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Purpose of review The prevalence and burden of obesity has reached alarming levels. The assessment of human energy expenditure enables the identification of obesity-prone and obesity-resistant individuals and helps to explain the short and long-term success of weight loss treatments. In this review, we describe the state-of-the-art methods used in the assessment of human energy expenditure and the impact of dietary intake on the interpretation of the data. Recent findings The reference techniques to assess energy expenditure in humans have not significantly changed during the last century. Today, indirect calorimetry, either using a metabolic chamber or a metabolic cart, is the favored method to assess human energy expenditure and is the only method enabling the assessment of macronutrient oxidation. The doubly labeled water method however provides accurate assessment of human energy expenditure under free living conditions. Summary Although energy expenditure and macronutrient oxidation can be assessed by simple calculations from oxygen consumption and carbon dioxide production, these calculations can provide erroneous results or require corrections and/or more complex interpretation when several biochemical pathways are simultaneously engaged. Such physiological mechanisms are often elicited by dietary interventions including, among other, gluconeogenesis, lipogenesis, ketogenesis, alcohol oxidation and under or overfeeding.

Introduction: Caloric restriction (CR) improves cardiometabolic risk, even among individuals without obesity. However, it is unclear whether these aging-related benefits are mediated by weight loss. Mediation analyses inform mechanisms underlying relationships between an exposure and outcome. Using mediation analyses, our aim was to test if 2-year weight loss mediates the beneficial effects of CR on cardiometabolic risk markers in individuals without obesity. Methods: Participants without obesity were randomized 2:1 to CR or ad libitum (AL) as part of the 2-year trial, Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE). The CR group aimed to enact 25% CR for 2 years, while AL maintained habitual energy intake. Baseline and year 2 assessments included weight and cardiometabolic risk markers. Using the approaches of Valeri and VanderWeele, mediation was quantified as the natural indirect effect (NIE), defined as the impact of an exposure on an outcome through a mediator. Here, the NIE was the effect of CR (exposure) on cardiometabolic risk markers (outcome) that was accounted for by weight change (mediator). Results: In total, 117 and 71 participants in the CR and AL groups, respectively, completed the trial. The CR group achieved 11.9 (± 0.7)% CR and 7.6 (± 0.3) kg of weight loss ( P < 0.01 versus AL). Weight loss significantly mediated the CR-induced improvements in total cholesterol (NIE = -10.4 ± 3.5 mg/dL), low-density lipoprotein cholesterol (NIE = -8.5 ± 2.8 mg/dL), high-density lipoprotein cholesterol (NIE = 2.9 ± 1.3 mg/dL), triglycerides (NIE = -0.20 ± 0.05 log mg/dL), the homeostatic model assessment of insulin resistance (NIE = -0.22 ± 0.06), and C-reactive protein (NIE = -0.39 ± 0.15 log ug/mL) ( P ≤ 0.02). Weight loss did not mediate CR-induced reductions in systolic (NIE = -0.9 ± 1.4 mmHg) and diastolic (NIE = -1.0 ± 1.1 mmHg) blood pressure ( P ≥ 0.37). Conclusion: In individuals without obesity, CR-induced improvements in multiple cardiometabolic risk markers are driven by weight loss after 2 years. These findings emphasize that, even in individuals without obesity, weight loss after prolonged CR plays a role in improving cardiometabolic disease risk; however, some CR benefits still occur independent of weight loss.

INTRODUCTION: The ability to maintain functional independence in a rapidly aging population results in an increased life expectancy without corresponding increases in health care costs. The accelerated decline in VO(2peak) after the age of 65 is primarily due to peripheral tissue changes rather than centrally mediated factors. The purpose of this study was to determine if the PRIME (Peripheral Remodeling through Intermittent Muscular Exercise) approach, consisting of a low mass, high repetition/duration skeletal muscle focused training regimen would provide superior functional benefits in participants above 70 years old and at risk for losing functional independence. METHODS: In this clinical trial, 107 participants were randomized to four weeks of either standard aerobic exercise training (AT) or PRIME [Phase 1]. This was followed by eight weeks of a progressive whole-body aerobic and resistance training (AT+RT) for all participants [Phase 2]. The major outcome measures were cardiorespiratory fitness (peak oxygen consumption-VO(2peak)), muscular fitness (1 repetition maximal strength -1RM) and physical function (Senior Fitness Test scores-SFT). Results were analyzed under a pro-protocol criterion. RESULTS: Thirty-eight PRIME and 38 AT participants completed the 3-month protocols. VO(2peak), 1RM, and SFT scores all increased significantly after 12 weeks for both treatment groups (p

