Compensatory Increase In Energy Intake Research Articles

Altered motivation states for physical activity and 'appetite' for movement as compensatory mechanisms limiting the efficacy of exercise training for weight loss.

Weight loss is a major motive for engaging in exercise, despite substantial evidence that exercise training results in compensatory responses that inhibit significant weight loss. According to the Laws of Thermodynamics and the CICO (Calories in, Calories out) model, increased exercise-induced energy expenditure (EE), in the absence of any compensatory increase in energy intake, should result in an energy deficit leading to reductions of body mass. However, the expected negative energy balance is met with both volitional and non-volitional (metabolic and behavioral) compensatory responses. A commonly reported compensatory response to exercise is increased food intake (i.e., Calories in) due to increased hunger, increased desire for certain foods, and/or changes in health beliefs. On the other side of the CICO model, exercise training can instigate compensatory reductions in EE that resist the maintenance of an energy deficit. This may be due to decreases in non-exercise activity thermogenesis (NEAT), increases in sedentary behavior, or alterations in sleep. Related to this EE compensation, the motivational states associated with the desire to be active tend to be overlooked when considering compensatory changes in non-exercise activity. For example, exercise-induced alterations in the wanting of physical activity could be a mechanism promoting compensatory reductions in EE. Thus, one's desires, urges or cravings for movement-also known as "motivation states" or "appetence for activity"-are thought to be proximal instigators of movement. Motivation states for activity may be influenced by genetic, metabolic, and psychological drives for activity (and inactivity), and such states are susceptible to fatigue-or reward-induced responses, which may account for reductions in NEAT in response to exercise training. Further, although the current data are limited, recent investigations have demonstrated that motivation states for physical activity are dampened by exercise and increase after periods of sedentarism. Collectively, this evidence points to additional compensatory mechanisms, associated with motivational states, by which impositions in exercise-induced changes in energy balance may be met with resistance, thus resulting in attenuated weight loss.

Performance nutrition for cold-weather military operations

ABSTRACT .High daily energy expenditure without compensatory increases in energy intake results in severe energy deficits during cold-weather military operations. The severity of energy deficits has been proportionally linked to declines in body mass, negative protein balance, suppression of androgen hormones, increases in systemic inflammation and degraded physical performance. Food availability does not appear to be the predominant factor causing energy deficits; providing additional rations or supplement snack bars does not reduce the severity of the energy deficits. Nutrition interventions that allow greater energy intake could be effective for reducing energy deficits during cold-weather military operations. One potential intervention is to increase energy density (i.e. energy per unit mass of food) by increasing dietary fat. Our laboratory recently reported that self-selected higher energy intakes and reductions in energy deficits were primarily driven by fat intake (r = 0.891, r2 = 0.475), which, of the three macronutrients. Further, soldiers who ate more fat lost less body mass, had lower inflammation, and maintained net protein balance compared to those who ate less fat. These data suggest that consuming high-fat energy-dense foods may be a viable nutritional intervention that mitigates the negative physiological effects of energy deficit and sustains physical performance during cold-weather military operations.

Topical application of the pharmacological cold mimetic menthol stimulates brown adipose tissue thermogenesis through a TRPM8, UCP1, and norepinephrine dependent mechanism in mice housed at thermoneutrality

