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Background: Active video games (AVGs) have been shown to acutely increase energy expenditure when compared with seated video games; however, the influence of AVGs on compensatory adjustments in energy intake and expenditure is largely unknown., Objective: The aim was to examine the acute effects of AVGs on energy intake and expenditure., Design: With the use of a randomized crossover design, 26 male adolescents (mean ± SD age: 14.5 ± 1.4 y) completed three 1-h experimental conditions: resting control, seated video game play (Xbox 360; Microsoft), and AVG play (Kinect Adventures on Xbox 360) followed by an ad libitum lunch. A validated food menu was used to assess food intake immediately after the conditions and for the remainder of the day, and a dietary record was used for the subsequent 3-d period. Energy expenditure was measured by using portable indirect calorimetry throughout each experimental condition, and an accelerometer was used to assess the subsequent 3-d period. Appetite sensations were assessed by using visual analog scales at different time points during the testing day. The primary outcomes were acute (immediately after the conditions and 24-h) and short-term (3-d) energy intake and expenditure., Results: Energy expenditure was significantly higher (~145%; P < 0.001) during the AVG condition than during the resting control and seated video game conditions; however, no significant differences in energy expenditure were observed 24 h (~6%; P > 0.49) and 3 d after the experimental conditions (~3%; P > 0.82). No significant differences were observed in absolute energy intake immediately after the conditions (~2%; P > 0.94) or in absolute energy intake 24 h (~5%; P > 0.63) and 3 d (~9%; P > 0.53) after the experimental conditions. Finally, appetite sensations were similar between conditions at all time points (P > 0.05)., Conclusions: The increase in energy expenditure promoted by a single session of Kinect AVG play is not associated with increased food intake but is compensated for after the intervention, resulting in no measurable change in energy balance after 24 h. These results suggest that the potential of Kinect to reduce the energy gap underlying weight gain is offset within 24 h in male adolescents. This trial was registered at clinicaltrials.gov as NCT01655901., (© 2015 American Society for Nutrition.)

Background: A short sleep (SS) duration has been linked to obesity in observational studies. However, experimental evidence of the potential mechanisms of sleep restriction on energy balance is conflicting and, to our knowledge, nonexistent in adolescents., Objective: We investigated the effects of 3 consecutive nights of partial sleep deprivation on components of energy balance., Design: In a randomized, crossover design, 21 healthy, normal-weight male adolescents (mean ± SD age: 16.8 ± 1.3 y) completed the following 2 experimental conditions, each for 3 consecutive nights: an SS (4 h/night) and a long sleep (LS; 9 h/night) duration. Endpoints were 24-h energy expenditure (EE), spontaneous physical activity (SPA), postintervention diet-induced thermogenesis (DIT), appetite sensations, ad libitum energy intake (EI), and profiles of plasma ghrelin and leptin., Results: The 24-h EE on day 3 was 370 ± 496 kJ higher in the SS condition than in the LS condition (P = 0.003). This difference in EE was explained by prolonged wakefulness in the SS condition and a 19% higher SPA (P = 0.003). In a postintervention breakfast-meal challenge, there was a 0.19-kJ/min smaller incremental AUC in DIT over 4 h in the SS condition than in the LS condition (P = 0.012) with no time × condition effect (P = 0.29). Subjects consumed 13% less energy in the ad libitum meal in the SS condition (P = 0.031), with a concomitant decreased motivation to eat. Concentrations of ghrelin and leptin remained unchanged with sleep restriction., Conclusion: Short-term sleep restriction in male adolescents is associated with a small negative energy balance driven by increased EE from prolonged wakefulness and a concomitant decreased EI and motivation to eat. This trial was registered at clinicaltrials.gov as NCT01198431.

Background: Video game playing has been linked to obesity in many observational studies. However, the influence of this sedentary activity on food intake is unknown., Objective: The objective was to examine the acute effects of sedentary video game play on various components of energy balance., Design: With the use of a randomized crossover design, 22 healthy, normal-weight, male adolescents (mean ± SD age: 16.7 ± 1.1 y) completed two 1-h experimental conditions, namely video game play and rest in a sitting position, followed by an ad libitum lunch. The endpoints were spontaneous food intake, energy expenditure, stress markers, appetite sensations, and profiles of appetite-related hormones., Results: Heart rate, systolic and diastolic blood pressures, sympathetic tone, and mental workload were significantly higher during the video game play condition than during the resting condition (P < 0.05). Although energy expenditure was significantly higher during video game play than during rest (mean increase over resting: 89 kJ; P < 0.01), ad libitum energy intake after video game play exceeded that measured after rest by 335 kJ (P < 0.05). A daily energy surplus of 682 kJ (163 kcal) over resting (P < 0.01) was observed in the video game play condition. The increase in food intake associated with video game play was observed without increased sensations of hunger and was not compensated for during the rest of the day. Finally, the profiles of glucose, insulin, cortisol, and ghrelin did not suggest an up-regulation of appetite during the video game play condition., Conclusion: A single session of video game play in healthy male adolescents is associated with an increased food intake, regardless of appetite sensations. The trial was registered at clinicaltrials.gov as NCT01013246.

Background: Clinical trials of low-fat diets characteristically produce small mean long-term weight loss but a large interindividual variation in response. This variation has been attributed to psychological and behavioral factors, although biological differences may also play a role., Objective: The objective was to determine whether physiologic differences in insulin secretion explain differences in weight gain among individuals consuming low- and high-fat diets., Design: Of 276 individuals followed in the Quebec Family Study for a mean of 6 y, we compared those in the lowest with those in the highest dietary fat tertiles. We performed oral-glucose-tolerance tests at baseline and examined the insulin concentration at 30 min (insulin-30) as a proxy measure of insulin secretion. Six-year changes in body weight and waist circumference were the primary endpoints. We determined the associations between insulin-30 and the primary endpoints by linear regression analysis, with adjustment for potentially confounding factors., Results: Mean changes in body weight and waist circumference did not differ significantly between the lowest- and highest-fat diet groups. However, these endpoints were strongly associated with insulin-30, especially among individuals consuming the lowest-fat diet. Insulin-30 at baseline was significantly associated with 6-y weight gain (r = 0.51, P < 0.0001) and change in waist circumference (r = 0.55, P < 0.0001) in the lowest diet fat, group [corrected], but not in the highest diet fat group (r = 0.18, P = 0.086 and r = 0.20, P = 0.058, respectively) [corrected] Individuals in the highest insulin-30 and lowest dietary fat group gained 1.8 kg more than did those in the highest insulin-30 and highest dietary fat group (51%; P = 0.034); they gained 4.5 kg more than did those in the lowest insulin-30 and lowest dietary fat group (6.5-fold; P = 0.0026)., Conclusion: A proxy measure of insulin secretion strongly predicts changes in body weight and waist circumference over 6 y in adults, especially among those consuming lower-fat diets, which demonstrates the existence of a novel diet-phenotype interaction.