A diet-induced negative energy balance triggers compensatory mechanisms, e.g., lower metabolic rate and increased appetite. However, knowledge about potential compensatory mechanisms triggered by increased aerobic exercise is limited. A randomized controlled trial was performed in healthy, sedentary, moderately overweight young men to examine the effects of increasing doses of aerobic exercise on body composition, accumulated energy balance, and the degree of compensation. Eighteen participants were randomized to a continuous sedentary control group, 21 to a moderate-exercise (MOD; 300 kcal/day), and 22 to a high-exercise (HIGH; 600 kcal/day) group for 13 wk, corresponding to ϳ30 and 60 min of daily aerobic exercise, respectively. Body weight (MOD: Ϫ3.6 kg, P Ͻ 0.001; HIGH: Ϫ2.7 kg, P ϭ 0.01) and fat mass (MOD: Ϫ4.0 kg, P Ͻ 0.001 and HIGH: Ϫ3.8 kg, P Ͻ 0.001) decreased similarly in both exercise groups. Although the exercise-induced energy expenditure in HIGH was twice that of MOD, the resulting accumulated energy balance, calculated from changes in body composition, was not different (MOD: Ϫ39.6 Mcal, HIGH: Ϫ34.3 Mcal, not significant). Energy balance was 83% more negative than expected in MOD, while it was 20% less negative than expected in HIGH. No statistically significant changes were found in energy intake or nonexercise physical activity that could explain the different compensatory responses associated with 30 vs. 60 min of daily aerobic exercise. In conclusion, a similar body fat loss was obtained regardless of exercise dose. A moderate dose of exercise induced a markedly greater than expected negative energy balance, while a higher dose induced a small but quantifiable degree of compensation.exercise; body weight regulation; compensatory mechanisms; energy balance ALTHOUGH A MODERN SEDENTARY lifestyle along with overeating has been put forward as "Big Two" factors in the etiology of obesity (3,10,29), the outcomes of structured exercise programs designed to promote weight loss are often modest (42,58). This has led to the general (mis)conception that exercise, in itself, is a poor weight management strategy (20,42,49). Apart from a potential lack of compliance, the discrepancy between predicted and observed weight loss is likely due to a combination of physiological and behavioral compensatory changes affecting energy balance. These compensatory changes cause the accumulated energy balance during an exercise intervention to be less negative than would be theoretically predicted from the exercise-induced energy expenditure (ExEE), i.e., the total amount of energy expenditure that is caused by the exercise intervention (12,32,34).Body energy stores are protected against long-term negative energy balance resulting from caloric restriction by a greater than predicted reduction in resting energy expenditure (REE) (28), a decrease in nonexercise activity thermogenesis (NEAT) (40,45), an increase in the metabolic efficiency of physical activity (16,35), and an increase in hedonic (21) and hormonal mediators o...

Emerging literature highlights the need to incorporate physical activity into every strategy intended to prevent weight gain as well as to maintain weight loss over time. Furthermore, physical activity should be part of any plan to lose weight. The stimulus of exercise provides valuable metabolic adaptations that improve energy and macronutrient balance regulation. A tight coupling between energy intake and energy expenditure has been documented at high levels of physical exercise, suggesting that exercise may improve appetite control. The regular practice of physical activity has also been reported to reduce the risk of stress-induced weight gain. A more personalized approach is recommended when planning exercise programs in a clinical weight loss setting in order to limit the compensatory changes associated to exercise-induced weight loss. With modern environment promoting overeating and sedentary behavior, there is an urgent need for a concerted action including legislative measures to promote healthy active living in order to curb the current epidemic of chronic diseases.

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(7), but in contrast to these previous studies, apart from including younger and only moderately overweight men, our exercise training program included bouts of high intensity exercise. We hypothesized that endurance training, also without a concomitant weight loss, would increase metabolic health. Methods and Procedures ParticipantsVolunteers were recruited through advertising in newspapers and on the internet. Inclusion criteria were male sex, age 20-40 years, BMI 25-30 kg/m 2

Objective: To elucidate if fat oxidation at rest predicts peak fat oxidation during exercise and/or metabolic phenotype in moderately overweight, sedentary men. Design: Cross-sectional study. Subjects: We measured respiratory exchange ratio (RER) at rest in 44 moderately overweight, normotensive and normoglycemic men and selected 8 subjects with a low RER (L-RER, body mass index (BMI): 27.9±0.9 kg m À2 , RER: 0.76±0.02) and 8 with a high RER (H-RER; BMI 28.1 ± 1.1 kg m À2 , RER: 0.89 ± 0.02). After an overnight fast, a venous blood sample was obtained and a graded exercise test was performed. Fat oxidation during exercise was quantified using indirect calorimetry. Results: Peak fat oxidation during exercise was higher in L-RER than in H-RER (0.333 ± 0.096 vs 0.169 ± 0.028 g min À1 ; Po0.01) and occurred at a higher relative intensity (36.2±6.6 vs 28.2±3.1% VO 2max , Po0.05). Using the International Diabetes Federation criteria, we found that there was a lower accumulation of metabolic risk factors in L-RER than in H-RER (1.6 vs 3.5, P ¼ 0.028), and no subjects in L-RER and four of eight subjects in H-RER had the metabolic syndrome. Resting RER was positively correlated with plasma triglycerides (Po0.01) and negatively with plasma free fatty acids (Po0.05), and peak fat oxidation during exercise was positively correlated with plasma free fatty acid concentration at rest (Po0.05). Conclusion: A low RER at rest predicts a high peak fat oxidation during exercise and a healthy metabolic phenotype in moderately overweight, sedentary men.

ObjectivesTo evaluate effects of active bike commuting or leisure-time exercise of two intensities on peripheral insulin sensitivity (primary outcome), cardiorespiratory fitness and intra-abdominal adipose tissue mass (secondary outcomes).Methods188 physically inactive, healthy women and men (20-45 years) with overweight or class 1 obesity were recruited. In the 6-month trial, 130 participants were randomised to either: no intervention (CON), active commuting (BIKE) or leisure-time exercise of moderate (MOD, 50% VO2peak) or vigorous (VIG, 70% VO2peak) intensity. 100 completed follow-up testing. Exercise prescription was 5 days/week with a weekly exercise energy expenditure of 1600 kcal for women and 2100 kcal for men. Testing was performed at baseline, 3 months and 6 months.ResultsPeripheral insulin sensitivity (ml/min/pmol insulin/L) increased (improved) by 24% (95% CI 6% to 46%, p=0.01) in VIG compared with CON at 3 months. Peripheral insulin sensitivity increased (improved) by 20% in BIKE (95% CI 1% to 43%, p=0.04) and 26% in VIG (95% CI 7% to 47%, p<0.01) compared with CON at 6 months. Cardiorespiratory fitness increased in all exercise groups compared with CON at 6 months; but the increase was higher in those that undertook vigorous exercise than those who did moderate exercise. Intra-abdominal adipose tissue mass diminished across all exercise groups in comparison to CON at 6 months.ConclusionsActive bike commuting improved cardiometabolic health; as did leisure-time exercise. Leisure-time exercise of vigorous intensity conferred more rapid effects on peripheral insulin sensitivity as well as additional effects on cardiorespiratory fitness than did moderate intensity exercise.Trial registrationNCT01962259

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A meaningful fat loss was obtained by 6 months of active commuting and leisure-time exercise, but fat loss was greater with vigorous compared with moderate intensity exercise. Active commuting is an alternative to leisure-time exercise in the management of overweight and obesity. The trial was registered at clinicaltrials.gov as NCT01962259 (main trial) and NCT01973686 (energy metabolism sub-study).