Exercise-induced Energy Deficit Research Articles

Comparative analysis of circulating metabolomic profiles identifies shared metabolic alterations across distinct multistressor military training exercises.

Military training provides insight into metabolic responses under unique physiological demands that can be comprehensively characterized by global metabolomic profiling to identify potential strategies for improving performance. This study identified shared changes in metabolomic profiles across three distinct military training exercises, varying in magnitude and type of stress. Blood samples collected before and after three real or simulated military training exercises were analyzed using the same untargeted metabolomic profiling platform. Exercises included a 2-wk survival training course (ST, n = 36), a 4-day cross-country ski march arctic training (AT, n = 24), and a 28-day controlled diet- and exercise-induced energy deficit (CED, n = 26). Log2-fold changes of greater than ±1 in 191, 121, and 64 metabolites were identified in the ST, AT, and CED datasets, respectively. Most metabolite changes were within the lipid (57-63%) and amino acid metabolism (18-19%) pathways and changes in 87 were shared across studies. The largest and most consistent increases in shared metabolites were found in the acylcarnitine, fatty acid, ketone, and glutathione metabolism pathways, whereas the largest decreases were in the diacylglycerol and urea cycle metabolism pathways. Multiple shared metabolites were consistently correlated with biomarkers of inflammation, tissue damage, and anabolic hormones across studies. These three studies of real and simulated military training revealed overlapping alterations in metabolomic profiles despite differences in environment and the stressors involved. Consistent changes in metabolites related to lipid metabolism, ketogenesis, and oxidative stress suggest a potential common metabolomic signature associated with inflammation, tissue damage, and suppression of anabolic signaling that may characterize the unique physiological demands of military training.NEW & NOTEWORTHY The extent to which metabolomic responses are shared across diverse military training environments is unknown. Global metabolomic profiling across three distinct military training exercises identified shared metabolic responses with the largest changes observed for metabolites related to fatty acids, acylcarnitines, ketone metabolism, and oxidative stress. These changes also correlated with alterations in markers of tissue damage, inflammation, and anabolic signaling and comprise a potential common metabolomic signature underlying the unique physiological demands of military training.

The impact of acute exercise on appetite control: Current insights and future perspectives

The interaction of exercise with appetite control and energy intake has been widely studied due to the ability of exercise-related energy expenditure to influence energy and substrate balance. Many empirical studies have explored appetite and energy intake responses to acute (single) exercise bouts involving a variety of protocols in diverse populations revealing several consistent trends. The balance of evidence suggests that acute moderate-to-vigorous intensity land-based exercise suppresses subjective appetite feelings and the orexigenic hormone acylated ghrelin and elevates the anorexigenic hormones peptide YY and glucagon-like peptide-1. These perturbations are transient and hormone concentrations usually return to resting values in the hours after exercise without evoking compensatory increases in appetite or energy intake on the same day. This evidence counters the popular assertion that exercise transiently increases appetite and may prompt greater energy intake at subsequent meals. The indifference of the appetite control system to acute exercise-induced energy deficits contrasts with the immediate increases in appetite and energy intake provoked by equivalent diet-induced energy deficits. There is, however, considerable inter-individual variability in subjective appetite and hormonal responses to acute exercise with some individuals experiencing greater exercise-induced appetite suppression than others. Current evidence supports the promotion of exercise as a strategy for inducing a short-term energy deficit but the relevance of this for long-term appetite regulation and the control of body mass remains uncertain.

Preoperative state of autonomic regulation in patients with adolescent idiopathic scoliosis

