Effects of High-Intensity Intermittent Exercise Training on Appetite Regulation AARON Y. SIM1, KAREN E. WALLMAN1, TIMOTHY J. FAIRCHILD2, and KYM J. GUELFI1 1 School of Sport Science, Exercise and Health, University of Western Australia, Perth, Western Australia, AUSTRALIA; and 2School of Psychology and Exercise Science, Murdoch University, Perth, Western Australia, AUSTRALIA
ABSTRACT SIM, A. Y., K. E. WALLMAN, T. J. FAIRCHILD, and K. J. GUELFI. Effects of High-Intensity Intermittent Exercise Training on Appetite Regulation. Med. Sci. Sports Exerc., Vol. 47, No. 11, pp. 2441–2449, 2015. Objective: An acute bout of high-intensity intermittent exercise suppresses ad libitum energy intake at the postexercise meal. The present study examined the effects of 12 wk of high-intensity intermittent exercise training (HIIT) compared with moderate-intensity continuous exercise training (MICT) on appetite ˙ O2peak, 35.3 T 5.3 mLIkgj1Iminj1) were regulation. Methods: Thirty overweight inactive men (body mass index, 27.2 T 1.3 kgImj2; V randomized to either HIIT or MICT (involving 12 wk of training, three sessions per week) or a control group (CON) (n = 10 per group). Ad libitum energy intake from a laboratory test meal was assessed after both a low-energy (847 kJ) and a high-energy preload (2438 kJ) before and after the intervention. Perceived appetite and appetite-related blood variables were also measured. Results: There was no significant effect of the intervention period on energy intake at the test meal after the two different preloads (P Q 0.05). However, the 95% confidence interval indicated a clinically meaningful decrease in energy intake after the high-energy preload compared with the lowenergy preload in response to HIIT (516 T 395 kJ decrease), but not for MICT or CON, suggesting improved appetite regulation. This was not associated with alterations in the perception of appetite or the circulating concentration of a number of appetite-related peptides or metabolites, although insulin sensitivity was enhanced with HIIT only (P = 0.003). Conclusions: HIIT seems to benefit appetite regulation in overweight men. The mechanisms for this remain to be elucidated. Key Words: ENERGY INTAKE, INSULIN SENSITIVITY, APPETITE-RELATED HORMONES, PRELOAD, OVERWEIGHT, INACTIVE
individuals by promoting more sensitive eating behavior in response to previous energy intake. Similar improvements in appetite regulation have been reported in inactive overweight participants in response to 12 wk of aerobic exercise training (five sessions per week at approximately 75% of HRmax) (24). However, there is evidence that the benefits of exercise training for appetite regulation may be optimized by manipulating the specific type of exercise used. For instance, Guelfi et al. (9) found that 12 wk (three sessions per week) of aerobic-based exercise training (stationary cycling and elliptical cross training at approximately 70%–80% of HRmax) increased both fasting and postprandial ratings of perceived fullness whereas an equivalent period of resistance training (machine and free weights) did not. Another important aspect of exercise prescription that may influence appetite regulation is the intensity of training. Support for this notion comes from a recent study by our laboratory showing that an acute bout of intermittent highintensity exercise (consisting of repeated bouts of 15 s at ˙ O2peak with an active recovery period approximately 170% V ˙ O2peak) attenuated energy of 60 s at approximately 32% V intake in the postexercise meal compared with a bout of continuous moderate-intensity exercise (approximately 60% ˙ O2peak) of matched total work and a resting control in V overweight and inactive men (30). The lower energy intake after intermittent exercise was associated with reduced active
Address for correspondence: Aaron Sim, Ph.D., School of Sport Science, Exercise and Health, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia; E-mail: [email protected]. Submitted for publication November 2014. Accepted for publication April 2015. 0195-9131/15/4711-2441/0 MEDICINE & SCIENCE IN SPORTS & EXERCISEÒ Copyright Ó 2015 by the American College of Sports Medicine DOI: 10.1249/MSS.0000000000000687
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A
growing body of research has demonstrated a link between exercise and the physiological mechanisms controlling appetite and energy intake, with inactivity potentially contributing to a positive energy balance and subsequent weight gain (18,22,31). Conversely, it is widely acknowledged that exercise plays a prominent role in weight management by 1) contributing to a negative energy balance by increasing energy expenditure (3,4,27) and 2) having a favorable influence on the sensitivity of appetite regulation (25), the total amount of energy consumed (30), feelings of hunger and fullness (3,9), and the circulating levels of a number of appetite-related hormones (1,3). More specifically, Martins et al. (25) demonstrated that 6 wk of moderate-intensity aerobic exercise training (four sessions per week at approximately 65%–75% of HRmax) improved appetite regulation in previously inactive normal-weight
ghrelin, together with elevated blood lactate and glucose. In addition, free-living energy intake in the 48 h after leaving the laboratory remained lower after the intermittent exercise compared with moderate continuous exercise and control. Whether these acute benefits of intermittent high-intensity exercise translate to differences in long-term appetite regulation and weight loss remains to be determined. Therefore, the purpose of this study was to examine the effect of 12 wk of supervised exercise (high-intensity intermittent exercise training (HIIT) compared with continuous moderate-intensity training (MICT) and a no-exercise control) on appetite regulation (using the high-energy vs low-energy preload test meal paradigm), perceptions of appetite and the circulating concentrations of appetite-related hormones (particularly active ghrelin, leptin, insulin, pancreatic peptide (PP), and peptide tyrosine tyrosine (PYY)) in the fasted state and in response to caloric consumption in previously inactive overweight men. It was hypothesized that 12 wk of supervised exercise would improve appetite regulation (i.e., promote more sensitive eating behavior) compared with a no-exercise control but that the improvement would be to a greater extent in response to HIIT compared with MICT.
