James A. Levine

Energy expenditure of sedentary screen time compared with active screen time for children.

OBJECTIVE. We examined the effect of activity-enhancing screen devices on childrens energy expenditure compared with performing the same activities while seated. Our hypothesis was that energy expenditure would be significantly greater when children played activity-promoting video games, compared with sedentary video games. METHODS. Energy expenditure was measured for 25 children aged 8 to 12 years, 15 of whom were lean, while they were watching television seated, playing a traditional video game seated, watching television while walking on a treadmill at 1.5 miles per hour, and playing activity-promoting video games. RESULTS. Watching television and playing video games while seated increased energy expenditure by 20 ± 13% and 22 ± 12% above resting values, respectively. When subjects were walking on the treadmill and watching television, energy expenditure increased by 138 ± 40% over resting values. For the activity-promoting video games, energy expenditure increased by 108 ± 40% with the EyeToy (Sony Computer Entertainment) and by 172 ± 68% with Dance Dance Revolution Ultramix 2 (Konami Digital Entertainment). CONCLUSIONS. Energy expenditure more than doubles when sedentary screen time is converted to active screen time. Such interventions might be considered for obesity prevention and treatment.

Measurement of energy expenditure.

Measurement of energy expenditure in humans is required to assess metabolic needs, fuel utilisation, and the relative thermic effect of different food, drink, drug and emotional components. Indirect and direct calorimetric and non-calorimetric methods for measuring energy expenditure are reviewed, and their relative value for measurement in the laboratory and field settings is assessed. Where high accuracy is required and sufficient resources are available, an open-circuit indirect calorimeter can be used. Open-circuit indirect calorimeters can employ a mask, hood, canopy or room/chamber for collection of expired air. For short-term measurements, mask, hood or canopy systems suffice. Chamber-based systems are more accurate for the long-term measurement of specified activity patterns but behaviour constraints mean they do not reflect real life. Where resources are limited and/or optimum precision can be sacrificed, flexible total collection systems and non-calorimetric methods are potentially useful if the limitations of these methods are appreciated. The use of the stable isotope technique, doubly labelled water, enables total daily energy expenditure to be measured accurately in free-living subjects. The factorial method for combining activity logs and data on the energy costs of activities can also provide detailed information on free-living subjects.

Activity-promoting video games and increased energy expenditure.

OBJECTIVES To test the hypothesis that both children and adults would expend more calories and move more while playing activity-promoting video games compared with sedentary video games. STUDY DESIGN In this single-group study, 22 healthy children (12 +/- 2 years; 11 male, 11 female) and 20 adults (34 +/- 11 years; 10 male, 10 female) were recruited. Energy expenditure and physical activity were measured while participants were resting, standing, watching television seated, sitting and playing a traditional sedentary video game, and while playing an activity-promoting video game (Nintendo Wii Boxing). Physical activity was measured with accelerometers, and energy expenditure was measured with an indirect calorimeter. RESULTS Energy expenditure was significantly greater than all other activities when children or adults played Nintendo Wii (mean increase over resting, 189 +/- 63 kcal/hr, P < .001, and 148 +/- 71 kcal/hr, P < .001, respectively). When examining movement with accelerometry, children moved significantly more than adults (55 +/- 5 arbitrary acceleration units and 23 +/- 2 arbitrary acceleration units, respectively, P < .001) while playing Nintendo Wii. CONCLUSION Activity-promoting video games have the potential to increase movement and energy expenditure in children and adults.

Non-Exercise Activity Thermogenesis. The Crouching Tiger Hidden Dragon of Societal Weight Gain

Non-exercise activity thermogenesis (NEAT) is the energy expenditure of all physical activities other than volitional sporting-like exercise. NEAT includes all the activities that render us vibrant, unique, and independent beings such as working, playing, and dancing. Because people of the same weight have markedly variable activity levels, it is not surprising that NEAT varies substantially between people by up to 2000 kcal per day. Evidence suggests that low NEAT may occur in obesity but in a very specific fashion. Obese individuals appear to exhibit an innate tendency to be seated for 2.5 hours per day more than sedentary lean counterparts. If obese individuals were to adopt the lean “NEAT-o-type,” they could potentially expend an additional 350 kcal per day. Obesity was rare a century ago and the human genotype has not changed over that time. Thus, the obesity epidemic may reflect the emergence of a chair-enticing environment to which those with an innate tendency to sit, did so, and became obese. To reverse obesity, we need to develop individual strategies to promote standing and ambulating time by 2.5 hours per day and also re-engineer our work, school, and home environments to render active living the option of choice.