Objective. To analyze the state of autonomic regulation of the heart rate in patients with adolescent idiopathic scoliosis before the upcoming surgical treatment of spinal deformity.Material and Methods. The study included 30 patients with adolescent idiopathic scoliosis who were admitted for surgical treatment from January to April 2021. There were 28 female and 2 male patients. The heart rate variability (HRV) registration was carried out on the VNS-micro vegetotester, with Poly-Spectrum.NET software, Neurosoft (Russia). The study was conducted for 5 minutes in the supine position and for 5 minutes after the active orthostatic test. Temporal and spectral indicators of heart rate were analyzed.Results. When analyzing HRV at rest, an increase in the temporal indicators of the heart rate and the power of high-frequency wave oscillations was recorded, which indicates both an increased activity of autonomic regulation in general and the predominance of the regulatory influence o of the parasympathetic division of the autonomic nervous system. A decrease in all spectral components during an active orthostatic test and an increase in stress index values by 3.5 times indicate a significant stress of regulatory systems.Conclusion. Analysis of HRV in patients with adolescent idiopathic scoliosis at rest revealed increased autonomic activity with a predominant effect of the parasympathetic division of the autonomic nervous system. The state of exercise-induced energy deficit, registered after an active orthostatic test, indicates a significant preoperative stress of the regulatory systems and refers this category of patients to a group of increased risk of complications associated with hemodynamic instability.

Testosterone Undecanoate Administration Prevents Fat-Free Mass Loss During Strenuous Multi-Stressor Military Operations

PURPOSE: The efficacy of administering testosterone (T) to restore eugonadal concentrations during multi-stressor, sustained military operations (SUSOPS) that suppress endogenous T synthesis to prevent declines in lean mass and physical performance is not well described. Therefore, the objective of this study was to test the effects of T on androgen status, body composition, and physical performance during a simulated SUSOPS. METHODS: After a baseline phase (P1), 32 healthy young males (26.5 ± 4.4 y) received a single injection of either T undecanoate (750 mg; TEST) or placebo (PLA) before completing four consecutive, 5-d simulated SUSOPS cycles (P2). Each cycle consisted of two low-stress days (~1230 kcal/d exercise-induced energy deficit [EDef]; 8 h sleep/night) and three high-stress days (~2800 kcal/d EDef; 4 h sleep/night). P2 was followed by a 23-d recovery period (P3). Circulating hormones, 4-compartment measures of body composition, and physical performance (vertical jump, 3-repetition maximum [RM] deadlift, Wingate anaerobic test, treadmill VO2peak, and 2.5-mile weighted ruck march) were examined at the end of each phase. RESULTS: Total T in TEST was greater by the end of P2 than P1 (mean ± SE between group difference at the end of P2: 6.7 ± 2.6 nmol/L, p < 0.001), which returned to P1 values in P3, but total T did not change in PLA. Despite increases in free T in TEST throughout P2, free T at the end of P2 was not different from P1, but decreased from P1 to P2 in PLA (-1.2 ± 0.6 pmol/L, p = 0.04) and was greater at the end of P3 compared to P1 in PLA (p < 0.05). FFM was maintained across phases in TEST, but decreased from P1 to P2 in PLA (-2.3 ± 1.0 kg, p = 0.02) and recovered in P3. Total body mass and fat mass decreased from P1 to P2 (p < 0.05) and recovered by P3 regardless of treatment. Vertical jump height, 3-RM deadlift, and Wingate peak power decreased, and 2.5-mile ruck march time increased from P1 to P2 (all p < 0.05) and recovered by P3 regardless of treatment. CONCLUSION: Administering T before a 20-d, simulated SUSOPS maintained eugonadal T concentrations and prevented FFM loss without impacting androgen status in recovery. However, T use did not attenuate performance decrements in response to the multi-stressor SUSOPS.