METHODS
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Participants Thirty overweight, physically inactive men (age, 31T 8 yr; ˙ O2peak, 35.3 T body mass index (BMI), 27.2 T 1.3 kgImj2; V j1 j1 5.3 mLIkg Imin ) were recruited from the local community. Physical inactivity was defined as not engaging in moderate-intensity exercise for more than 75 minIwkj1 (35). To minimize any influence of dietary restraint on the results, participants were excluded if they scored Q3.5 on the restraint scale of the Dutch Eating Behavior Questionnaire (33). Ethics approval was granted by the human research ethics committee at the University of Western Australia, and a written consent was obtained from all participants. Study Design Participants were randomly allocated (using a random number generator software (32) into one of the following three experimental groups: 1) HIIT, 2) MICT, or 3) no exercise training control (CON). Appetite regulation was assessed before and after the intervention on the basis of a preload-test meal paradigm, originally introduced by Schachter et al. (29) (involving the assessment of ad libitum energy intake in response to previous energy intake of differing caloric contents). The effect of the intervention period on perceived appetite, appetite-related blood variables, free-living energy intake, physical activity levels, anthropometric measures, aerobic fitness, dietary restraint, and physical activity enjoyment were also assessed. Baseline testing and familiarization. Participants completed an initial baseline testing and familiarization session. This included the assessment of 1) body composition
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using dual-energy x-ray absorptiometry (GE Lunar Prodigy Vision; GE Medical Systems, Madison, WI), 2) peak aero˙ O2peak) using a continuous incremental bic capacity (V exercise test performed on an air-braked cycle ergometer as previously described (30), 3) dietary restraint via the Dutch Eating Behavior Questionnaire (33), and 4) whether they were regular breakfast consumers (Q5 times per week). Familiarization with the questionnaires and protocols to be used for the subsequent assessment of pre- and postintervention outcome measures (i.e., blood sampling, laboratory test meal) was also performed during this session to minimize the novelty of these tasks. Body compo˙ O2peak, and dietary restraint were reassessed at the sition, V end of the study period. Pre- and postintervention testing. Participants attended the laboratory at approximately 0700 h, having fasted for 10–12 h, on two separate occasions both before and after intervention (i.e., four visits in total) for the assessment of outcomes measures. In the 24 h before the first visit, participants were required to document their food and drink consumption and to refrain from vigorous physical activity. The documented dietary information was reviewed by the investigator upon arrival at the laboratory, and participants were instructed to replicate their food and drink intake before each subsequent visit, with compliance confirmed by the inspection of the records upon arrival to the laboratory and later nutritional analyses. All postintervention testing was conducted within the week and at least 48 h after the last training session. Enjoyment of physical activity was assessed before and after intervention (i.e., first and final exercise training session) via the Physical Activity Enjoyment Scale (16). Preload test meal. Upon arrival at the laboratory, participants were provided with either a high-energy preload (HEP, 2438 kJ) or low-energy preload (LEP, 847 kJ) in a counterbalanced, single-blind design (preloads were of similar volume and sensory properties for consumption). The HEP consisted of 250 mL of UP&GOÒ liquid breakfast (Sanitariumi; Berkeley Vale, New South Wales, Australia), 100 g of maltodextrin (Poly-JouleÒ; Nutricia, Macquarie Park, New South Wales, Australia), and approximately 100 mL of water to make a total volume of 450 mL, whereas the LEP consisted of 250-mL UP&GOÒ liquid breakfast, 2 g of ResourceÒ ThickenUpi Clear (Nestle´, Notting Hill, Victoria, Australia), 5-mL SugarlessÒ Liquid Sweetener, (Sugarlessi, Chipping Norton, New South Wales, Australia), and approximately 193-mL water to make a total volume of 450 mL. Participants remained seated for 70 min after consuming the preload, at which point they were given access to a laboratory test meal for 20 min, during which time they were instructed to consume ad libitum until they felt ‘‘comfortably full.’’ The test meal consisted of porridge made from a mixture of instant oats (Oats Quick Sachet—Creamy Honey; Uncle TobysÒ, Nestle´, Rhodes, New South Wales, Australia) and milk (HiLo Milk; PuraÒ, Melbourne, Victoria, Australia) of known quantity and nutrition content. In favor of external
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activity based on accelerometry were determined using ActiLife software (ActiGraph, Pensacola, FL). Exercise intervention. Both exercise training groups (HIIT and MICT) were required to participate in three training sessions each week over 12 wk. All training was conducted on calibrated front-access air-braked cycle ergometers (model EX-10; Repco Cycle, Huntingdale, Victoria, Australia) that were interfaced with a customized software program (Cyclemax; School of Sport Science, Exercise and Health, University of Western Australia, Perth, Western Australia, Australia). Participants randomized to HIIT were required to complete repeated bouts of high-intensity exercise (15 s at a power output equivalent to approximately ˙ O2peak) with an active recovery period (60 s at a power 170% V ˙ O2peak) between efforts. This output approximately 32% V protocol was intended to replicate the intensity and duration of intervals (and corresponding work-to-recovery ratio) shown to attenuate short-term ad libitum energy intake in our previous