Compared with the control condition, DIET represented a greater acute challenge to appetite regulation than EX, as demonstrated by greater appetite and ad libitum EI. This study confirms that compared with depletions by exercise alone, acute caloric restriction results in rapid changes in appetite that result in compensatory eating, which may initially dissuade potential success in weight-loss efforts. This trial was registered at clinicaltrials.gov as NCT02653378.
Evidence suggests that fat-free mass and resting metabolic rate (RMR), but not fat mass, are strong predictors of energy intake (EI). However, body composition and RMR do not explain the entire variance in EI, suggesting that other factors may contribute to this variance. We aimed to investigate the associations between body mass index (in kg/m), fat mass, fat-free mass, and RMR with acute (1 meal) and daily (24-h) EI and between fasting appetite ratings and certain eating behavior traits with daily EI. We also evaluated whether RMR is a predictor of the error variance in acute and daily EI. Data collected during the control condition of 7 studies conducted in Ottawa, Ontario, Canada, were included in these analyses ( = 191 and 55 for acute and daily EI, respectively). These data include RMR (indirect calorimetry), body composition (dual-energy X-ray absorptiometry), fasting appetite ratings (visual analog scales), eating behavior traits (Three-Factor Eating Questionnaire), and EI (food buffet or menu). Fat-free mass was the best predictor of acute EI ( = 0.46; < 0.0001). The combination of fasting prospective food consumption ratings and RMR was the best predictor of daily EI ( = 0.44; < 0.0001). RMR was a statistically significant positive predictor of the error variance for acute ( = 0.20; < 0.0001) and daily ( = 0.23; < 0.0001) EI. RMR did, however, remain a statistically significant predictor of acute ( = 0.32; < 0.0001) and daily ( = 0.30; < 0.0001) EI after controlling for this error variance. Our findings suggest that combined measurements of appetite ratings and RMR could be used to estimate EI in weight-stable individuals. However, greater error variance in acute and daily EI with increasing RMR values was observed. Future studies are needed to identify whether greater fluctuations in daily EI over time occur with increasing RMR values. This trial was registered at clinicaltrials.gov as NCT02653378.
This study explored the relationship between muscle fat infiltration derived from mid‐thigh computed tomography (CT) scan, central fat distribution and insulin sensitivity in postmenopausal women. Mid‐thigh CT scans were used to measure low attenuation muscle surface (LAMS) (0–34 Hounsfield units (HU)), which represented a specific component of fat‐rich muscle. Whole‐body insulin sensitivity (M/I) was evaluated by an euglycemic‐hyperinsulinemic clamp. A group of 103 women aged 57.0 ± 4.4 years was studied. Women with higher levels of LAMS presented higher metabolic risk features, particularly elevated fasting, 2‐h plasma glucose (2hPG) concentrations and diminished M/I (P < 0.05). To further study the contribution of muscle fat infiltration and central adiposity on metabolic parameters, we divided the whole group based on the median of LAMS and visceral adipose tissue (VAT). As expected, the best metabolic profile was found in the Low‐LAMS/Low‐VAT group and the worst in the High‐LAMS/High‐VAT group. Women with Low‐LAMS/High‐VAT presented similar metabolic risks to those with High‐LAMS/High‐VAT. There was no difference between High‐LAMS/Low‐VAT and Low‐LAMS/Low‐VAT, which presents the most healthy metabolic and glycemic profiles as reflected by the lowest levels of cardiovascular disease risk variables. This suggests that High‐LAMS/Low‐VAT is also at low risk of metabolic deteriorations and that High‐LAMS, only in the presence of High‐VAT seems associated with deteriorated risks. Although increased mid‐thigh fat‐rich muscle was related to a deteriorated metabolic profile, VAT appears as a more important contributor to alterations in the metabolic profile in postmenopausal women.
Background/Objectives Body composition (BC) does not always vary as a function of exercise induced energy expenditure (exercise EE – resting EE). Energy balance variables were measured to understand energy compensation (EC) in response to an exercise intervention performed at low (LOW) or moderate (MOD) intensity. Subjects/Methods Twenty-one women with overweight/obesity (33 ± 5 kg/m 2 ; 29 ± 10 yrs; 31 ± 4 ml O 2 /kg/min) were randomized to a 3-month LOW or MOD (40 or 60% of VȮ 2reserve , respectively) matched to expend 1500 kcal/week (compliance = 97 ± 5%). Body energy stores (DXA), energy intake (EI) (food menu and food diaries), resting EE (indirect calorimetry), total EE (doubly-labeled water), time spent in different activities (accelerometers), appetite (visual analog scale), eating behavior traits and food reward (liking and wanting) were assessed at baseline, after weeks 1 and 2 and at the end of the 3-month exercise intervention. Results EC based on BC changes (fat mass and fat-free mass) was 49 ± 79% and 161 ± 88% in LOW and MOD groups, respectively ( p = 0.010). EI did not change significantly during the intervention. However, eating behavior traits and food reward had changed by the end of the 3-month supervised exercise. Non-structured physical activity (NSPA) decreased across the intervention ( p < 0.002), independent of the intensity of the exercise training. Conclusion Women with overweight/obesity training at LOW presented lower EC for a given energy cost of exercise. Our results strongly suggest that NSPA plays a major role in mediating the effects of exercise on energy balance and ultimately on changes in BC. Clinical Trial Registration www.ClinicalTrials.gov , identifier ISRCTN31641049.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.