Increasing whole-body energy expenditure via the pharmacological activation of uncoupling protein 1 (UCP1)-dependent brown adipose tissue (BAT) thermogenesis is a promising weight management strategy, yet most therapeutics studied in rodents to date either induce compensatory increases in energy intake, have thermogenic effects that are confounded by sub-thermoneutral housing temperatures or are not well tolerated in humans. Here, we sought to determine whether the non-invasive topical application of the pharmacological cold mimetic and transient receptor potential (TRP) cation channel subfamily M member 8 (TRPM8) agonist L-menthol (MNTH), could be used to stimulate BAT thermogenesis and attenuate weight gain in mice housed at thermoneutrality. Using three different strains of mice and multiple complimentary approaches to quantify thermogenesis in vivo, coupled with ex vivo models to quantify direct thermogenic effects, we were able to convincingly demonstrate the following: (1) acute topical MNTH application induces BAT thermogenesis in a TRPM8- and UCP1-dependent manner; (2) MNTH-induced BAT thermogenesis is sufficient to attenuate weight gain over time without affecting energy intake in lean and obese mice; (3) the ability of topical MNTH application to stimulate BAT thermogenesis is mediated, in part, by a central mechanism involving the release of norepinephrine. These data collectively suggest that topical application of MNTH may be a promising weight management strategy.

Ectoparasites reduce scope for growth in a rocky-shore mussel (Perna perna) by raising maintenance costs

Endolithic cyanobacteria are ubiquitous colonisers of organic and inorganic carbonate substrata that frequently attack the shells of mussels, eroding the shell to extract carbon, often with population infestation rates of >80%. This reduces host physiological condition and ultimately leads to shell collapse and mortality, compromising the services provided by these important ecosystem engineers. While the ecological implications of this and similar interactions have been examined, our understanding of the underlying mechanisms driving the physiological responses of infested hosts remains limited. Using field and laboratory experiments, we assessed the energetic costs of cyanobacterial infestation to the intertidal brown mussel (Perna perna). In the field we found that growth (measured as both increase in shell length and rate of biomineralization) and reproductive potential of clean mussels are greater than those of infested individuals. To explore the mechanisms behind these effects, we compared the energy allocation of parasite-free and infested mussels using the scope for growth (SFG) framework. This revealed a lower SFG in parasitized mussels attributed to an energetic imbalance caused by increased standard metabolic rates, without compensation through increased feeding or reduced excretion of ammonia. Separate laboratory assays showed no differences in calcium uptake rates, indicating that infested mussels do not compensate for shell erosion through increased mineralization. This suggests that the increased maintenance costs detected reflect repair of the organic component of the inner nacreous layer of the shell, an energetically more demanding process than mineralization. Thus, parasite-inflicted damage reduces SFG directly through the need for increased basal metabolic rate to drive shell repair without compensatory increases in energy intake. This study provides a first perspective of the physiological mechanisms underlying this parasite-host interaction, a critical step towards a comprehensive understanding of the ecological processes driving dynamics of this intertidal ecosystem engineer.

Association of Exercise with Control of Eating and Energy Intake

This narrative review examines the association of acute and chronic exercise with control of eating and energy intake, which could provide important insights for interventions targeting weight loss and weight management. Despite considerable variability in study results, acute exercise is generally associated with a decline in appetite. This effect, however, is short-lived, and changes in 24-h energy intake in response to exercise have been limited. Chronic exercise may induce some compensatory increase in energy intake due to an increase in hunger. Nevertheless, higher activity levels have been associated with a better regulation of energy intake. The better coupling of energy intake and energy expenditure with exercise indicates beneficial effects of exercise in weight management. In order to enhance the efficacy of exercise-based strategies targeting weight loss, additional research—particularly on differential effects of various exercise modes and individual traits that characterize participants at increased risk for compensatory energy intake—is warranted.

Structured, aerobic exercise reduces fat mass and is partially compensated through energy intake but not energy expenditure in women