study (30). Participants allocated to MICT exercised ˙ O2peak continuously for at a power output equivalent to 60% V the duration of each training session. Relative total work was matched between exercise protocols, and the workload for each participant was determined using their individual base˙ O2peak results. line V All training sessions were fully supervised by an exercise physiologist (A.Y.S.). Training sessions commenced with a 5-min warm-up that involved easy pedaling followed by light static/dynamic stretching of the lower limbs. Heart rate (HR) and rating of perceived exertion (RPE) were measured during each exercise session. To accommodate for an increase in fitness throughout the intervention period, the workload and duration of the training sessions were progressively increased. Training workloads were adjusted on the basis of a conservative 1% improvement in aerobic capacity per week, whereas duration progressed as follows: weeks 1–3 (30 min), weeks 4–6 (35 min), weeks 7–9 ˙ O2peak (40 min), and weeks 10–12 (45 min). In addition, the V test was repeated during week 6 of the intervention and training workloads were further adjusted accordingly. Statistical Analysis Insulin sensitivity was calculated using the homeostatic model assessment (HOMA-IR) index (based on fasting blood glucose and insulin concentration) (34). Repeated-measures ANOVA were used to compare the estimated energy intake and energy expenditure for the 24 h before each laboratory visit for the assessment of outcome measures to confirm that these factors were well matched. Mixed-model ANOVA was applied to determine treatment effects for each outcome variable, as follows: 1) two-way (pre- vs postintervention condition (HIIT, MICT, and CON)) for aerobic fitness, anthropometric measures, physical activity enjoyment, and dietary restraint, 2) three-way (pre- vs postintervention preload (HEP vs LEP) condition) for energy intake at the laboratory test meal and 24-h cumulative energy intake, 3)
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validity (i.e., there is typically free access to water intake when consuming a meal), a standardized bottle of plain drinking water (approximately 1000 mL) was also available for ad libitum consumption. The porridge and drinking water were weighed before and after consumption. Measures were taken to minimize the influence of environmental factors on eating behavior as previously described (30). Assessment of perceptions of appetite. Subjective perceptions of appetite (fullness, hunger, satiation, desire to eat, and prospective food consumption) were assessed using a 100-mm visual analog scale (13) in the fasted state (before preload consumption) and in response to caloric consumption (immediately and 30, 60, and 90 min after preload). Assessment of appetite-related blood variables. Blood was sampled in the fasted state (before preload consumption) and in response to caloric consumption (30 and 60 min after preload). To prepare the sampling site, the entire hand was placed into a box heated with warm air (approximately 60-C). Capillary blood (535 KL) was then collected from the warmed fingertip using a sterile lancet (Unistik 2 Normal; Owen Mumford, Oxford, United Kingdom). Blood glucose concentration was measured using a blood gas analyzer (35-KL ABL 735; Radiometer, Copenhagen, Denmark). The remaining blood was treated with EDTA (Microtainer Tubes with K2E (K2EDTA); BD Microtainer, Franklin Lakes, NJ) and serine protease inhibitor (20 KL per 500 KL of blood; Pefabloc SC, Roche Diagnostics, Sydney, New South Wales, Australia) before being centrifuged at 1020g for 10 min. Plasma obtained was stored at approximately j80-C, and samples from the HEP condition only were later analyzed for a range of appetiterelated hormones leptin, insulin, active ghrelin, PP, and PYY using a commercially available assay kit (Milliplex Map Human Metabolic Hormone Magnetic Bead Panel; Millipore Corporation, Billerica, MA). The minimum detectable concentrations of the respective peptides are as follows: ghrelin, 1.8 pgImLj1; leptin, 157.2 pgImLj1; PP, 2.4 pgImLj1; PYY, 8.4 pgImLj1; insulin, 44.5 pgImLj1. The intraassay variation (%coefficient of variation) of the Milliplex multiplex assay is G11%. Assessment of free-living energy intake and physical activity levels. Free-living energy intake and physical activity levels in the 24 h before and for the remainder of the day after leaving the laboratory sessions were assessed using a self-recorded food diary and accelerometry (GT1M Activity Monitor; ActiGraph, Pensacola, FL), respectively. The food diary required participants to record the portion size (weighing scales were provided to assist) and describe the food consumed. Detailed instructions on the use of the food diary and the necessity for timely and accurate recordings after food and drink consumption were emphasized. Energy intake from food records was calculated using a commercially available software program (Foodworks; Xyris Software, Queensland, Australia). The total number of steps and estimated energy expenditure from physical
TABLE 1. Aerobic fitness and body composition before and after 12 wk of HIIT (n = 10), MICT (n = 10), or no exercise training control (CON, n = 10). HIIT V˙O2peak (mLIkgj1Iminj1) Body mass (kg) BMI (kgImj2) Body fat percentage (%)
Preintervention Postintervention Preintervention Postintervention Preintervention Postintervention Preintervention Postintervention
34.8 40.4 87.4 86.6 27.4 27.1 32.0 30.9
T 4.5 T 4.4*,** T 7.7 T 7.5 T 1.6 T 1.4 T 2.9 T 2.7
MICT 34.8 T 39.7 T 86.5 T 85.9 T 27.2 T 27.0 T 31.1 T 30.2 T
CON
6.2 6.9*,** 8.6 8.5 1.5 2.3 5.0 6.5
36.3 35.8 85.6 87.1 27.0 27.5 32.2 32.5
T 5.6 T 5.5 T 6.4 T 6.7 T 0.9 T 0.9** T 3.9 T 3.9
Values are presented as mean T SD. *Indicates significant difference from preintervention (P e 0.050). **Indicates moderate-to-large Cohen d effect size from preintervention.