The energy expenditure of using a "walk-and-work" desk for office workers with obesity

Objective: For many people, most of the working day is spent sitting in front of a computer screen. Approaches for obesity treatment and prevention are being sought to increase workplace physical activity because low levels of physical activity are associated with obesity. Our hypothesis was that a vertical workstation that allows an obese individual to work while walking would be associated with significant and substantial increases in energy expenditure over seated work. Methods: The vertical workstation is a workstation that allows an office worker to use a standard personal computer while walking on a treadmill at a self-selected velocity. 15 sedentary individuals with obesity (14 women, one man; 43 (7.5) years, 86 (9.6) kg; body mass index 32 (2.6) kg/m2) underwent measurements of energy expenditure at rest, seated working in an office chair, standing and while walking at a self-selected speed using the vertical workstation. Body composition was measured using dual x ray absorptiometry. Results: The mean (SD) energy expenditure while seated at work in an office chair was 72 (10) kcal/h, whereas the energy expenditure while walking and working at a self-selected velocity of 1.1 (0.4) mph was 191 (29) kcal/h. The mean (SD) increase in energy expenditure for walking-and-working over sitting was 119 (25) kcal/h. Conclusions: If sitting computer-time were replaced by walking-and-working, energy expenditure could increase by 100 kcal/h. Thus, if obese individuals were to replace time spent sitting at the computer with walking computer time by 2–3 h/day, and if other components of energy balance were constant, a weight loss of 20–30 kg/year could occur.

Variability in energy expenditure and its components

Purpose of reviewTo review factors contributing to variation in total daily energy expenditure and its primary components: (1) resting metabolic rate; (2) diet-induced thermogenesis; and (3) activity thermogenesis, including exercise energy expenditure and nonexercise activity. For each component, the expected magnitude of intra-individual variability is also considered. We also reviewed studies that quantified the variability in 24 h energy expenditure. Recent findingsIn humans, the coefficient of variation in the components of total daily energy expenditure is around 5-8% for resting metabolic rate, 1-2% for exercise energy expenditure, and around 20% for diet-induced thermogenesis. The coefficient of variance for 24 h energy expenditure measured using a room calorimeter for resting metabolic rate is around 5-10%. Thus, these measures are all rather reproducible. Total daily energy expenditure varies several-fold in humans, not due to variation in resting metabolic rate, diet-induced thermogenesis, or exercise thermogenesis, but rather, due to variations in nonexercise activity. A variety of factors impact nonexercise activity, including occupation, environment, education, genetics, age, gender, and body composition, but little is known about the magnitude of effect. SummaryResting metabolic rate, diet-induced thermogenesis, exercise energy expenditure, and 24 h energy expenditure are highly reproducible. Coefficient of variation is smallest for exercise energy expenditure, followed by resting metabolic rate, 24 h energy expenditure, and diet-induced thermogenesis. There is considerable variability in total daily energy expenditure, largely due to variations in nonexercise activity. Although the factors that impact upon nonexercise activity are understood, their contribution to variation in total daily energy expenditure is unclear.

Deleted in breast cancer-1 regulates SIRT1 activity and contributes to high-fat diet-induced liver steatosis in mice.

The enzyme sirtuin 1 (SIRT1) is a critical regulator of many cellular functions, including energy metabolism. However, the precise mechanisms that modulate SIRT1 activity remain unknown. As SIRT1 activity in vitro was recently found to be negatively regulated by interaction with the deleted in breast cancer-1 (DBC1) protein, we set out to investigate whether DBC1 regulates SIRT1 activity in vivo. We found that DBC1 and SIRT1 colocalized and interacted, and that DBC1 modulated SIRT1 activity, in multiple cell lines and tissues. In mouse liver, increased SIRT1 activity, concomitant with decreased DBC1-SIRT1 interaction, was detected after 24 hours of starvation, whereas decreased SIRT1 activity and increased interaction with DBC1 was observed with high-fat diet (HFD) feeding. Consistent with the hypothesis that DBC1 is crucial for HFD-induced inhibition of SIRT1 and for the development of experimental liver steatosis, genetic deletion of Dbc1 in mice led to increased SIRT1 activity in several tissues, including liver. Furthermore, DBC1-deficient mice were protected from HFD-induced liver steatosis and inflammation, despite the development of obesity. These observations define what we believe to be a new role for DBC1 as an in vivo regulator of SIRT1 activity and liver steatosis. We therefore propose that the DBC1-SIRT1 interaction may serve as a new target for therapies aimed at nonalcoholic liver steatosis.