BackgroundExercise-induced weight loss is often less than expected and highly variable in men and women. Behavioural compensation for the exercise-induced energy deficit could be through energy intake (EI), non-exercise physical activity (NEPA) or sedentary behaviour (SB). We investigated this issue in women. MethodsTwenty-four overweight [body mass index (BMI) M = 27.9 kg/m2, SD = 2.7] women [age M = 33.1 years, SD = 11.7] completed 12-weeks of supervised exercise (5×500kcal per week) in a non-randomised, pre-post intervention study. Body mass (BM), waist circumference (WC), body composition, resting metabolic rate (RMR), total daily EI, individual meals, appetite sensations and appetite-related peptides were measured at baseline (week 0) and post-intervention (week 12). Free-living physical activity (PA) and SB were measured (SenseWear) at baseline, week 1 and 10 of the exercise intervention, and at post-intervention (week 13). ResultsFollowing the 12-week exercise intervention BM [p = .04], BMI [p = .035], WC [p < .001] and fat mass (FM) [p = .003] were significantly reduced, and fat-free mass (FFM) significantly increased [p = .003]. Total [p = .028], ad libitum [p = .03] and snack box EI [p = .048] were significantly increased and this was accompanied by an increase in hunger [p = .01] and a decrease in fullness [p = .03] before meals. The peptides did not explain changes in appetite [p > .05]. There was no compensatory reduction in NEPA [p > .05] and no increase in SB, rather there was a decrease in SB during the exercise intervention [p = .03]. ConclusionsTwelve-weeks of supervised aerobic exercise resulted in a significant reduction in FM and an increase in FFM. Exercise increased hunger and EI which only partially compensated for the increase in energy expenditure. There was no evidence for a compensatory reduction in NEPA or an increase in SB. Dietary intervention, as an adjunct to exercise, may offset the compensatory increase in EI and result in a greater reduction in BM. Trial registrationOur trial was retrospectively registered on the International Standard Randomised Controlled Trials Registry (ISRCTN78021668, 27th September 2016) and can be found here: https://doi.org/10.1186/ISRCTN78021668

Diet-Quality and Socio-Demographic Factors Associated with Non-Nutritive Sweetener Use in the Australian Population.

Non-nutritive sweeteners (NNS) are used in the food supply to replace sugar and/or to reduce dietary energy intake. The aim of this research was to assess the consumption prevalence and food sources of NNS in the Australian population. Food group and nutrient intakes were assessed to compare diet quality of NNS consumers and non-consumers. Secondary analysis of the Australian National Nutrition and Physical Activity Survey, 2011/12 was conducted (n = 12,435) after identifying all NNS products consumed in the population. The proportion of participants that reported intake of NNS per day was 18.2% for adults (19+ years), and 8.5% for children (2–18 years), with the most common food sources being carbonated soft drinks, tabletop sweeteners, and yoghurt. Characteristics associated with NNS consumption in adults included being female, higher body mass index (BMI), self-reported diabetes status, and being on a weight-loss diet. For adults, NNS consumers had lower free sugar intake but energy intake did not differ from non-consumers. However, for children, no differences in free sugar or energy intake were observed between consumers and non-consumers. While these results support the use of NNS in reducing sugar intake, these data suggest compensatory increases in energy intake may occur.

Changes in Energy Balance during Dapagliflozin Therapy in Type 2 Diabetes—The Energize Study

Weight loss during SGLT2i therapy is less than predicted from urinary glucose loss. Modelling suggests a 10-15% compensatory increase in energy intake. We compared effects of 12 weeks’ dapagliflozin 10mg od vs. placebo on food intake in a double-blind, placebo-controlled study with short (1 week) and long-term (12 week) crossover periods. Food intake was measured during test meals at baseline, pre and post each crossover using the Sussex Ingestion Pattern Monitor, continuously recording intake during the meal; primary outcome was the difference after 12 weeks’ treatment. 52 patients with T2DM treated with diet or oral agents were recruited (45 completed;43% female). Median age 60y, weight 98.4 kg, BMI 34, HbA1c 59.5 mmol/mol. Analysis used a linear mixed model with the random effect as study subject and fixed effects of sex, visit, study arm and arm:visit interaction. Dapagliflozin use was associated with a reduction in HbA1c -9.73mmol/mol (95% CI 3.91, 16.27; p=0.004), and body weight (-2.84 vs. -0.87 kg) vs. placebo. There was no difference in test meal food intake between dapagliflozin and placebo at 12 weeks median difference, 2.63g (95% CI,-31.65,36.9); p=0.659 or at other time points. Dapagliflozin was not associated with a compensatory increase in food intake. Disclosure S. Rajeev: None. C.A. Roberts: None. D.J. Cuthbertson: None. V.S. Sprung: None. E. Brown: Research Support; Self; AstraZeneca. J.C. Halford: Advisory Panel; Self; Novo Nordisk A/S. Speaker's Bureau; Self; Novo Nordisk A/S. J.A. Harrold: None. G.J. Kemp: None. A. Stancak: None. J.P. Wilding: Other Relationship; Self; Astellas, AstraZeneca, Boehringer Ingelheim GmbH, Janssen Pharmaceuticals, Inc., Novo Nordisk Inc., Sanofi, Eli Lilly and Company, Orexigen Therapeutics, Inc., Merck &amp; Co., Inc..