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four-way (pre- vs postintervention preload time (0 min, immediately after preload, 30 min after preload, 60 min after preload, and 90 min post-preload) condition) for perceived appetite, and 4) three-way (pre-vs postintervention time (0 min, 30 min after preload, and 60 min after preload) condition) for appetite-related hormone concentration in response to caloric intake. The effect of the intervention and condition (HIIT, MICT, and CON) on HR and RPE was assessed using a mixed-model ANOVA. Post hoc comparisons were conducted where appropriate. Statistical significance was accepted at P e 0.050 (SPSS version 20; IBM Corporation, Armonk, NY). In addition, 95% confidence intervals (CI) were presented as follows: lower bound value–upper bound value. Furthermore, Cohen d effect sizes (d) were also calculated for pairwise comparisons; only moderate (0.50–0.79) and large (90.80) effect sizes are reported. All results are presented as mean T SD, unless otherwise indicated.
RESULTS There were no dropouts in any of the treatment groups, with every participant in the study completing all the required testing sessions. Furthermore, training attendance was similar between groups (P = 0.712), with 98% T 3% (mean, 35 of 36 sessions; minimum, 33 sessions) compliance for HIIT and 97% T 4% (mean, 35 of 36; minimum, 33 sessions) for MICT. Training intervention. A main effect of condition revealed higher average HR (P G 0.001) and RPE (P = 0.034) during HIIT (HR, 158 T 3 bpm; RPE, 14 T 1) compared with MICT (HR, 133 T 5 bpm; RPE, 13 T 1). A main effect of training time point showed that average HR (P G 0.001) and
RPE (P G 0.001) increased through the course of both training interventions. ˙ O2peak was improved in After the 12-wk study period, V both the HIIT and MICT groups (P G 0.001) (Table 1) to a similar extent but remained unchanged in the CON group. There were no significant changes in anthropometric measures (body mass, P = 0.234; BMI, P = 0.204; body fat, P = 0.187) in response to the interventions (Table 1). With respect to the enjoyment of exercise, there was a main effect of the exercise intervention period (P = 0.006), with an increase in enjoyment after intervention compared with baseline (preintervention, 93 T 15; postintervention, 102 T 13; d = 0.64); however, there was no difference between HIIT and MICT (P = 0.172). Furthermore, there was no interaction effect of pre- vs postintervention condition on dietary restraint (pre- vs postintervention, HIIT: 2.7 T 0.4 vs 2.6 T 0.5; MICT, 2.4 T 0.6 vs. 2.5 T 0.8; CON, 2.2 T 0.5 vs 2.4 T 0.5; P = 0.829). Ad libitum energy intake at the laboratory test meal. Energy intake and energy expenditure from physical activity in the 24 h before each preload test session were well-matched (energy intake = 8327 T 2191 kJ, P = 0.416; energy expenditure = 1905 T 573 kJ, P = 0.768). Likewise, the environmental conditions were consistent during the preload test sessions (temperature = 21.3-C T 0.9-C, P = 0.996; humidity = 52.6% T 7.2 %, P = 0.700). Absolute ad libitum energy intake during the laboratory test meal after the HEP and LEP assessed pre- and postintervention is shown in Figure 1, with differences in energy intake pre- and postintervention displayed in Table 2. Energy intake during the test meal after the two different preloads was similar at baseline in all groups (P = 0.396),
FIGURE 1—Mean (T SE) ad libitum energy intake at laboratory test meal after HEP and LEP before (preintervention) and after (postintervention) 12 wk of HIIT, MICT, or no exercise training (CON) (n = 10 in each group).