Acute Exercise Increases Attentional Bias Towards Food Cues

Although exercise is a common weight loss strategy, the amount of weight loss resulting from exercise training is often less than expected. This is often attributed to exercise promoting greater energy intake, resisting the exercise-induced negative energy balance required for weight loss. Prior research on how exercise can influence hormonal mediators of appetite offer conflicting results, with some demonstrating longitudinal exercise increases the satiety response to a meal and changes in hunger hormones do not predict weight loss. Research on other underlying mechanisms working to promote energy intake during exercise is scarce. PURPOSE: To determine if acute exercise influences attentional bias towards food cues. METHODS: Thirty (30) participants (BMI ≥ 25, aged 18-50 years) completed the Dot-Probe task before and 15 minutes after a bout of aerobic exercise where they expended an estimated 500 kcal and before and after a 60-minute bout of television watching (sedentary condition) on separate sessions. Sessions were separate by one week and order was counterbalanced across participants. The Dot-Probe task uses an eye-tracking device to measure the amount of time (ms) participants spent fixated on image pairs projected on a computer screen. Images included either highly appealing food (critical task stimuli) or neutral (non-food) images. Images were presented for 3,000 ms. A yellow dot appeared on either side of the screen in place of one of the previously presented images. Participants responded as quickly as possible to indicate which side the probe appeared by pressing a corresponding computer key. Mean fixation time (amount of time looking at each image) was recorded in ms. RESULTS: A condition (exercise vs sedentary) by time (pre vs post) interaction (p = 0.001) was observed where the percent of time fixated on food cues increased from 48.3% pre to 56.6% post-exercise while fixation percent changed from 50.6% pre to 49.7% post-sedentary. CONCLUSION: Acute aerobic exercise increases the environmental salience of food cues, which may increase the motivational drive to eat and resist an exercise-induced energy deficit. Attentional bias training has been successfully used to change eating behaviors and may represent a novel adjunct therapy to increase the success of an exercise for weight loss intervention.

Carbohydrate-Energy Replacement Following High-Intensity Interval Exercise Blunts Next-Day Glycemic Control in Untrained Women.

BackgroundImproved glycemic control has been reported for ∼24 h following low-volume high-intensity interval exercise (HIIE), but it is unclear if this is a direct effect of exercise or an indirect effect of the exercise-induced energy deficit. The purpose of this study was to investigate the effect of carbohydrate-energy replacement after low-volume HIIE on 24 h glycemic control in women.MethodsSeven untrained women (age: 22 ± 2 yr; BMI: 22 ± 3 kg/m2; VO2peak: 33 ± 7 ml/kg/min) completed three 2-day trials in the mid-follicular phase of the menstrual cycle. Continuous glucose monitoring was used to measure blood glucose concentrations during, and for 24 h following three conditions: (1) HIIE followed by a high-carbohydrate energy replacement drink (EX-HC); (2) HIIE followed by a non-caloric taste-matched placebo drink (EX-NC); and (3) seated control with no drink (CTL). HIIE involved an evening session (1,700 h) of 10 × 1-min cycling efforts at ∼90% maximal heart rate with 1 min recovery. Diet was standardized and identical across all three 2-day trials, apart from the post-exercise carbohydrate drink in EX-HC, which was designed to replenish the exercise-induced energy expenditure. Postprandial glycemic responses to the following days breakfast, snack, lunch, and dinner, as well as 24 h indices of glycemic control, were analyzed.ResultsThe day after HIIE, postprandial glycemia following breakfast and snack were reduced in EX-NC compared to EX-HC, as reflected by lower 3 h glucose mean (breakfast: 5.5 ± 0.5 vs. 6.7 ± 1, p = 0.01, Cohen’s d = 1.4; snack: 4.9 ± 0.3 vs. 5.7 ± 0.8 mmol/L, p = 0.02, d = 1.4) and/or area under the curve (AUC) (breakfast: 994 ± 86 vs. 1,208 ± 190 mmol/L x 3 h, p = 0.01, d = 1.5). Postprandial glycemic responses following lunch and dinner were not different across conditions (p > 0.05). The 24 h glucose mean (EX-NC: 5.2 ± 0.3 vs. EX-HC: 5.7 ± 0.7 mmol/L; p = 0.02, d = 1.1) and AUC (EX-NC: 7,448 ± 425 vs. EX-HC: 8,246 ± 957 mmol/L × 24 h; p = 0.02, d = 1.1) were reduced in EX-NC compared to EX-HC.ConclusionPost-exercise carbohydrate-energy replacement attenuates glycemic control the day following a single session of low-volume HIIE in women.