Isosorbide mononitrate in heart failure with preserved ejection fraction

BACKGROUND Nitrates are commonly prescribed to enhance activity tolerance in patients with heart failure and a preserved ejection fraction. We compared the effect of isosorbide mononitrate or placebo on daily activity in such patients. METHODS In this multicenter, double-blind, crossover study, 110 patients with heart failure and a preserved ejection fraction were randomly assigned to a 6-week dose-escalation regimen of isosorbide mononitrate (from 30 mg to 60 mg to 120 mg once daily) or placebo, with subsequent crossover to the other group for 6 weeks. The primary end point was the daily activity level, quantified as the average daily accelerometer units during the 120-mg phase, as assessed by patient-worn accelerometers. Secondary end points included hours of activity per day during the 120-mg phase, daily accelerometer units during all three dose regimens, quality-of-life scores, 6-minute walk distance, and levels of N-terminal pro-brain natriuretic peptide (NT-proBNP). RESULTS In the group receiving the 120-mg dose of isosorbide mononitrate, as compared with the placebo group, there was a nonsignificant trend toward lower daily activity (-381 accelerometer units; 95% confidence interval [CI], -780 to 17; P=0.06) and a significant decrease in hours of activity per day (-0.30 hours; 95% CI, -0.55 to -0.05; P=0.02). During all dose regimens, activity in the isosorbide mononitrate group was lower than that in the placebo group (-439 accelerometer units; 95% CI, -792 to -86; P=0.02). Activity levels decreased progressively and significantly with increased doses of isosorbide mononitrate (but not placebo). There were no significant between-group differences in the 6-minute walk distance, quality-of-life scores, or NT-proBNP levels. CONCLUSIONS Patients with heart failure and a preserved ejection fraction who received isosorbide mononitrate were less active and did not have better quality of life or submaximal exercise capacity than did patients who received placebo. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT02053493.).

Feeding and activity induced by orexin A in the lateral hypothalamus in rats.

Orexin A injected into the lateral hypothalamus (LH) stimulates feeding and activates neurons in brain sites regulating feeding and arousal. The feeding effects of orexin A have been demonstrated during the light cycle, a time when rats are normally resting, and the effect of orexin A on activity after injection into the LH has not been previously measured. Thus, it is unclear whether LH orexin A-induced feeding is secondary to enhanced arousal. To address this, LH-cannulated rats habituated to a running wheel were injected with either orexin A (1000 pmol) or vehicle during light and dark cycles. Food intake and running wheel rotations were measured for 2 h. Spontaneous physical activity (SPA) was also measured during the dark cycle. During the light cycle, orexin A in the LH stimulated feeding in the presence and absence of a running wheel and increased number of running wheel rotations in the presence and absence of food. During the dark cycle, orexin A in the LH induced SPA (+/- presence of food), but had no effect on feeding. These data show that LH orexin A stimulation of feeding is not always coincident with increased activity, suggesting that feeding induced by LH-injected orexin A is not consequent to enhanced arousal.

ADIPOCYTE MACROPHAGE COLONY-STIMULATING FACTOR IS A MEDIATOR OF ADIPOSE TISSUE GROWTH

Adipose tissue growth results from de novo adipocyte recruitment (hyperplasia) and increased size of preexisting adipocytes. Adipocyte hyperplasia accounts for the severalfold increase in adipose tissue mass that occurs throughout life, yet the mechanism of adipocyte hyperplasia is unknown. We studied the potential of macrophage colony-stimulating factor (MCSF) to mediate adipocyte hyperplasia because of the profound effects MCSF exerts on pluripotent cell recruitment and differentiation in other tissues. We found that MCSF mRNA and protein were expressed by human adipocytes and that adipocyte MCSF expression was upregulated in rapidly growing adipose tissue that encircled acutely inflamed bowel and in adipose tissue from humans gaining weight (4-7 kg) with overfeeding. Localized overexpression of adipocyte MCSF was then induced in rabbit subcutaneous adipose tissue in vivo using adenoviral-mediated gene transfer. Successful overexpression of MCSF was associated with 16-fold increases in adipose tissue growth compared with a control adenovirus expressing beta-galactosidase. This occurred in the absence of increased cell size and in the presence of increased nuclear staining for MIB-1, a marker of proliferation. We conclude that MCSF participates in adipocyte hyperplasia and the physiological regulation of adipose tissue growth.