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TABLE 2. Difference in ad libitum energy intake from a laboratory test meal and cumulative 24-h energy intake (kJ) after HEP and LEP before and after 12 wk of HIIT, MICT, or no exercise training (CON; n = 10 in each group). Study Time Point/Preload $ Energy intake at test meal (i.e., HEP j LEP) $ 24-h energy intake (i.e., HEP j LEP) $ Energy intake at test meal (i.e., preintervention j postintervention) $ 24-h energy intake (i.e., preintervention j postintervention)
Preintervention Postintervention Preintervention Postintervention HEP LEP HEP LEP
HIIT x¯ T SD (95% CI) j43 j516 402 186 517 43 928 712
T 585 (320, j406) T 395 (j271, j762) T 1597 (1392, j588) T 1108 (873, j500) T 736 (61, 973) T 640 (j354, 439) T 1590 (j58, 1913) T 1241 (j57, 1481)
MICT x¯ T SD (95% CI) 219 j68 649 j617 199 j89 758 j509
T 523 (544, j105) T 677 (351, j488) T 2103 (1953, j654) T 2445 (898, j2133) T 1043 (j447, 845) T 783 (j574, 397) T 1917 (j430, 1946) T 1265 (j1293, 275)
CON x¯ T SD (95% CI) j88 T j66 T j204 T 265 T j223 T j202 T j199 T 104 T
494 (218, j394) 688 (360, j493) 1054 (449, j857) 1345 (1099, j569) 628 (j612, 166) 736 (j658, 254) 648 (j601, 203) 1354 (j735, 943)
Values are presented as mean (x¯) and 95% CI for preintervention energy intake minus postintervention energy intake (lower bound, upper bound). Where the 95% CI does not cross zero, the value was set in bold.
Appetite-related blood variables. An interaction effect of pre- versus postintervention time condition was observed for insulin (P = 0.050) (Fig. 3A), with post hoc analysis revealing lower insulin concentration in a fasted state after HIIT (P = 0.003, d = 0.60) and 60 min after caloric consumption in MICT (P = 0.010, d = 0.77) compared with preintervention. There was an interaction effect of preversus postintervention condition on leptin (P = 0.017) (Fig. 3B), revealing lower leptin concentration after HIIT but not after MICT and CON. There were no interaction effects observed for active ghrelin (P = 0.736) (Fig. 4A), PP (P = 0.060) (Fig. 4B), PYY (P = 0.077) (Fig. 4C), or blood glucose (P = 0.926) (Fig. 4D). However, there was a main effect of test session time (P e 0.001) for each of these blood variables, with increased PP, PYY, insulin, and blood glucose in response to caloric consumption, whereas active ghrelin and leptin decreased over time. HOMA-IR was similar between groups at baseline (P = 0.48). There was an interaction effect of pre- versus postintervention condition on HOMA-IR (P = 0.016), with post hoc analysis revealing significantly lower HOMA-IR after HIIT (pre, 3.8 T 1.9; post, 2.9 T 1.6; P = 0.018; d = 0.61) but not for MICT and CON.
DISCUSSION The main aim of the present study was to compare the effects of 12 wk of HIIT with an equivalent period of MICT or inactivity on appetite regulation in previously inactive overweight men. There were no statistically significant
FIGURE 2—Mean (T SE) cumulative 24-h energy intake after HEP and LEP before (preintervention) and after (postintervention) 12 wk of HIIT, MICT, or no exercise training (CON) (n = 10 in each group).
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suggesting a lack of appropriate compensation for previous energy intake. With respect to the effect of the intervention period on energy intake from the test meals, there was no significant interaction of pre- versus postintervention preload condition (P = 0.333); however, the 95% CI indicated a decrease in energy intake after the HEP after 12 wk of HIIT compared with the LEP postintervention (Table 2), suggesting a tendency for enhanced appetite regulation based on more appropriate adjustment for previous energy intake. There was no difference in ad libitum water intake at the laboratory test meal between trials (P = 0.601). Cumulative 24-h energy intake. Cumulative energy intake for the remainder of the day after the ad libitum laboratory meal is shown in Figure 2, and the differences in cumulative energy intake before to after intervention are presented in Table 2. Cumulative energy intake values after the two different preloads were similar at baseline in all groups (P = 0.644). The interaction effect of pre- versus postintervention preload condition on cumulative energy intake over 24 h was not significant (P = 0.082). Perception of appetite. There were no significant interactions of pre- versus postintervention preload time condition on perceived hunger (P = 0.691), fullness (P = 0.260), satiation (P = 0.352), desire to eat (P = 0.434), or prospective food consumption (P = 0.657; results not displayed). However, there was a main effect of time within each test session for each of these variables (P G 0.001), with increased feelings of fullness and satiation along with decreased hunger, desire to eat, and prospective food consumption after the test meal.
FIGURE 3—Mean (T SE) concentrations of insulin (A) and leptin (B) in the fasted state (time, 0 min) and in response to caloric consumption (indicated by an upward arrow, j) before (represented by black circles, ) and after (represented by white circles, )) 12 wk of HIIT, MICT, or no exercise training control (CON) (n = 10 in each group). #Significantly different from preintervention. *Significant interaction effect of pre- vs postintervention, test session time (0, 35, and 65 min), and condition (HIIT, MICT, and CON). †Significant main effect of test session time point (0, 35, and 65 min) is different from preintervention (P e 0.050).
the test meal after the HEP compared with LEP in response to HIIT but not for MICT or CON. The tendency for lower energy intake after HEP compared with LEP in response to HIIT suggests improved appetite regulation (based on a more appropriate adjustment of energy intake in response to
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differences in energy intake at the laboratory test meal or cumulative energy intake after leaving the laboratory as a result of the intervention period. However, the 95% CI indicated improved appetite regulation after HIIT on the basis of a clinically meaningful decrease (14) in energy intake at
FIGURE 4—Mean (T SE) concentrations of active ghrelin (A), PP (B), PYY (C), and glucose (D) in the fasted state (time, 0 min) and in response to caloric consumption (indicated by upward arrow, j) before (represented by black circles, ) and after (represented by white circles, )) 12 wk of HIIT, MICT, or no exercise training control (CON) (n = 10 in each group). †Significant main effect of test session time point (0, 35, and 65 min) is different from preintervention (P e 0.050).