Influence of fat-free mass and resting metabolic rate on increased food reinforcement after exercise training

PurposeModels of appetite control have been largely based on negative feedback from gut and adipose signaling to central appetite centers. However, contemporary models posit that fat-free mass (FFM) or the energy demand of FFM [i.e., resting metabolic rate (RMR)] may play a primary role in the motivational drive for food intake (i.e., food reinforcement). The relative reinforcing value of food (RRVfood) is associated with energy intake (EI) and increases with an acute energy deficit. Chronic exercise-induced energy deficits lead to alterations in fat mass (FM), FFM, and RMR and provide an opportunity to test whether change in (∆) FM, ∆FFM, ∆usual EI, or ∆RMR are associated with ∆RRVfood.MethodsParticipants (n = 29, BMI = 25–35 kg/m2) engaged in aerobic exercise expending 300 or 600 kcal, 5 days/weeks for 12 weeks. The reinforcing value of food (PMaxfood) was measured via a computer-based operant responding task and RRVfood was calculated as the reinforcing value of food relative to non-eating sedentary behaviors. RMR was determined by indirect calorimetry and body composition by DXA.ResultsPost-training FFM correlated with usual post-training EI (rs = 0.41, p < 0.05), PMaxfood (rs=0.52, p < 0.01), and RMR (rs = 0.85, p < 0.0001). ∆RMR negatively correlated with ∆PMaxfood (rs = − 0.38, p < 0.05) and with ∆RRVfood (rs = − 0.37, p < 0.05). ∆PMaxfood and ∆RRVfood were not associated with ∆FFM (p = 0.71, p = 0.57, respectively).ConclusionsReductions in RMR with weight loss may increase food reinforcement as means of restoring FFM and RMR to pre-weight loss amounts. Limiting reductions in RMR during weight loss may benefit weight maintenance by restricting increases in food reinforcement after weight loss.

Effect of acute dietary- versus combined dietary and exercise-induced energy deficits on subsequent energy intake, appetite and food reward in adolescents with obesity

BackgroundAcute dietary-induced energy deficits have been shown to favor compensatory appetitive responses. The aim of this study was to compare energy intake (EI), appetite sensations and the hedonic responses to equivalent energy deficits induced by dietary restriction alone and combined with exercise in adolescents with obesity. MethodsIn a within-subjects design, seventeen adolescents with obesity (12–16 years, Tanner stage 3–5, 6 males) randomly completed three 14 h conditions: (i) control (CON); (ii) deficit induced by diet only (Def-EI) and; (iii) deficit induced by combined diet and physical exercise (Def-mixed). Breakfast and lunch were calibrated to generate a 500 kcal deficit in Def-EI and 250 kcal deficit in Def-mixed. A 250 kcal deficit was created through a cycling exercise set at 65% VO2peak in Def-mixed. Ad libitum EI, macronutrients and relative EI (REI) were assessed at dinner, subjective appetite sensations taken at regular intervals, and food reward measured before dinner. ResultsEI at dinner was significantly lower in Def-EI compared to CON (p = 0.014; Effect size (ES): -0.59 [-1.07; -0.12]), with no difference between Def-mixed and both CON and Def-EI. Total REI was lower in both deficit conditions compared with CON (Def-mixed: p < 0.001; ES: -3.80 [-4.27; -3.32], Def-EI: p < 0.001; ES: -4.90 [-5.37; -4.42] respectively), indicating incomplete compensation for the energy deficits. Absolute protein ingestion at dinner was lower in Def-EI than Def-mixed (p = 0.037; ES: -0.50 [-0.98; -0.03]) and absolute lipid ingestion was lower in Def-EI than in CON (p = 0.033; ES: -0.51 [-0.99; -0.04]). A higher proportion of protein and a lower proportion of carbohydrates was observed in Def-mixed than in Def-EI (p = 0.078; ES: -0.42 [-0.90; 0.04] and p = 0.067; ES: 0.44 [-0.03; 0.92] respectively). Total area under the curve for appetite sensations were similar between conditions. Explicit liking for sweet relative to savoury food was lower in Def-mixed compared to CON (p = 0.027; ES: -0.53 [-1.01; -0.06]) with no difference in food reward between Def-EI and CON. ConclusionNeither of the two acute isoenergetic deficits led to subsequent appetitive compensation, with the dietary deficit even inducing a lower ad libitum EI at the subsequent dinner. Further studies are needed to better understand the appetitive response to dietary and exercise energy balance manipulations in this population.

Exercise for Weight Loss: Further Evaluating Energy Compensation with Exercise.

