Psychological and cognitive factors that influence post -exercise energy intake in normal weight and overweight sedentary males

Physical activity is recommended to facilitate weight management. However, some individuals may be unable to successfully manage their weight due to certain psychological and cognitive factors that trigger them to compensate for calories expended in exercise. The primary purpose of this study was to evaluate the effect of moderate-intensity exercise on lunch and 12-hour post-exercise energy intake (PE-EI) in normal weight and overweight sedentary males. Perceived hunger, mood, carbohydrate intake from beverages, and accuracy in estimating energy intake (EI) and energy expenditure (EE) were also assessed. The study consisted of two conditions, exercise (treadmill walking) and rest (sitting), with each participant completing each condition, in a counterbalanced-crossover design on two days. Eighty males, mean age 30 years (SD=8) were categorized into five groups according to weight (normal-/overweight), dietary restraint level (high/low), and dieting status (yes/no). Results of repeated measures, 5x2 ANOVA indicated that the main effects of condition and group, and the interaction were not significant for lunch or 12-hour PE-EI. Among overweight participants, dieters consumed significantly (p<0.05) fewer calories than non-dieters at lunch (M=822 vs. M=1149) and over 12 hours (M=1858 vs. M =2497). Overall, participants’ estimated exercise EE was significantly (p<0.01) higher than actual exercise EE, and estimated resting EE was significantly (p<0.001) lower than actual resting EE. Participants significantly (p<0.001) underestimated EI at lunch on both experimental days. Perceived hunger was significantly (p<0.05) lower after exercise (M=49 mm, SEM=3) than after rest (M=57 mm, SEM=3). Mood scores and carbohydrate intake from beverages were not influenced by weight, dietary restraint, and dieting status. In conclusion, a single bout of moderate-intensity exercise did not influence PE-EI in sedentary males in reference to weight, dietary restraint, and dieting status, suggesting that this population may not be at risk for overeating in response to exercise. Therefore, exercise can be prescribed and used as an effective tool for weight management. Results also indicated that there was an inability to accurately estimate EI (ad libitum lunch meal) and EE (60 minutes of moderate-intensity exercise). Inaccuracies in the estimation of calories for EI and EE could have the potential to unfavorably impact weight management.

The impact of dieting status and restraint on post-exercise energy intake in overweight females

This study investigated the impact of an acute bout of physical activity on postexercise energy intake (PE-EI) in overweight females who were dieting with high restraint (D-HR) and non-dieting with either high restraint (ND-HR) or low restraint (ND-LR). PE-EI at lunch and 12-hours after was compared on the exercise (E) and a nonexercise (NE) day. There was a significant interaction (F (2,33)= 4.12, p = 0.025) of dieting/restraint status and condition (E vs. NE day) on the 12-hour El. The D-HR ate 519 ± 596 kcal more on the E than on the NE day; while the ND-HR ate 177 ± 392 kcal less on the E than on the NE day. The results of this study demonstrate that the impact of exercise on PE-EI is determined by both a physiological and psychological response. Dieting status, dietary restraint, level of disinhibition and cognitive factors may influence PE-EI and weight.

Overweight/Obesity and HIV Disease Progression in HIV+ Adults in Botswana

Studies indicate that overweight and obesity protect against HIV-disease progression in antiretroviral therapy (ART)-naïve patients. We examined retrospectively the relationship of overweight/obesity with HIV-disease progression in ART-naïve HIV+ adults in Botswana in a case-control study with 18-month follow-up, which included 217 participants, 139 with BMI 18.0-24.9 kg/m2 and 78 with BMI ≥25 kg/m2. Archived plasma samples were used to determine inflammatory markers: leptin and bacterial endotoxin lipopolysaccharide (LPS), and genotype single nucleotide polymorphisms (SNPs) of the Fat Mass and Obesity Associated Gene (FTO). At baseline, BMI was inversely associated with risk for AIDS-defining conditions (HR=0.218; 95%CI=0.068, 0.701, P=0.011), and higher fat mass was associated with reduced risk of the combined outcome of CD4+cell count ≤250/µL and AIDS-defining conditions, whichever occurred earlier (HR=0.918; 95%CI=0.847, 0.994, P=0.036) over 18 months, adjusting for age, gender, marriage, children, and baseline CD4+cell count and HIV-viral load. FTO-SNP rs17817449 was associated with BMI (OR=1.082; 95%CI=1.001, 1.169; P=0.047). Fat mass was associated with the risk alleles of rs1121980 (OR=1.065; 95%CI=1.009, 1.125, P=0.021), rs8050136 (OR=1.078; 95%CI=1.021, 1.140; P=0.007), and rs17817449 (OR=1.086; 95%CI=1.031, 1.145; P=0.002), controlling for age, gender, tribe, total energy intake, and activity. There were no associations of SNPs with markers of disease progression. Leptin levels were positively associated with BMI (β=1.764; 95%CI=0.788, 2.739; P=0.022) and fat mass (β=0.112; 95%CI=0.090, 0.135; P<0.001), but inversely with viral load (β=-0.305; 95%CI=-0.579, -.031; P=0.030). LPS levels were inversely associated with BMI (OR=0.790, 95%CI=0.630, 0.990; P=0.041), and fat mass (OR=0.852, 95%CI=0.757, 0.958; P=0.007) and directly with viral load (OR=2.608, 95%CI=1.111, 6.124; P=0.028), adjusting for age, gender, smoking and %fat mass. In this cohort, overweight/obesity predicted slower HIV-disease progression. Obesity may confer an advantage in maintaining fat stores to support the overactive immune system. FTO-SNPs may contribute to the variation in fat mass; however, they were not associated with HIV-disease progression. Our findings suggest that the obesity paradox may be explained by the association of increased LPS with lower BMI and higher viral load; while viral load decreased with increasing leptin levels. Studies in African populations are needed to clarify whether genetic variation and inflammation mediate the obesity paradox in HIV-disease progression.