Obese Mice Are Protected From Increased Energy Intake in Response to Voluntary Wheel Running

Diseases of metabolism pose an increasing threat to public health that has led to greater demand for effective treatments. Obesity is a highly prevalent metabolic disease that afflicts over 100 million Americans and increases the risk of developing diabetes and cardiovascular disease. Lifestyle modifications that incorporate exercise are a standard prescription for obesity, but its effectiveness is limited due to variability in compliance and physiological adaptations (e.g. compensatory increases in energy intake). Previous studies have shown that voluntary exercise fails to induce weight loss in high fat fed mice, but little is known regarding the onset of exercise. Here, we tested the hypothesis that chronic overnutrition from high fat feeding will mitigate the compensatory increase in food intake that commonly accompanies increased energy expenditure from voluntary exercise.Starting at 12 weeks of age, male C57BL/6J mice were weight matched, singly housed and fed a chow (n=8) or high fat diet (HFD; 60% calories from fat; n=6) for 4 weeks. At 18 weeks of age, mice were housed in a Promethion Metabolic Analyzer to measure energy expenditure, food intake and physical activity. Experiments were performed at 21°C with running wheels locked for four days then unlocked for the subsequent nine days. Body composition was assessed both prior to and immediately following indirect calorimetry experiments. Ethoscan (Sable Systems) analysis was performed to examine voluntary wheel running (VWR) distance, duration and speed and measured the time and distance for off‐wheel activities (i.e. roaming and feeding).HF‐fed mice were heavier (WT: 26.9 ± 1.1 vs. HF: 36.8 ± 4.2 g; p &lt; 0.05) and had greater fat mass (WT: 3.5 ± 0.6 vs. HF: 11.1 ± 3.1 g; p &lt; 0.05) than chow‐fed mice prior to energy balance studies. VWR caused a decrease in whole body (WT: −0.3 ± 0.8 vs. HF: −4.0 ± 1.3 g; p &gt; 0.05) and fat mass (WT: 0.3 ± 0.6 vs. HF: −3.0 ± 0.9 g; p &lt; 0.05) in HFD‐fed, but not in chow‐fed mice. VWR distance, duration, and speed were not affected by diet. VWR increased energy expenditure (EE) with both diets equally, but energy intake (EI) only increased in chow‐fed mice. VWR decreased overall off‐wheel activity (OWA) regardless of diet.These data demonstrate that 9 days of VWR cause weight loss in HFD‐fed mice but not mice fed a chow‐diet. Because VWR did not vary between diets, the efficacy of VWR in HFD‐fed mice could instead be attributed to resistance to specific behavioral compensations (i.e. increased food intake) that occur with the introduction of VWR in lean mice.Support or Funding InformationDSL (16POST29910001); D.H.W. (NIH DK054902 and DK076169)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Chronic Effect of Interval Training on Energy Intake: A Systematic Review and Meta-Analysis.