ABSTRACTPurposeThis study assessed how individuals compensate for energy expended during a 12-wk aerobic exercise intervention, elucidating potential mechanisms and the role exercise dose plays in the compensatory response.Participants and DesignThree-arm, randomized controlled trial among sedentary adults age 18 to 40 yr, body mass index of 25 to 35. Groups included six exercise sessions per week, two sessions per week, and sedentary control.MethodsRate of exercise energy expenditure was calculated from a graded exercise test averaged across five heart rate zones. Energy compensation was calculated as the difference between expected weight loss (based on exercise energy expenditure) and changes in fat and fat-free mass (DXA). Resting energy expenditure was assessed via indirect calorimetry and concentrations of acylated ghrelin, leptin, insulin, and Glucagon-like peptide 1 (GLP-1) were assessed fasting and postprandial (six timepoints over 2 h).ResultsThe 6-d·wk−1 group expended more energy (2753.5 kcal) and exercised longer (320.5 min) per week than the 2-d·wk−1 group (1490.7 kcal, 1888.8 min, P < 0.05), resulting in greater fat loss compared with the 2-d or control groups (P < 0.05). Exercise groups did not differ in the % or total kcal compensated. Greater decreases in area under the curve (AUC) for acylated ghrelin predicted greater fat loss, regardless of group, energy expended per week, exercise duration, or exercise intensity. Changes in leptin AUC was the only independent predictor for energy compensation, with a greater decrease in leptin AUC predicting less energy compensation. Exercise frequency, energy expended, duration, or intensity did not influence energy compensation.ConclusionsLeptin is an important factor in successful weight loss through exercise, with greater postprandial decreases promoting less compensation. Greater amounts of exercise do not influence the compensatory response to an exercise-induced energy deficit.

Energy replacement diminishes the postprandial triglyceride-lowering effect from accumulated walking in older women.

Dietary replacement of an acute exercise-induced energy deficit offsets the postprandial triglyceride (TG)-lowering effect of exercise in young boys and middle-aged men. It is unclear whether these findings are observed when exercise is accumulated in older adults. This study examined the effect of accumulating short bouts of exercise, with and without dietary replacement of an exercise-induced energy deficit, on postprandial TG in older women. Seventeen older women (≥ 65years) underwent three, 8-h trials: (1) control, (2) accumulated walking and (3) accumulated walking with energy replacement. During the control trial, participants rested for 8h. The accumulated walking trials comprised twenty 1.5min brisk walking bouts performed at a pre-determined self-selected pace separated by 15min seated rest. In each trial, participants consumed a standardised breakfast and lunch. The breakfast in the accumulated walking with energy replacement trial included replacement of the energy deficit (0.62MJ, 149kcal) induced by exercise. Venous blood samples were collected fasted and at 2, 4, 6 and 8h after breakfast. Time-averaged postprandial serum TG concentrations over 8h were lower after accumulated walking than control and accumulated walking with energy replacement (mean ± SD: 1.46 ± 0.93 vs 1.71 ± 1.01 vs 1.60 ± 0.98mmol/L, respectively: main effect of trial p = 0.017). There was little difference between control and accumulated walking with energy replacement. Replacing the energy expenditure induced by accumulating 30min of brisk walking in short (1.5min) bouts diminishes the postprandial TG-lowering effect in older women.

Energy Deficit Required for Exercise-induced Improvements in Glycemia the Next Day.