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This is in contrast with the reported increases in fasting and postprandial feelings of fullness in the study by Guelfi et al. (9) after an aerobic exercise intervention of similar duration and frequency to that used here. With respect to the appetite-related blood variables, we observed attenuated insulin concentration in a fasted state after HIIT and in a postprandial state after MICT compared with preintervention. However, improved insulin sensitivity (based on the HOMA-IR index) was only noted after HIIT but not after MICT. Given that insulin sensitivity has been reported to have a negative relation with ad libitum energy intake during a test meal in an overweight population (8,12), the tendency for enhanced appetite regulation after HIIT may be mediated by improved insulin sensitivity. Our findings are in line with those of Matinhomaee et al. (26), who also reported that 12 wk of HIIT improved insulin sensitivity (HOMA-IR index). Importantly, the present study may lend further support to the role of aerobic exercise training as a first line of defense in the management of insulin resistance. The decrease in leptin concentration after HIIT may be associated with the fat loss (although not significant) observed in the HIIT group (19). In contrast, active ghrelin, PP, and PYY were not altered in response to the intervention period. The lack of response of these appetite-related hormones after aerobic exercise training is consistent with the study of Guelfi et al. (9), who reported no change in active ghrelin, PP, and PYY concentration in sedentary overweight/ obese men after 12 wk of aerobic exercise training (three times weekly at 70%–80% of HRmax). In contrast, Martins et al. (23) reported that 12 wk of aerobic training (five times per week at 75% of HRmax) resulted in a significant increase in fasting acylated ghrelin concentration, together with feelings of hunger in sedentary overweight/obese men and women. Reasons that may explain the discrepancy in outcomes between these studies include differences in the volume of exercise performed and the characteristics of the participants. For instance, the study by Martins et al. (23) involved exercise training five times per week compared with three times per week in the study of Guelfi et al. (9) and the present study. Furthermore, given that active ghrelin has been shown to respond differently to aerobic exercise training in men and women (higher active ghrelin concentration in women) (11), the inclusion of women in the study by Martins et al. (23) may partially explain the difference in findings. Regardless, this raises the question of the potential mechanisms besides appetite-related blood variables that may have contributed to the tendency for enhanced appetite regulation after HIIT. Firstly, it should be acknowledged that the range of appetite-related peptides measured in this present study was not exhaustive and other appetite-related hormones such as glucagon-like peptide 1, cholecystokinin, and obestatin also influence appetite regulation. Furthermore, a series of recent studies have suggested that exercise may have a dampening effect (attenuated neural activity) on the food reward pathways located in the brain, which is consistent with reduced general palatability of food, reduced anticipation to eat, and
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previous caloric consumption). No significant changes in the perception of appetite were noted as a result of the intervention, and the circulating concentrations of glucose, active ghrelin, PP, and PYY were not altered across the intervention period. However, insulin was lower after both exercise interventions (fasting—HIIT, postprandial—MICT) but unaltered in CON, whereas leptin was reduced after HIIT only. Both exercise interventions resulted in a significant increase in aerobic fitness. Previous research has demonstrated improved appetite regulation in response to a period of aerobic exercise training (24,25). However, to our knowledge, this is the first study that has compared the effect of different types of exercise training (specifically HIIT with MICT) on appetite regulation. Despite no significant interaction effects being observed in energy intake in response to the intervention, the reported 95% CI suggests (i.e., lower and upper bound values do not cross zero) that 12 wk of HIIT improved appetite regulation in response to previous energy intake of differing caloric content. Specifically, participants ate less at the test meal after HEP compared with that after LEP (by 516 T 395 kJ) after the HIIT intervention, whereas intake remained unaltered in the MICT and CON groups. When comparing the preintervention and postintervention energy intake at the test meals, it is evident that this compensation was related to a reduction in energy intake after the postintervention HEP test meal compared with preintervention in the HIIT group (517 T 736 kJ decrease). Considering that an energy deficit of 419 kJIdj1 and 795 kJIdj1 has been calculated to prevent weight gain (maintain weight loss) and achieve weight loss, respectively (14), the energy deficits presented previously may be considered a clinically meaningful and important consideration for weight management. However, it is important to note that despite the mentioned changes in energy intake in the meal directly after the HEP or LEP, there were no significant differences in cumulative energy intake for the remainder of the day between preloads or conditions. This may be related to the level of accuracy of assessing energy intake at a laboratory test meal compared with that obtained from self-reported food diaries, with the former being a more precise measure. The lack of improvement in appetite regulation (based on the similar energy intake after HEP vs LEP) observed after MICT in the present study is in contrast with previous research of similar duration (24,25). Martins et al. (24) reported a significant within-group improvement in 24-h cumulative energy compensation after 12 wk of MICT. This discrepancy between studies may be explained by differences in the volume of exercise performed. The study of Martins et al. (23) involved exercise training five times per week compared with three times per week in the present study. Of note, exercise intensities used in both studies were similar; Martins et al. ˙ (24), 75% HRmax, versus present study, 60% VO 2peak (21). In addition, it was surprising that the tendency for improved appetite regulation in response to HIIT in the present study was not accompanied by changes in perception of appetite.