OBJECTIVE To conduct a secondary analysis designed to test whether gestational weight gain is the result of increased energy intake or adaptive changes in energy expenditures. METHODS In this secondary analysis, energy intake and energy expenditure of 45 pregnant women (body mass index [BMI] 18.5-24.9 [n=33] and BMI 25 or greater [n=12]) were measured preconceptionally and at 22 and 36 weeks of gestation. Energy intake was calculated as the sum of total energy expenditure measured by doubly-labeled water and energy deposition determined by the four-compartment body composition model. Measurements of weight, body composition, and basal metabolic rate were completed preconceptionally and 9, 22, and 36 weeks of gestation. Basal metabolic rate was measured by indirect calorimetry in a room calorimeter and activity energy expenditure by doubly-labeled water. RESULTS Energy intake from 22 to 36 weeks of gestation was significantly higher in high gainers (n=19) (3,437±99 kcal per day) compared with low+ideal gainers (n=26) (2,687±110, P

Obesity is a significant health challenge, with the latest projections estimating that there will be 2.16 billion overweight and 1.12 billion obese individuals globally by 2030. In addition to social stigmatization and impaired quality of life, obese people are faced with significantly increased risk of cardiovascular disease, type 2 diabetes mellitus, and a number of cancers. Weight gain results from a sustained imbalance between energy intake (calories consumed) and energy expenditure (calories burned), resulting in positive energy balance. To tip energy balance toward weight loss, not only should food intake be decreased, but increasing physical activity may help. It is important to realize, however, that the secular rises in obesity over the past 3 to 4 decades can be explained by both physiological and environmental drivers and a number of putative factors (Figure 1).1,2 At one level, the obesity epidemic is a classic gene-environment interaction in which the human genotype is susceptible to environmental influences that affect energy intake and expenditure, with the obesogenic environment being dominant. These environmental factors include the 2 obvious explanations, ie, reduced physical activity and increased energy intake from high-calorie food and drinks, with the latter likely being the dominant factor.3 However, other less studied factors have been implicated, including longer time spent awake, increased mean age of mothers at first birth, decreased prevalence of smoking, presence of environmental pollutants, ingestion of many novel medications, and reduction in the variability of seasonal ambient temperature owing to the presence of almost ubiquitous air conditioning.4 Fundamentally, the obesity epidemic is explained by a dysregulation of energy balance in our obesogenic environment. Understanding the cause of obesity requires the study of how genetic and environmental factors interact to produce long-term positive energy balance. Figure 1. The effects of genes and environment on adiposity. Effects …

There is a debate over the independent effects of aerobic fitness and body fatness on mortality and disease risks.To determine whether a 25% energy deficit that produces equal change in body fatness leads to greater cardiometabolic benefits when aerobic exercise is included.Thirty-six overweight participants (16 males/20 females) (39 +/- 1 yr; 82 +/- 2 kg; body mass index = 27.8 +/- 0.3 kg x m2, mean +/- SEM) were randomized to one of three groups (n = 12 for each) for a 6-month intervention: control (CO, weight-maintenance diet), caloric restriction (CR, 25% reduction in energy intake), or caloric restriction plus aerobic exercise (CR + EX, 12.5% reduction in energy intake plus 12.5% increase in exercise energy expenditure). Food was provided during weeks 1-12 and 22-24. Changes in fat mass, visceral fat, VO2peak (graded treadmill test), muscular strength (isokinetic knee extension/flexion), blood lipids, blood pressure, and insulin sensitivity/secretion were compared.As expected, VO2peak was significantly improved after 6 months of intervention in CR + EX only (22 +/- 5% vs 7 +/- 5% in CR and -5 +/- 3% in CO), whereas isokinetic muscular strength did not change. There was no difference in the losses of weight, fat mass, or visceral fat and changes in systolic blood pressure (BP) between the intervention groups. However, only CR + EX had a significant decrease in diastolic BP (-5 +/- 3% vs -2 +/- 2% in CR and -1 +/- 2% in CO), in low-density lipoprotein (LDL) cholesterol (-13 +/- 4% vs -6 +/- 3% in CR and 2 +/- 4% in CO), and a significant increase in insulin sensitivity (66 +/- 22% vs 40 +/- 20% in CR and 1 +/- 11% in CO).Despite similar effect on fat losses, combining CR with exercise increased aerobic fitness in parallel with improved insulin sensitivity, LDL cholesterol, and diastolic BP. The results lend support for inclusion of an exercise component in weight loss programs to improve metabolic fitness.