This study determined the impact of an exercise-induced energy deficit on postprandial and 24 h glycemic control the day after a session of exercise. Fifteen healthy participants (m/f = 5/10, 27 ± 6 yr, body mass index = 24 ± 3 kg·m, peak oxygen consumption [V˙O2peak] = 36 ± 9 mL·kg·min) completed two separate 5-d experimental trials performed under "free-living" conditions. On day 1 of each trial, participants were fitted with a continuous glucose monitor and abstained from exercise. Day 2 served as a nonexercise control (NoEx). On day 3, participants exercised at 3:00 PM (65% V˙O2peak) until they expended 350 kcals (~45 min). The diet during both experimental trials was identical with the exception of meals after this exercise session. During one trial, the dinner after exercise did not replenish the 350 kcal expended during exercise, thereby establishing an exercise energy deficit (ExDEF). During the other experimental trial, the dinner after exercise contained an additional 350 kcal to compensate for the energy expended during exercise, and thereby maintained energy balance after exercise (ExBAL). Free-living glycemia was measured the day before exercise (NoEx) and the day after exercise under ExDEF and ExBAL conditions. The day after exercise, 3 h postprandial area under the curve was lower after breakfast in ExDEF compared with ExBAL (16.0 ± 1.8 vs 17.0 ± 1.6 mmol·L·h per 3 h, P = 0.01), but did not differ between groups after lunch (P = 0.24), dinner (P = 0.39), or evening snack (P = 0.45). Despite differences in the glycemic response to breakfast, 24 h glycemia did not differ between ExDEF and ExBAL (area under the curve = 128 ± 10 vs 131 ± 10 mmol·L·h per 24 h, respectively; P = 0.54). An exercise-induced energy deficit lowered the glycemic response to breakfast the next day-but this energy deficit did not impact total 24 h glycemia, the day after exercise in metabolically healthy adults.

Post-moderate-intensity exercise energy replacement does not reduce subsequent appetite and energy intake in adolescents with obesity.

Exercise modifies energy intake (EI) in adolescents with obesity, but whether this is mediated by the exercise-induced energy deficit remains unknown. The present study examined the effect of exercise with and without dietary replacement of the exercise energy expenditure on appetite, EI and food reward in adolescents with obesity. Fourteen 12-15-year-old adolescents with obesity (eight girls; Tanner 3-4; BMI 34·8 (sd 5·7) kg/m2; BMI z score 2·3 (sd 0·4)) randomly completed three experimental conditions: (i) rest control (CON); (ii) 30-min cycling (EX) and (iii) 30-min cycling with dietary energy replacement (EX + R). Ad libitum EI was assessed at lunch and dinner, and food reward (Leeds Food Preference Questionnaire) before and after lunch. Appetite was assessed at regular intervals. Lunch, evening and total EI (excluding the post-exercise snack in EX - R) were similar across conditions. Lunch and total EI including the post-exercise snack in EX + R were higher in EX - R than CON and EX; EX and CON were similar. Total relative EI was lower in EX (6284 (sd 2042) kJ) compared with CON (7167 (sd 2218) kJ; P < 0·05) and higher in EX + R (7736 (sd 2033) kJ) compared with CON (P < 0·001). Appetite and satiety quotients did not differ across conditions (P ≥ 0·10). Pre-meal explicit liking for fat was lower in EX compared with CON and EX + R (P = 0·05). There was time by condition interaction between EX and CON for explicit wanting and liking for fat (P = 0·01). Despite similar appetite and EI, adolescents with obesity do not adapt their post-exercise food intake to account for immediate dietary replacement of the exercise-induced energy deficit, favouring a short-term positive energy balance.

Effects of a 12-Week Exercise Intervention on Subsequent Compensatory Behaviors in Adolescent Girls: An Exploratory Study.

Chronic exercise programs can induce adaptive compensatory behavioral responses through increased energy intake (EI) and/or decreased free-living physical activity in adults. These responses can negate the benefits of an exercise-induced energy deficit; however, it is unclear whether young people experience similar responses. This study examined whether exercise-induced compensation occurs in adolescent girls. Twenty-three adolescent girls, heterogeneous for weight status, completed the study. Eleven adolescent girls aged 13 years completed a 12-week supervised exercise intervention (EX). Twelve body size-matched girls comprised the nonexercise control group (CON). Body composition, EI, free-living energy expenditure (EE), and peak oxygen uptake (V˙O2) were measured repeatedly over the intervention. Laboratory EI (EX: 9027, 9610, and 9243kJ·d-1 and CON: 9953, 9770, and 10,052kJ·d-1 at 0, 12, and 18 wk, respectively; effect size [ES] = 0.26, P = .46) and free-living EI (EX: 7288, 6412, and 5273, 4916kJ·d-1 and CON: 7227, 7128, and 6470, 6337kJ·d-1 at 0, 6, 12, and 18 wk, respectively; ES ≤ 0.26, P = .90) did not change significantly over time and were similar between groups across the duration of the study. Free-living EE was higher in EX than CON (13,295 vs 12,115kJ·d-1, ES ≥ 0.88, P ≥ .16), but no significant condition by time interactions were observed (P ≥ .17). The current findings indicate that compensatory changes in EI and EE behaviors did not occur at a group level within a small cohort of adolescent girls. However, analysis at the individual level highlights large interindividual variability in behaviors, which suggests a larger study may be prudent to extend this initial exploratory research.

