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/m 2 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/m 2 , 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.
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 < 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.
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 role of physical activity in normal weight obesity (NWO), which is associated with increased cardiometabolic risk, is not clear. This study aimed to determine body composition phenotype-specific differences in objectively measured physical activity and sedentary time in adults in the United States. A total of 2055 adults with a body mass index (BMI) ≥ 18.5 m2 were studied using 2003–2006 National Health and Nutrition Examination Surveys. Physical activity and percent body fat (BF%) were measured using accelerometer and dual-energy X-ray absorptiometry, respectively. A BF% > 23.1% and >33.3% for men and women, respectively, was considered excess. A BMI of 18.5–24.9 kg/m2 with excess BF% was defined as NWO, while those with normal BF%, as normal weight lean (NWL). A BMI of ≥25 kg/m2 with excess BF% was considered overweight/obesity (OB). Compared to NWL, moderate to vigorous physical activity was significantly lower by 8.3 min (95% confidence interval/CI = −15.20, −1.40) and 10.18 min (95% CI = −14.83, −5.54) per day in NWO and OB, respectively. Low-intensity physical activity was also significantly lower by 17.71 min (95% CI = −30.61, −4.81) per day in NWO compared to NWL. However, sedentary time was not different. Objectively measured physical activity is significantly lower in NWO compared to NWL, while sedentary time is not.
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