18) kcal/exercise session, five sessions/week, for 12 weeks. Methods: The RRVexercise was determined by how much work was performed for exercise relative to a sedentary alternative in a progressive ratio schedule task. Preference and tolerance for exercise intensity were determined by questionnaire. Results: RRVexercise increased (P < 0.05) in both groups. Exercise reinforcement, defined as the amount of work completed for exercise without taking sedentary activity into account, increased (P < 0.01) in the 600 kcal group only. Preference and tolerance for exercise intensity increased (P < 0.01) in both groups, which predicted increases in RRVexercise. Conclusion: Expending 300 or 600 kcal, 5 days/week increases RRVexercise, while 600 kcal, 5 days/week may be needed to increase exercise reinforcement.

Active Videogames to Promote Traditional Active Play: Increasing the Reinforcing Value of Active Play Among Low-Active Children.

Background: Exercise reinforcement predicts physical activity of children. Repeated exposures of physical activity may increase physical activity reinforcement (incentive sensitization). Active videogame (AVG) play produces light-to-moderate-intensity physical activity. Ideally, AVG play would transition to nonscreen-based active play through incentive sensitization of traditional active play (TAP), providing AVG does not increase sedentary videogame (SVG) reinforcement. Greater autonomy increases motivation toward traditional physical activity, but whether autonomy enhances incentive sensitization has not been studied. Objectives: To determine whether autonomy over AVG play promotes incentive sensitization of TAP or SVG. Methods: Inactive children (ages 8-12; 5th-97th body mass index percentile) were provided with AVG and SVG for 6 weeks and assigned to either a high autonomy (n = 25) or low autonomy (n = 24) group, differentiated by AVG choice and more freedom over amount of play. Both groups played AVG 3 days per week. SVG were played ad libitum. Participants completed an operant responding task to measure the relative reinforcing value (RRV) of AVG versus SVG (RRVAVG vs. SVG) and AVG versus TAP (RRVAVG vs. TAP) at baseline, 6 weeks, and 10 weeks. Results: RRVAVG vs. SVG increased over time (P = 0.056) but did not differ by autonomy or autonomy × time (P = 0.184). RRVAVG vs. TAP decreased over time (P = 0.033) but did not differ by autonomy or autonomy × time (P = 0.73). Conclusion: AVG play does not increase motivation toward SVG and increases motivation to play AVG relative to TAP. Providing higher autonomy did not promote incentive sensitization of play.

Inducing incentive sensitization of exercise reinforcement among adults who do not regularly exercise-A randomized controlled trial.

BACKGROUND: Increasing exercise reinforcement, or decreasing sedentary reinforcement, may reduce sedentary activity and promote habitual exercise. Repeated exposures to a reinforcer may increase its reinforcing value (i.e., incentive sensitization). It is not yet known whether incentive sensitization occurs for exercise or factors associated with incentive sensitization for exercise reinforcement. The purpose was to determine whether exercise exposures increase exercise reinforcement relative to a sedentary alternative and whether this sensitization of exercise reinforcement would alter physical or sedentary behavior. This work also determined whether exercise dose, intensity, and preference and tolerance for exercise intensity were associated with incentive sensitization of exercise. METHODS: 104 sedentary men and women were randomized to exercise training groups with 89 completing the study. Groups included exercise exposures of 150 (n = 35) or 300 kcal/session (n = 34), 3 sessions/week for 6 weeks, or a non-exercise control group (n = 35). Assessments for exercise and sedentary behavior reinforcement (primary dependent variables) and activity and tolerance for exercise intensity were performed at baseline (week 0), post training (week 6), and post washout (week 10). RESULTS: The control group reduced (P = 0.022) relative reinforcing value of exercise, such that the 150 kcal group had a greater relative reinforcing value of exercise after the exercise treatment 150 kcal: 0.69 ± 0.07 to 0.74 ± 0.07; 300 kcal: 0.72 ± 0.07 to 0.63 ± 0.08, control: 0.72 ± 0.07 to 0.57 ± 0.08 mean ± SE. Increases in tolerance for exercise intensity discomfort were associated with increases in relative reinforcing value of exercise. Sedentary behavior reinforcement decreased in both exercise groups (150 kcal: 5.4 ± 4.3 to 1.8 ± 1.3; 300 kcal: 5.4 ± 4.3 to 3.1 ± 2.4, P<0.05), but remained unchanged in the control group (5.1 ± 4.0 to 6.1 ± 4.9, P>0.05). Sedentary activity decreased baseline to post-training in the 300 kcal group (546.5 ± 10.7 to 503.8 ± 11.8 minutes, P<0.01). CONCLUSION: Small amounts of regular exercise may reduce the reinforcing value sedentary behavior. The process of incentive sensitization of exercise may include reducing the reinforcing value of competing sedentary activities. Developing tolerance to exercise discomfort of exercise may be critical to increasing exercise reinforcement.