Testosterone Administration During Energy Deficit Suppresses Hepcidin Concentrations and Increases Iron Utilization in Healthy Males (OR15-08-19)

ObjectivesMilitary personnel are exposed to periods of energy deficit and stress, which is typically accompanied by reductions in testosterone concentrations and declines in iron status. Exogenous testosterone administration may increase erythropoiesis and iron availability.The objective of this study was to determine the effects of exogenous testosterone on iron homeostasis in healthy young males during energy deficit. MethodsFifty males (24.8 ± 5.0 y, 78.6 ± 12.2 kg) completed this randomized, double-blind, placebo-controlled trial. Participants were provided a eucaloric diet during a 2-week free-living phase (day 1–14). Following the free-living phase, participants completed a 4-week live-in phase (day 15–42). During the live-in phase participants were randomized to 200 mg testosterone enanthate/week (n = 24) or 1 mL sesame oil/week (placebo, n = 26) and were in an energy- and exercise-induced energy deficit equal to 53 ± 4%. Blood was collected on days 14 and 42 to determine concentrations of testosterone, hemoglobin, hematocrit, ferritin, hepcidin, and erythroferrone. Data are reported as change scores (mean ± SD). ResultsTotal testosterone concentrations increased with testosterone and declined with placebo (569 ± 271 nmol/L and −83 ± 142 nmol/L, P < 0.0001). Testosterone attenuated the decline in hemoglobin (−0.04 ± 0.7 g/L and −0.6 ± 0.8 g/dL, P < 0.01) and hematocrit (0.6 ± 2.2% and −1.3 ± 2.1%, P < 0.01) that occurred with placebo. Hepcidin (−3.7 ± 5.0 ng/mL and 2.1 ± 5.0 ng/mL, P < 0.001) and ferritin (−32.5 ± 38.6 ng/mL and 15.4 ± 41.2 ng/mL, P < 0.0001) were reduced with testosterone as compared to placebo. Erythroferrone (−0.5 ± 2.1 ng/mL and 0.5 ± 2.0 ng/mL, P = 0.11) did not differ when comparing testosterone to placebo. ConclusionsTestosterone administration during energy deficit suppressed hepcidin concentrations and increased iron utilization in healthy young males. The reduction in hepcidin with testosterone administration appears to occur through an erythroferrone-independent mechanism. Funding SourcesThe views expressed are those of the authors and do not reflect the official policy of the Army, DoD, or the U.S. Government. Supported by the Collaborative Research to Optimize Warfighter Nutrition II and III projects and the Defense Health Program Joint Program Committee-5.

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

Exercise-induced Energy Deficit Lowers Glycemia At Breakfast The Next Day, But Not Over 24-hours.

Exercise-induced Energy Deficit Lowers Glycemia At Breakfast The Next Day, But Not Over 24-hours.

Compensatory Mechanisms to Exercise Induced Energy Deficit

Compensatory Mechanisms to Exercise Induced Energy Deficit

Appetite and Energy Intake Responses to Acute Energy Deficits in Females versus Males.