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reduced food consumption (5–7). Specifically, Crabtree et al. (6) demonstrated that high-intensity exercise resulted in suppressed neural responses during the viewing of highcalorie foods. Another potential mechanism by which regular exercise training may enhance appetite regulation is via changes to substrate metabolism, particularly increased fatty acid oxidation, which may reduce energy intake via alterations to vagal afferent activity that report satiety signals to appetite centers in the brain (2). Furthermore, changes in psychological approaches to food may result from regular exercise. However, the lack of change in dietary restraint scores observed in the present study suggests minimal influence of eating attitudes on appetite regulation. Clearly, further research is required to determine the mechanisms through which exercise training may affect and improve appetite regulation. Average HR and RPE over the course of the intervention were found to be higher during HIIT compared with those during MICT. Considering the nature of the HIIT protocol (i.e., repeated short bouts of supramaximal high-intensity exercise), this was not unexpected. Despite this, physical activity enjoyment was not different between HIIT and MICT and enjoyment was greater after both training interventions. These findings are of importance, given that enjoyment of physical activity has been reported to be a key factor in physical activity performance and exercise adherence (10,28). The high attendance rate of study participants in both exercise groups seems to reflect the levels of enjoyment observed in the present study. Our study also demonstrated that 12 wk of aerobic exercise, regardless of exercise protocol, resulted in an increase in aerobic fitness. This is significant, given that improvement in aerobic fitness, independent of weight loss, has been associated with decreased mortality (20). Finally, it should be noted that even though HIIT may have resulted in a tendency for improved appetite regulation, the lack of significant alterations in anthropometric measures
(i.e., body mass and body fat) is consistent with previous literature reporting that exercise alone may not be the most effective method for weight loss (15). However, it is important to note that the magnitude of change in body fat after HIIT (d = 0.39) was comparable with previous studies that reported statistically significant body fat loss after aerobic exercise interventions of a similar duration, as follows: Martins et al. (24), d = 0.31; Guelfi et al. (9), d = 0.22. The lack of statistical significance in the present study may be related to the method of analysis used, with the present study comparing differences within (pre vs post) and between intervention/control groups, whereas Martins et al. (24) and Guelfi et al. (9) analyzed differences within (pre vs post) the intervention groups only. More studies with a larger sample size are needed to further investigate these findings. In summary, we found that HIIT resulted in clinically meaningful improvements in appetite regulation whereas an equivalent period of MICT and CON did not. The mechanisms behind this are unclear, with no alterations in the perception of appetite or a number of circulating appetiterelated peptides and metabolites in either the fasted or postprandial state, although insulin sensitivity was enhanced in response to HIIT only. Together with previous evidence suggesting the benefits of HIIT for various comorbidities of obesity (17), findings from the present study may have important implications for current exercise prescription guidelines for individuals exercising for weight loss/maintenance and the management of insulin sensitivity.
The hormone assays were carried out with the facilities at the Centre for Microscopy, Characterisation and Analysis, University of Western Australia, that are supported by the funding of the university, state, and federal government. T. J. F. is in receipt of a McCusker Charitable Foundation grant, which was used to help defray costs of the appetite hormone assays. The authors declare no conflict of interest. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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7. Evero N, Hackett LC, Clark RD, Phelan S, Hagobian TA. Aerobic exercise reduces neuronal responses in food reward brain regions. J Appl Physiol (1985). 2012;112(9):1612–9. 8. Flint A, Gregersen NT, Gluud LL, et al. Associations between postprandial insulin and blood glucose responses, appetite sensations and energy intake in normal weight and overweight individuals: a meta-analysis of test meal studies. Br J Nutr. 2007; 98(1):17–25. 9. Guelfi KJ, Donges CE, Duffield R. Beneficial effects of 12 weeks of aerobic compared with resistance exercise training on perceived appetite in previously sedentary overweight and obese men. Metabolism. 2013;62(2):235–43. 10. Hagberg L, Lindahl B, Nyberg L, Helle´nius ML. Importance of enjoyment when promoting physical exercise. Scand J Med Sci Sports. 2009;19(5):740–7. 11. Hagobian TA, Sharoff CG, Stephens BR, et al. Effects of exercise on energy-regulating hormones and appetite in men and women. Am J Physiol Regul Integr Comp Physiol. 2009;296(2):R233–42.