Single bouts of acute exercise do not appear to increase subsequent energy intake (EI), even when energy deficit is large. However, studies have shown a compensatory effect on EI following chronic exercise, and it remains unclear whether this is affected by exercise intensity. We investigated the chronic effect of high-intensity interval training (HIIT) and sprint interval training (SIT) on EI when compared with moderate-intensity continuous training (MICT) or no exercise (CON). Databases were searched until 13 March 2017 for studies measuring EI in response to chronic exercise (≥4 weeks of duration) of a high-intensity interval nature. Meta-analysis was conducted for between-group comparisons on EI (kilojoules) and bodyweight (kg). Results showed large heterogeneity, and therefore, metaregression analyses were conducted. There were no significant differences in EI between HIIT/SIT versus MICT (P=0.282), HIIT/SIT versus CON (P=0.398), or MICT versus CON (P=0.329). Although bodyweight was significantly reduced after HIIT/SIT versus CON but not HIIT/SIT versus MICT (in studies measuring EI), this was not clinically meaningful (<2% mean difference). In conclusion, there is no compensatory increase in EI following a period of HIIT/SIT compared to MICT or no exercise. However, this review highlights important methodological considerations for future studies.

Body Weight and Energy Intake Changes in Overweight Individuals Treated with Canagliflozin, Phentermine, or Canagliflozin+Phentermine

SGLT2 inhibitors (SGLT2i) induce a caloric loss by increasing urinary glucose excretion (UGE) leading to a modest yet sustained weight loss (WL) of ~2-4% in patients with type 2 diabetes. This WL is much less than predicted based on the UGE caloric deficit alone due to compensatory increases in energy intake (EI) that occur in response to WL. A 26-week study in overweight, otherwise healthy individuals (N=334, 82% female, mean (SD) age=46 (11) y, body weight (BW)=103 (18) kg, BMI=37 (5) kg/m2) tested the hypothesis that combining the appetite suppressant phentermine (PHEN 15 mg) with the SGLT2i canagliflozin (CANA 300 mg) results in greater WL than either monotherapy. Changes in EI were estimated using a previously validated mathematical model of energy balance using measured BW profiles and an estimated UGE of 55 g/day with CANA. As expected, WL was greatest with CANA+PHEN, and estimated EI was increased with CANA and decreased with PHEN (Figure). Surprisingly, despite the greater WL with CANA+PHEN, EI with CANA+PHEN was virtually identical to EI with PHEN alone, suggesting that co-administration of PHEN was able to fully block the compensatory EI increase that occurs with CANA alone. This effect led to greater-than-additive WL with CANA+PHEN, and individuals were still in negative energy balance and losing weight at Week 26. Longer-term studies with CANA+PHEN are warranted.

Effect Of Exercise-induced Weight Loss On 24 Hour Energy Metabolism

Exercise usually results in less weight loss than expected. It is therefore postulated that changes in energy expenditure (EE) and/or compensatory increases in energy intake (EI) occur to counteract energy deficits induced by exercise. PURPOSE: Compare changes in all components of daily energy expenditure (24hrEE) after 24 weeks of exercise training between varying doses of exercise recommended for weight loss. METHODS: Forty-one (28 F, 13 M) obese (35.2±3.7 kg/m2) middle aged (47.8±12.5 y), sedentary individuals from the Examination of Mechanisms of Exercise-induced Weight Compensation (E-MECHANIC) study were randomized to either a healthy living control group (HL, n=13) or a supervised, controlled aerobic exercise intervention that achieved 8 kcal/kg of body weight/week (KKW, n=14) or 20 KKW (n=14). 24hEE (metabolic chamber), total daily energy expenditure (TDEE, by doubly labeled water), energy intake (by Intake-Balance method), and VO2peak (by graded exercise test) were measured before and after the intervention. RESULTS: Compared to the HL group, VO2peak increased in the 8 KKW (p=.004) and 20 KKW (p<.0001) groups. With 20 KKW, TDEE (and 24hrEE) increased (p=.04) and weight loss (-2.5±0.9 kg, p=.04) was significant but approximately half of what was expected based on the increase in energy expenditure from exercise. Fat mass (-2.1±0.8 kg, p=.02) but not fat-free mass (-0.4±0.3 kg, p=.79) was also significantly reduced. A 151 kcal/d energy deficit was detected at week 24. The increase in TDEE is attributed to the increased physical activity (p=.03) and not to changes in EE during sleep, arousal or the thermic effect of food. Besides physical activity, the largest change in EE was a reduction in spontaneous physical activity by ~15% (p=.04). With 8 KKW, there was no significant weight or body composition change and no significant increase in TDEE. An energy deficit of 23 kcal/d was detected at week 24. None of the components of EE were changed in the 8 KKW group. CONCLUSIONS: Structured aerobic exercise that expends up to 1800 kcal/wk increased TDEE but produces less weight loss than expected possibly due to compensatory increases in EI and behavioral adaptations that could lead to reduced spontaneous physical activity.

