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Time-restricted eating and concurrent exercise training reduces fat mass and increases lean mass in overweight and obese adults.

ABSTRACT: The purpose of this study was to determine whether time-restricted eating (TRE), also known as time-restricted feeding, was an effective dietary strategy for reducing fat mass and preserving fat-free mass while evaluating changes in cardiometabolic biomarkers, hormones, muscle performance, energy intake, and macronutrient intake after aerobic and resistance exercise training in physically inactive and overweight or obese adults. This study was a randomized, controlled trial. Overweight and obese adults (mean ± SD; age: 44 ± 7 years; body mass index [BMI]: 29.6 ± 2.6 kg/m² ; female: 85.7%) were randomly assigned to a TRE or normal eating (NE) dietary strategy group. The TRE participants consumed all calories between 12:00 p.m. and 8:00 p.m., whereas NE participants maintained their dietary habits. Both groups completed 8 weeks of aerobic exercise and supervised resistance training. Body composition, muscle performance, energy intake, macronutrient intake, physical activity, and physiological variables were assessed. A total of 21 participants completed the study (NE: n = 10; TRE: n = 11). A mild energy restriction was observed for TRE (~300 kcal/day, 14.5%) and NE (~250 kcal/day, 11.4%). Losses of total body mass were significantly greater for TRE (3.3%) relative to NE (0.2%) pre- to post-intervention, of which TRE had significantly greater losses of fat mass (9.0%) compared to NE (3.3%). Lean mass increased during the intervention for both TRE (0.6%) and NE (1.9%), with no group differences. These data support the use of TRE and concurrent exercise training as a short-term dietary strategy for reducing fat mass and increasing lean mass in overweight and obese adults.

SUBMITTER: Kotarsky CJ

PROVIDER: S-EPMC8157764 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Weight gain in pregnancy is an essential physiologic adaptation that supports growth and development of a fetus and is distributed among lean mass that includes total body water and fat mass gains. Although gestational weight gain provides a source of energy for the mother and fetus, excess gestational weight gain may underlie reported associations between parity and future metabolic disorders and is linked to postpartum weight retention and insulin resistance. Although weight gain often is proposed as a modifiable variable to mitigate adverse maternal and offspring health outcomes, our knowledge of specific maternal body composition changes with weight gain and the potential metabolic consequences is limited. Furthermore, although gestational weight gain alters maternal body composition, the impact of excess weight gain on fat and lean mass is not well-studied. Understanding the accrual of fat and lean body mass may improve our understanding of the role of excessive gestational weight gain and metabolic dysfunction.The purpose of our study was to quantify the relationship between gestational weight gain and maternal fat and lean body mass accrual and to compare fat and lean body mass accrual according to the 2009 Institute of Medicine Guidelines for Gestational Weight Gain in Pregnancy adherence. We hypothesized that exceeding current weight gain guidelines would be associated with greater fat, compared with lean body, mass accrual.This is a secondary analysis of a randomized controlled trial of 49 overweight/obese women; all 49 are included in this secondary analysis. Maternal weight and body composition were collected in early (13 0/6 to 16 6/7 weeks gestation) and late (34 0/7 to 36 6/7 weeks gestation) pregnancy with the use of air densitometry. Correlations were drawn between gestational weight gain and change in fat and lean body mass. We compared change in fat and lean body mass by adherence to the 2009 Institute of Medicine Guidelines for Gestational Weight Gain in Pregnancy. Nonparametric tests and chi-square analyses were performed; a probability value of <.05 was significant.Early pregnancy body mass index was 30.3 kg/m(2) (interquartile range [IQR], 28.5-35.2 kg/m(2)); women gained 9.0 kg (IQR, 5.3-13.2 kg). Overweight and obese women were equally likely to gain excess weight (48% vs 35%; P = .6). Weight gain correlated strongly with fat mass change (r = 0.87; P < .001); women with excess vs adequate vs inadequate weight gain had greater fat mass change overall (5.2 [IQR, 4.2-8.1] vs 0.2 [IQR, -0.4-2.2] vs -2.7 [IQR, -5.2- -0.7] kg, respectively; P < .001) and in all pairwise comparisons. Weight gain also correlated with lean body mass change (r = 0.52; P = .001), but women with excess vs adequate weight gain had similar lean body mass change (8.4 [IQR, 7.2-10.1] vs 7.8 [IQR, 6.0-8.7] kg; P = .1).Excess gestational weight gain is associated primarily with maternal fat, but not with lean body mass accrual. Our results may help explain the reason that excess gestational weight gain or fat mass accrual is associated with long-term obesity, metabolic dysfunction, and cardiovascular disease risk.