ABSTRACTPurposeTo explore whether compensatory responses to acute energy deficits induced by exercise or diet differ by sex.MethodsIn experiment one, 12 healthy women completed three 9-h trials (control, exercise-induced (Ex-Def) and food restriction–induced energy deficit (Food-Def)) with identical energy deficits being imposed in the Ex-Def (90-min run, ∼70% of V˙O2max) and Food-Def trials. In experiment two, 10 men and 10 women completed two 7-h trials (control and exercise). Sixty minutes of running (∼70% of V˙O2max) was performed at the beginning of the exercise trial. The participants rested throughout the remainder of the exercise trial and during the control trial. Appetite ratings, plasma concentrations of gut hormones, and ad libitum energy intake were assessed during main trials.ResultsIn experiment one, an energy deficit of approximately 3500 kJ induced via food restriction increased appetite and food intake. These changes corresponded with heightened concentrations of plasma acylated ghrelin and lower peptide YY3–36. None of these compensatory responses were apparent when an equivalent energy deficit was induced by exercise. In experiment two, appetite ratings and plasma acylated ghrelin concentrations were lower in exercise than in control, but energy intake did not differ between trials. The appetite, acylated ghrelin, and energy intake response to exercise did not differ between men and women.ConclusionsWomen exhibit compensatory appetite, gut hormone, and food intake responses to acute energy restriction but not in response to an acute bout of exercise. Additionally, men and women seem to exhibit similar acylated ghrelin and PYY3–36 responses to exercise-induced energy deficits. These findings advance understanding regarding the interaction between exercise and energy homeostasis in women.

Energy replacement diminishes the effect of exercise on postprandial lipemia in boys

PurposeAcute bouts of exercise reduce postprandial triacylglycerol concentrations ([TAG]) in healthy boys and girls; however, it is not known whether this effect is mediated by the energy deficit. This study examined whether the exercise-induced reduction in postprandial [TAG] persists after immediate dietary replacement of the exercise energy expenditure (EE). MethodsEighteen healthy 11- to 13-year-old boys (mean (SD): body mass 41.3 (8.4)kg; peak oxygen uptake (V̇O2) 55 (5)mL·kg−1·min−1) completed three, 2-day conditions in a within-measures, crossover design separated by 14days. On day 1, participants rested (CON), exercised at 60% peak V̇O2 inducing a net EE of 32kJ·kg−1 body mass (EX-DEF) or completed the same exercise with the net EE replaced immediately (EX-REP). On day 2, capillary blood samples were taken in the fasted state and at pre-determined intervals throughout the 6.5h postprandial period. A standardised breakfast and lunch meal were consumed immediately and 4h, respectively, after the fasting sample. ResultsBased on ratios of the geometric means (95% confidence intervals (CI) for ratios), EX-DEF fasting [TAG] was 19% and 15% lower than CON (−32 to −4%, ES=1.15, P=0.02) and EX-REP (−29 to 0%, ES=0.91, P=0.05) respectively; CON and EX-REP were similar (−4%; P=0.59). The EX-DEF total area under the [TAG] versus time curve was 15% and 16% lower than CON (−27 to 0%, ES=0.55, P=0.05) and EX-REP (−29 to −2%, ES=0.62, P=0.03) respectively; CON and EX-REP were not different (2%; −13 to 20%, P=0.80). ConclusionImmediate replacement of the exercise-induced energy deficit negates the reduction in postprandial [TAG] in boys; this highlights the importance of maintaining a negative energy balance immediately post-exercise to maximise the metabolic health benefits of exercise.

Predictors of Energy Compensation during Exercise Interventions: A Systematic Review

Weight loss from exercise-induced energy deficits is usually less than expected. The objective of this systematic review was to investigate predictors of energy compensation, which is defined as body energy changes (fat mass and fat-free mass) over the total amount of exercise energy expenditure. A search was conducted in multiple databases without date limits. Of 4745 studies found, 61 were included in this systematic review with a total of 928 subjects. The overall mean energy compensation was 18% ± 93%. The analyses indicated that 48% of the variance of energy compensation is explained by the interaction between initial fat mass, age and duration of exercise interventions. Sex, frequency, intensity and dose of exercise energy expenditure were not significant predictors of energy compensation. The fitted model suggested that for a shorter study duration, lower energy compensation was observed in younger individuals with higher initial fat mass (FM). In contrast, higher energy compensation was noted for younger individuals with lower initial FM. From 25 weeks onward, energy compensation was no longer different for these predictors. For studies of longer duration (about 80 weeks), the energy compensation approached 84%. Lower energy compensation occurs with short-term exercise, and a much higher level of energy compensation accompanies long-term exercise interventions.