Sex Differences In Total Pyy And Glp-1 After Moderate-intensity Continuous And Sprint Interval Cycling Exercise.

Exercise is often used as a weight-loss strategy, however, exercise interventions are sometimes less effective in females than males for improving body composition. One possible explanation is that exercise affects appetite regulating hormones differently in males and females such that females increase post-exercise energy intake. Recently, sprint interval training was shown to reduce body fat in females despite relatively low energy expenditure during exercise. PURPOSE: To examine sex differences in circulating anorexigenic hormones and perceived hunger following an acute session of sprint interval training (SIT) and moderate-intensity continuous training (MICT). METHODS: Twenty-one active participants (11 females in early follicular phase) participated in 3 sessions in a randomized crossover design: 1) MICT, 30 min cycling at 65% VO2max; 2) SIT, 6 x 30 sec “all-out” cycling sprints with 4 min recovery periods (27 min total); and 3) control (CTRL; no exercise). Participants arrived at the lab fasted and consumed a standardized breakfast 1 hour before exercise. Blood samples were collected pre-exercise, immediately and 90 min post-exercise for the measurement of total peptide tyrosine tyrosine (PYY) and glucagon-like peptide-1 (GLP-1). Subjective perceptions of hunger were assessed using a visual analogue scale before breakfast and before all blood draws. Hormone data were analysed as change in concentration from baseline. Changes in hormones and hunger were analysed using a 3 x 3 x 2 mixed factor (session x time x sex) repeated measures ANOVA. RESULTS: Increases in GLP-1 and PYY were greater during the MICT session (P<0.05) and SIT session (P<0.01) compared to CTRL. Total PYY increased more immediately post-exercise in males than females (P=0.030). GLP-1 increased only in females following MICT (P=0.034) and SIT (P=0.024) compared to CTRL. Perceived hunger was lower immediately post-MICT (P=0.016) and SIT (P=0.006) compared to CTRL, but there were no sex differences. CONCLUSION: Total PYY and GLP-1 appear to respond similarly to submaximal and supramaximal exercise, however, these results suggest they may respond differently to exercise in males and females over 90 min. The post-exercise hormonal response we observed in females would not be expected to create a compensatory increase in energy intake.

Sex differences in the response of total PYY and GLP-1 to moderate-intensity continuous and sprint interval cycling exercise.