Psychological and Cognitive Factors that Influence Post-Exercise Energy Intake in Normal Weight and Overweight Sedentary Males

The primary purpose of this study was to evaluate the effects of a single bout of moderate-intensity exercise on acute (ad libitum lunch) post-exercise energy intake (PE-EI) and 12-hour energy intake in normal-weight and overweight sedentary males. Accuracy in estimating energy intake (EI) and energy expenditure (EE), solid vs. liquid carbohydrate intake, mood, and perceived hunger were also assessed. The study consisted of two conditions, exercise and rest, with each subject participating in each condition, in a counterbalanced-crossover design on two days. The participants were randomly assigned to either the exercise or resting (seated) control condition on the first day of the experiment, and then the condition was reversed on the second day. Exercise consisted of walking on a treadmill at moderate-intensity for 60 minutes. Eighty males, mean age 30+8 years were categorized into five groups according to weight status (overweight/normal-weight), dietary restraint status (high/low), and dieting status (yes/no). The main effects of condition and group, and the interaction were not significant for acute (lunch) or 12-hour PE-EI. Overall, participants estimated EE for exercise at 46% higher than actual exercise EE, and they estimated EE for rest by 45% lower than actual resting EE. Participants significantly underestimated EI at lunch on both the exercise and rest days by 43% and 44%, respectively. Participants with high restraint were significantly better at estimating EE on the exercise day, and better at estimating EI on the rest day. Mood, perceived hunger, and solid vs. liquid carbohydrate intake were not influenced by dietary restraint, weight, or dieting status. In conclusion, a single bout of moderate-intensity exercise did not influence PE-EI in sedentary males in reference to dietary restraint, weight, and dieting status. Results also suggested that among sedentary males, there is a general inability to accurately estimate calories for moderate-intensity physical activity and EI. Inaccurate estimates of EE and EI have the potential to influence how males manage their weight.

Overweight/obesity and HIV disease progression in HIV+ adults in Botswana

Studies indicate that overweight and obesity protect against HIV-disease progression in antiretroviral therapy (ART)-naïve patients. We examined retrospectively the relationship of overweight/obesity with HIV-disease progression in ART-naïve HIV+ adults in Botswana in a case-control study with 18-month follow-up, which included 217 participants, 139 with BMI 18.0-24.9 kg/m 2 and 78 with BMI ≥25 kg/m2. Archived plasma samples were used to determine inflammatory markers: leptin and bacterial endotoxin lipopolysaccharide (LPS), and genotype single nucleotide polymorphisms (SNPs) of the Fat Mass and Obesity Associated Gene (FTO). ^ At baseline, BMI was inversely associated with risk for AIDS-defining conditions (HR=0.218; 95%CI=0.068, 0.701, P=0.011), and higher fat mass was associated with reduced risk of the combined outcome of CD4+cell count ≤250/µL and AIDS-defining conditions, whichever occurred earlier (HR=0.918; 95%CI=0.847, 0.994, P=0.036) over 18 months, adjusting for age, gender, marriage, children, and baseline CD4+cell count and HIV-viral load. ^ FTO-SNP rs17817449 was associated with BMI (OR=1.082; 95%CI=1.001, 1.169; P=0.047). Fat mass was associated with the risk alleles of rs1121980 (OR=1.065; 95%CI=1.009, 1.125, P=0.021), rs8050136 (OR=1.078; 95%CI=1.021, 1.140; P=0.007), and rs17817449 (OR=1.086; 95%CI=1.031, 1.145; P=0.002), controlling for age, gender, tribe, total energy intake, and activity. There were no associations of SNPs with markers of disease progression. ^ Leptin levels were positively associated with BMI (β=1.764; 95%CI=0.788, 2.739; P=0.022) and fat mass (β=0.112; 95%CI=0.090, 0.135; P<0.001), but inversely with viral load (β=-0.305; 95%CI=-0.579, -.031; P=0.030). LPS levels were inversely associated with BMI (OR=0.790, 95%CI=0.630, 0.990; P=0.041), and fat mass (OR=0.852, 95%CI=0.757, 0.958; P=0.007) and directly with viral load (OR=2.608, 95%CI=1.111, 6.124; P=0.028), adjusting for age, gender, smoking and %fat mass. ^ In this cohort, overweight/obesity predicted slower HIV-disease progression. Obesity may confer an advantage in maintaining fat stores to support the overactive immune system. FTO-SNPs may contribute to the variation in fat mass; however, they were not associated with HIV-disease progression. Our findings suggest that the obesity paradox may be explained by the association of increased LPS with lower BMI and higher viral load; while viral load decreased with increasing leptin levels. Studies in African populations are needed to clarify whether genetic variation and inflammation mediate the obesity paradox in HIV-disease progression.^