The focus of this review is on current research involving long-term calorie restriction and the resulting changes observed in possible biomarkers of aging. Special emphasis will be given to the basic and clinical science studies which are currently investigating the effects of controlled, high-quality energy-restricted diets on both biomarkers of longevity and on the development of chronic diseases related to age and obesity in humans.Prolonged calorie restriction has been shown to extend both the median and maximal lifespan in a variety of lower species such as yeast, worms, fish, rats, and mice. Mechanisms of this lifespan extension via calorie restriction are not fully elucidated, but possibly involve significant alterations in energy metabolism, oxidative damage, insulin sensitivity, and functional changes in both the neuroendocrine and sympathetic nervous systems. Ongoing studies of prolonged energy restriction in humans are now making it possible to analyze changes in these aging biomarkers to unravel some of the mechanisms of its antiaging phenomenon.With the incremental expansion of research endeavors in the area of energy or calorie restriction, data on the effects of calorie restriction in animal models and humans are becoming more accessible. Detailed analyses from controlled human trials involving long-term calorie restriction will allow investigators to link observed alterations in body composition down to changes in molecular pathways and gene expression, with their possible effects on the biomarkers of aging.

Almost one-quarter of U.S. children are now obese, a dramatic increase of over 20% in the past decade. It is intriguing that the increase in prevalence has been occurring while overall fat consumption has been declining. Body mass and composition are influenced by genetic factors, but the actual heritability of juvenile obesity is not known. A low physical activity (PA) is characteristic of obese children and adolescents, and it may be one cause of juvenile obesity. There is little evidence, however, that overall energy expenditure is low among the obese. There is a strong association between the prevalence of obesity and the extent of TV viewing. Enhanced PA can reduce body fat and blood pressure and improve lipoprotein profile in obese individuals. Its effect on body composition, however, is slower than with low-calorie diets. The three main dietary approaches are: protein sparing modified fast, balanced hypocaloric diets, and comprehensive behavioral lifestyle programs. To achieve long-standing control of overweight, one should combine changes in eating and activity patterns, using behavior modification techniques. However, the onus is also on society to reduce incentives for a sedentary lifestyle and over-consumption of food. To address the key issues related to childhood weight management, the American College of Sports Medicine convened a Scientific Roundtable in Indianapolis.

Context:An important goal during weight loss is to maximize fat loss while preserving metabolically active fat-free mass (FFM). Massive weight loss typically results in substantial loss of FFM potentially slowing metabolic rate.Objective:Our objective was to determine whether a weight loss program consisting of diet restriction and vigorous exercise helped to preserve FFM and maintain resting metabolic rate (RMR).Participants and Intervention:We measured body composition by dual-energy x-ray absorptiometry, RMR by indirect calorimetry, and total energy expenditure by doubly labeled water at baseline (n = 16), wk 6 (n = 11), and wk 30 (n = 16).Results:At baseline, participants were severely obese (×± sd; body mass index 49.4 ± 9.4 kg/m2) with 49 ± 5% body fat. At wk 30, more than one third of initial body weight was lost (−38 ± 9%) and consisted of 17 ± 8% from FFM and 83 ± 8% from fat. RMR declined out of proportion to the decrease in body mass, demonstrating a substantial metabolic adaptation (−244 ± 231 and −504 ± 171 kcal/d at wk 6 and 30, respectively, P < 0.01). Energy expenditure attributed to physical activity increased by 10.2 ± 5.1 kcal/kg·d at wk 6 and 6.0 ± 4.1 kcal/kg·d at wk 30 (P < 0.001 vs. zero).Conclusions:Despite relative preservation of FFM, exercise did not prevent dramatic slowing of resting metabolism out of proportion to weight loss. This metabolic adaptation may persist during weight maintenance and predispose to weight regain unless high levels of physical activity or caloric restriction are maintained.

The 24-h energy expenditure (24-h EE), resting EE (REE), sleeping EE (SEE), and spontaneous physical activity (SPA) were compared between six male endurance athletes whose reported energy intake was low (LOW) and did not match that theoretically required for weight maintenance and four whose reported energy intake appeared adequate (ADQ) and matched their estimated EE. Groups did not differ in age, body weight, fat-free mass, and daily EE estimated from activity records. The LOW athletes reported an energy intake 6338 +/- 2164 kJ.d-1 less than estimated EE. The 24-h EE, REE, SEE, and SPA of the LOW athletes were significantly lower than the ADQ athletes (862, 523, 770 kJ.d-1, and 43 min.d-1, respectively). Using all subjects, there was a significant positive correlation between REE and free thyroxine (FT4) (r = 0.82) and SEE and FT4 (r = 0.66). Thus, part of the LOW athlete's ability to maintain body weight on a seemingly low energy intake appears due to a lower daily sedentary EE.