Exercise interventions are often less effective at improving body composition for females than males, potentially due to post-exercise hormonal responses that increase energy intake in females. Recently, sprint interval training was shown to effectively reduce body fat in females despite being relatively low during exercise energy expenditure. To determine whether any sex difference in total PYY, GLP-1 or perceived hunger exists following moderate-intensity continuous exercise (MICT) and sprint interval exercise (SIT) METHODS: Twenty-one active participants (11 females) participated in three sessions in a randomized crossover design: (1) MICT, 30-min cycling at 65% VO2max; (2) SIT, 6 × 30s "all-out" sprints with 4-min recovery periods; (3) control (CTRL; no exercise). Blood samples were collected pre-exercise, immediately and 90min post-exercise for the measurement of total PYY and GLP-1. Subjective perceptions of hunger were assessed using a visual analogue scale pre-breakfast and before all blood samples. Concentrations of total PYY and GLP-1 were greater during MICT (P = 0.05) and SIT (P = 0.005) compared to CTRL. Total PYY increased more immediately post-exercise in males than females (P = 0.030). GLP-1 only increased in females following MICT (P = 0.034) and SIT (P = 0.024) compared to CTRL. Perceived hunger was lower immediately post-MICT (P = 0.016) and SIT (P = 0.006) compared to CTRL. These results suggest that total PYY and GLP-1 respond differently to exercise in males and females over 90min following various exercise intensities. The observed post-exercise hormonal response would not be expected to create a compensatory increase in energy intake in females.

Compensatory changes in energy balance during dapagliflozin treatment in type 2 diabetes mellitus: a randomised double-blind, placebo-controlled, cross-over trial (ENERGIZE)—study protocol

IntroductionSodium glucose cotransporter 2 (SGLT2) inhibitors are effective blood-glucose-lowering medications with beneficial effects on body weight in patients with type 2 diabetes mellitus (T2DM). However, observed weight loss is less...

Nonprescribed physical activity energy expenditure is maintained with structured exercise and implicates a compensatory increase in energy intake

Nonprescribed physical activity energy expenditure is maintained with structured exercise and implicates a compensatory increase in energy intake

Breakfast Consumption Affects Appetite, Energy Intake, and the Metabolic and Endocrine Responses to Foods Consumed Later in the Day in Male Habitual Breakfast Eaters

The effects of breakfast consumption on energy intake and the responses to foods consumed later in the day remain unclear. Twelve men of healthy body weight who reported regularly consuming breakfast (mean ± SD age 23.4 ± 7.3 y; BMI 23.5 ± 1.7 kg/m2) completed 2 trials using a randomized crossover design. Participants were provided with a 1050-kJ liquid preload 150 min after consuming a standardized breakfast (B) (10% daily energy requirement and 14, 14, and 72% energy from protein, fat, and carbohydrate, respectively), or no breakfast (NB). Blood glucose and serum insulin responses to the preload (area under the curve) were higher in the NB condition (P<0.05). Plasma FFA responses to the preload were higher in the NB condition (P<0.01). Plasma glucagon-like peptide 1 (P<0.01) and plasma peptide Y (P<0.05) responses were higher after the preload in the B condition. Desire to eat, fullness, and hunger ratings collected immediately prior to consuming the preload were all different from the fasting values in the NB condition (P<0.05). Thus, immediately prior to consuming the preload, the fullness rating was lower and hunger and desire to eat ratings were higher in the NB condition (P<0.05). Energy intake at the lunchtime test meal was ~17% lower in the B condition (P<0.01). In conclusion, missing breakfast causes metabolic and hormonal differences in the responses to foods consumed later in the morning as well as differences in subjective appetite and a compensatory increase in energy intake.

Nonprescribed physical activity energy expenditure is maintained with structured exercise and implicates a compensatory increase in energy intake