Project description:It is often assumed that some individuals reliably increase energy intake (EI) post-exercise ('compensators') and some do not ('non-compensators'), leading researchers to examine the characteristics that distinguish these two groups. However, it is unclear whether EI post-exercise is stable over time. The present study examined whether compensatory eating responses to a single exercise bout are consistent within individuals across three pairs of trials. Physically inactive, overweight/obese women (n 28, BMI 30·3 (SD 2·9) kg/m²) participated in three pairs of testing sessions, with each pair consisting of an exercise (30 min of moderate-intensity walking) and resting testing day. EI was measured using a buffet meal 1 h post-exercise/rest. For each pair, the difference in EI (EIdiff = EIex - EIrest) was calculated, where EIex is the EI of the exercise session and EIrest is the EI of the resting session, and women were classified as a 'compensator' (EIex > EIrest) or 'non-compensator' (EIex ? EIrest). The average EI on exercise days (3328·0 (SD 1686·2) kJ) was similar to those on resting days (3269·4 (SD 1582·4) kJ) (P= 0·67). Although EI was reliable within individuals across the three resting days (intraclass correlation coefficient (ICC) 0·75, 95 % CI 0·60, 0·87; P< 0·001) and three exercise days (ICC 0·83, 95 % CI 0·70, 0·91; P< 0·001), the ICC for EIdiff across the three pairs of trials was low (ICC 0·20, 95 % CI -0·02, 0·45; P= 0·04), suggesting that compensatory eating post-exercise is not a stable construct. Moreover, the classification of 'compensators'/'non-compensators' was not reliable (? = -0·048; P= 0·66). The results were unaltered when 'relative' EI was used, which considers the energy expenditure of the exercise/resting sessions. Acute compensatory EI following an exercise bout is not reliable in overweight women. Seeking to understand what distinguishes 'compensators' from 'non-compensators' based on a single eating episode post-exercise is not justified.

Project description:BackgroundLeucine deprivation modulates the dietary amino acid composition, reducing the fat content and improving the glucose tolerance, thus protecting the organism against obesity. However, a complete deprivation of leucine can lead to an extremely rapid fat loss in mice, accompanied by prolonged adverse effects such as weakness and mental fatigue. Therefore, in this study we aimed to seek the optimal concentration of dietary leucine that can reduce fat mass and improve the metabolism without the onset of severe effects.MethodsTo investigate whether there is a better concentration of diet leucine restriction (LR), based on the diet we conducted (A10021B), that can reduce fat mass and improve metabolism status without taking many negative effects, we fed 8 weeks old male C57Bl/6J mice with increasing degrees of leucine restriction diet 0% LR (control group), 25% LR, 50% LR, and 75% LR groups (4-6 mice each group). Fat mass and blood glucose levels were measured. The expression levels of genes involved in lipid metabolism in white adipose tissue (WAT) and liver, and proteins in insulin signaling were assessed in WAT, liver and muscle.ResultsWe found that the 50% LR group is the most proper group here at the lowest leucine effective concentration, which reduced fat mass (p < 0.05) and improved glucose regulation in mice over a 90 days feeding. Further studies revealed that lipid synthesis pathway (Fas, Scd1and Srebp1, p < 0.05) was downregulated and lipolysis (Atgl, p < 0.05) was upregulated in WAT in 50% LR group, compared to that in control group. Furthermore, glucose regulation (glucose tolerance test, p < 0.05) was also improved, and insulin signaling (p < 0.05) in the muscle was enhanced in 50% LR group while in WAT and liver were not changed.ConclusionsCollectively, a 50% LR in mice reduced fat mass and improved glucose regulation, which may function through modulating lipid synthesis and lipolysis pathway in adipose tissue as well as enhancing insulin signaling in muscle. So far, we provide a further consideration for carrying out the diet of leucine restriction to reduce fat and improve metabolism status before clinical study.

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Time-restricted eating and concurrent exercise training reduces fat mass and increases lean mass in overweight and obese adults.

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