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

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

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 \u3c 0.05), but remained unchanged in the control group (5.1 ± 4.0 to 6.1 ± 4.9, P \u3e 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 \u3c 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

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−1 group expended more energy (2753.5 kcal) and exercised longer (320.5 min) per week than the 2-d·wk−1 group (1490.7 kcal, 1888.8 min, P \u3c 0.05), resulting in greater fat loss compared with the 2-d or control groups (P \u3c 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

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 \u3c 0.05) in both groups. Exercise reinforcement, defined as the amount of work completed for exercise without taking sedentary activity into account, increased (P \u3c 0.01) in the 600 kcal group only. Preference and tolerance for exercise intensity increased (P \u3c 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

Genetic Variations in the Dopamine Reward System Influence Exercise Reinforcement and Tolerance for Exercise Intensity

Background: Exercise is a reinforcing behavior and finding exercise highly reinforcing is characteristic of habitual exercisers. Genotypes related to dopamine metabolism moderate the reinforcing value of behaviors, but genetic moderators of exercise reinforcement have not been established. Purpose: Determine whether singular nucleotide polymorphisms (SNPs) that moderate central reward pathways and pain neurotransmission are associated with exercise reinforcement, tolerance for exercise intensity, and usual physical activity. Methods: Adults (n = 178) were measured for the reinforcing value of exercise relative to sedentary activities (RRVexercise), minutes of moderate-to-vigorous physical activity (MVPA) and completed the Preference for and Tolerance of the Intensity of Exercise Questionnaire. Genotyping of 23 SNPs known to influence central dopamine tone, pain, or physical activity was performed. ANOVA tested differences in RRVexercise, tolerance, and MVPA among genotype groups. Linear regression controlling for BMI, sex, and liking of exercise was used to further predict the association of genotype on RRVexercise, tolerance, and MVPA. Results: Having at least one copy of the G allele for the DRD2/ANKK1 polymorphism (rs1800497) conferred greater RRVexercise. Greater tolerance for exercise intensity was observed among those homozygous for the T allele for the CNR1 polymorphism (rs6454672), had at least one copy of the G allele for the GABRG3 polymorphism (rs8036270), or had at least one copy of the T allele for the LPR polymorphism (rs12405556). Homozygous individuals for the T allele at rs6454672 exhibited greater MVPA. Conclusion: Similar to other reinforcing behaviors, there is a genetic contribution to exercise reinforcement, tolerance for exercise intensity, and MVPA

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

Aging, Resistance Training, and Diabetes Prevention

With the aging of the baby-boom generation and increases in life expectancy, the American population is growing older. Aging is associated with adverse changes in glucose tolerance and increased risk of diabetes; the increasing prevalence of diabetes among older adults suggests a clear need for effective diabetes prevention approaches for this population. The purpose of paper is to review what is known about changes in glucose tolerance with advancing age and the potential utility of resistance training (RT) as an intervention to prevent diabetes among middle-aged and older adults. Age-related factors contributing to glucose intolerance, which may be improved with RT, include improvements in insulin signaling defects, reductions in tumor necrosis factor-α, increases in adiponectin and insulin-like growth factor-1 concentrations, and reductions in total and abdominal visceral fat. Current RT recommendations and future areas for investigation are presented

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

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