Exercise interventions elicit only modest weight loss, which might reflect a compensatory reduction in nonprescribed physical activity energy expenditure (PAEE). The objective was to investigate whether there is a reduction in nonprescribed PAEE as a result of participation in a 6-mo structured exercise intervention in middle-aged men. Sedentary male participants [age: 54 ± 5 y; body mass index (in kg/m²): 28 ± 3] were randomly assigned to a 6-mo progressive exercise (EX) or control (CON) group. Energy expenditure during structured exercise (prescribed PAEE) and nonprescribed PAEE were determined with the use of synchronized accelerometry and heart rate before the intervention, during the intervention (2, 9, and 18 wk), and within a 2-wk period of detraining after the intervention. Structured prescribed exercise increased total PAEE and had no detrimental effect on nonprescribed PAEE. Indeed, there was a trend for greater nonprescribed PAEE in the EX group (P = 0.09). Weight loss in the EX group (-1.8 ± 2.2 kg compared with +0.2 ± 2.2 kg in the CON group, P < 0.02) reflected only ≈40% of the 300-373 kcal/kg body mass potential energy deficit from prescribed exercise. Serum leptin concentration decreased by 24% in the EX group (compared with 3% in the CON group, P < 0.03), and we estimate that this was accompanied by a compensatory increase in energy intake of ≈100 kcal/d. The adoption of regular structured exercise in previously sedentary, middle-aged, and overweight men does not result in a negative compensatory reduction in nonprescribed physical activity. The less-than-predicted weight loss is likely to reflect a compensatory increase in energy intake in response to a perceived state of relative energy insufficiency.

Effects of Exercise on Postprandial Responses to Ad Libitum Feeding in Overweight Men

Previous exercise reduces the lipemic response to meals of fixed size. It is not known whether this triglyceride (TG) attenuation also occurs in response to ad libitum feeding because exercise might induce a compensatory increase in energy intake. It is also unclear whether the effects of a single exercise session on lipemia would be augmented by repeated exercise sessions on consecutive days. Ten sedentary overweight/obese men (aged 35 ± 6 yr) each participated in three 4-d trials in random order: CON (no exercise on days 1-3), EX-1 (exercise session on day 3), and EX-3 (exercise sessions on days 1-3). Each exercise session expended 33.5 kJ·kg−¹ body mass. Subjects consumed an isocaloric diet (provided by experimenters) and avoided alcohol on days 1-3 of all trials. On day 4 of each trial, participants underwent a 7-h metabolic assessment, during which an ad libitum buffet breakfast and lunch was provided, and postprandial plasma and expired air responses were assessed. Day 4 ad libitum energy intake was higher than CON in EX-3 (9216 ± 669 vs 7859 ± 492 kJ, P < 0.05) but not EX-1 (8335 ± 683 kJ). Postprandial TG responses were 27% and 25% lower in EX-1 and EX-3, respectively, than in CON (both P < 0.05), and postprandial insulin responses were 26% (P = 0.06) and 31% (P < 0.05) lower in EX-1 and EX-3, respectively, than in CON. Compared with CON, postprandial fat oxidation was 20% higher in EX-1 and 27% higher in EX-3 (both P < 0.05). Previous exercise attenuates the lipemic response to ad libitum meals, suggesting that exercise's TG-lowering effect will extend into "real-world" settings where food intake is not carefully controlled. This response is not augmented by exercising on repeated days.

Acute and long-term effects of exercise on appetite control: is there any benefit for weight control?

To examine the relationship between energy intake, appetite control and exercise, with particular reference to longer term exercise studies. This approach is necessary when exploring the benefits of exercise for weight control, as changes in body weight and energy intake are variable and reflect diversity in weight loss. Recent evidence indicates that longer term exercise is characterized by a highly variable response in eating behaviour. Individuals display susceptibility or resistance to exercise-induced weight loss, with changes in energy intake playing a key role in determining the degree of weight loss achieved. Marked differences in hunger and energy intake exist between those who are capable of tolerating periods of exercise-induced energy deficit, and those who are not. Exercise-induced weight loss can increase the orexigenic drive in the fasted state, but for some this is offset by improved postprandial satiety signalling. The biological and behavioural responses to acute and long-term exercise are highly variable, and these responses interact to determine the propensity for weight change. For some people, long-term exercise stimulates compensatory increases in energy intake that attenuate weight loss. However, favourable changes in body composition and health markers still exist in the absence of weight loss. The physiological mechanisms that confer susceptibility to compensatory overconsumption still need to be determined.