Decreasing the Consumption of Foods with Sugar Increases Their Reinforcing Value: A Potential Barrier for Dietary Behavior Change.

BACKGROUND: The Dietary Guidelines for Americans (DGA) have recommended reducing added sugar intake since its inception in 1980. Nearly 40 years later, added sugar consumption still exceeds 2015-2020 DGA recommendations among most of the population. The reinforcing value of food influences eating behaviors, and foods high in added sugars are highly reinforcing. Restricting intake of foods high in added sugars as part of a low-sugar diet may increase their reinforcing value such that reducing consumption may be difficult to maintain. If so, this would present a mechanistic barrier to making the necessary dietary changes to meet 2015-2020 DGA recommendations. PURPOSE: To determine whether the relative reinforcing value of foods high in added sugars is altered when reducing intake of all foods high in sugars. METHODS: Obese (n=19) and normal weight (n=23) men and woman who habitually consumed over 10% of their calories from added sugars completed the study. Reinforcing value of foods high in added sugars was measured via progressive ratio schedules of reinforcement before and on day 7 of a weeklong controlled feeding intervention where added sugars comprised 2.5% to 4.0% of daily calories and total sugars 7.3% to 8.6% of daily calories. RESULTS: The reinforcing value of foods high in added sugars increased (P<0.01) after consuming a diet low in total added sugars for 1 week in both obese and normal weight participants. CONCLUSION: Adhering to a low-sugar diet for 1 week increases the reinforcing value of foods high in added sugars. Future studies should examine whether consuming a diet low in added sugars, but not other sugar, increases reinforcing value of foods high in added sugars and whether high-added sugar food reinforcement returns to baseline after longer-term reductions in added sugars.

Energy compensation in response to aerobic exercise training in overweight adults.

Weight loss from exercise is often less than expected. Putative compensatory mechanisms may limit exercise-induced reductions in body fat and might be proportional to exercise energy expenditure (ExEE). This study was conducted to determine compensation for (the difference between accumulated exercise energy expenditure and changes in body tissue energy stores) and compensatory responses to 1,500 or 3,000 kcal/wk of ExEE. Overweight-to-obese ( n = 36) sedentary men and women were randomized to groups expending 300 or 600 kcal/exercise session, 5 days/wk, for 12 wk. Fourteen participants in the 300-kcal group and 15 in the 600-kcal group completed the study. The primary outcome was energy compensation assessed through changes in body tissue energy stores. Secondary outcomes were putative compensatory responses of resting metabolic rate, food reinforcement, dietary intake, and serum acylated ghrelin and glucagon-like peptide-1. All measures were determined pre- and posttraining. The 3,000 kcal/wk group decreased ( P < 0.01) percentage and kilograms of body fat, while the 1,500 kcal/wk group did not. The 1,500 and 3,000 kcal/wk groups compensated for 943 (-164 to 2,050) and 1,007 (32 to 1,982) kcal/wk (mean, 95% CI, P ≥ 0.93), or 62.9% and 33.6% of ExEE, respectively. Resting metabolic rate and energy intake did not change. Food reinforcement and glucagon-like peptide-1 decreased ( P < 0.02), whereas acylated ghrelin increased ( P ≤ 0.02). Compensation is not proportional to ExEE. Similar energy compensation occurred in response to1,500 and 3,000 kcal/wk of ExEE. ExEE of 3,000 kcal/wk is sufficient to exceed compensatory responses and reduce fat mass.