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12. Han JC, Rutledge MS, Kozlosky M, et al. Insulin resistance, hyperinsulinemia, and energy intake in overweight children. J Pediatr. 2008;152(5):612–7. 13. Hill AJ, Blundell JE. Nutrients and behaviour: research strategies for the investigation of taste characteristics, food preferences, hunger sensations and eating patterns in man. J Psychiatr Res. 1982;17(2):203–12. 14. Hill JO, Peters JC, Wyatt HR. Using the energy gap to address obesity: a commentary. J Am Diet Assoc. 2009;109(11): 1848–53. 15. Jakicic JM. The effect of physical activity on body weight. Obesity (Silver Spring). 2009;17(3 Suppl):S34–8. 16. Kendzierski D, DeCarlo KJ. Physical activity enjoyment scale: two validation studies. J Sport Exerc Psy. 1991;13(1):50–64. 17. Kessler HS, Sisson SB, Short KR. The potential for high-intensity interval training to reduce cardiometabolic disease risk. Sports Med. 2012;42(6):489–509. 18. King NA, Tremblay A, Blundell JE. Effects of exercise on appetite control: implications for energy balance. Med Sci Sports Exerc. 1997;29(8):1076–89. 19. Kraemer RR, Chu H, Castracane VD. Leptin and exercise. Exp Biol Med (Maywood). 2002;227(9):701–8. 20. Lee DC, Artero EG, Sui X, Blair SN. Mortality trends in the general population: the importance of cardiorespiratory fitness. J Psychopharmacol. 2010;24(4 Suppl):27–35. 21. Londeree BR, Thomas TR, Ziogas G, Smith TD, Zhang Q. %VO2max versus %HRmax regressions for six modes of exercise. Med Sci Sports Exerc. 1995;27(3):458–61. 22. Long SJ, Hart K, Morgan LM. The ability of habitual exercise to influence appetite and food intake in response to high- and lowenergy preloads in man. Br J Nutr. 2002;87(5):517–23. 23. Martins C, Kulseng B, King NA, Holst JJ, Blundell JE. The effects of exercise-induced weight loss on appetite-related peptides and motivation to eat. J Clin Endocrinol Metab. 2010;95(4): 1609–16.
24. Martins C, Kulseng B, Rehfeld JF, King NA, Blundell JE. Effect of chronic exercise on appetite control in overweight and obese individuals. Med Sci Sports Exerc. 2013;45(5):805–12. 25. Martins C, Truby H, Morgan LM. Short-term appetite control in response to a 6-week exercise programme in sedentary volunteers. Brit J Nutr. 2007;98(4):834–42. 26. Matinhomaee H, Banaei J, Azarbayjani MA, Zolaktaf V. Effects of 12-week high-intensity interval training on plasma visfatin concentration and insulin resistance in overweight men. J Exerc Sci Fitness. 2014;12(1):20–5. 27. Okay DM, Jackson PV, Marcinkiewicz M, Papino MN. Exercise and obesity. Prim Care. 2009;36(2):379–93. 28. Ryan RM, Frederick CM, Lepes D, Rubio N, Sheldon KM. Intrinsic motivation and exercise adherence. Int J Sport Exerc Psychol. 1997;28: 335–54. 29. Schachter S, Goldman R, Gordon A. Effects of fear, food deprivation, and obesity on eating. J Pers Soc Psychol. 1968;10(2):91–7. 30. Sim AY, Wallman KE, Fairchild TJ, Guelfi KJ. High-intensity intermittent exercise attenuates ad-libitum energy intake. Int J Obes (Lond). 2014;38(3):417–22. 31. Stubbs RJ, Hughes DA, Johnstone AM, Horgan GW, King N, Blundell JE. A decrease in physical activity affects appetite, energy, and nutrient balance in lean men feeding ad libitum. Am J Clin Nutr. 2004;79(1):62–9. 32. Urbaniak GC, Plous S Research randomizer (version 3.0) [computer software]. 2011. 33. Van Strien T, Frijters JER, Bergers G, Defares PB. The Dutch Eating Behavior Questionnaire (DEBQ) for assessment of restrained, emotional, and external eating behavior. Int J Eat Disorder. 1986;5(2):295–315. 34. Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care. 2004;27(6):1487–95. 35. World Health Organization. Physical activity and adults. Available from: http://www.who.int/dietphysicalactivity/factsheet_adults/en/. Accessed 13 Oct 2014]. 2014.
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EXERCISE TRAINING AND APPETITE REGULATION
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ABSTRACT SIM, A. Y., K. E. WALLMAN, T. J. FAIRCHILD, and K. J. GUELFI. Effects of High-Intensity Intermittent Exercise Training on Appetite Regulation. Med. Sci. Sports Exerc., Vol. 47, No. 11, pp. 2441–2449, 2015. Objective: An acute bout of high-intensity intermittent exercise suppresses ad libitum energy intake at the postexercise meal. The present study examined the effects of 12 wk of high-intensity intermittent exercise training (HIIT) compared with moderate-intensity continuous exercise training (MICT) on appetite ˙ O2peak, 35.3 T 5.3 mLIkgj1Iminj1) were regulation. Methods: Thirty overweight inactive men (body mass index, 27.2 T 1.3 kgImj2; V randomized to either HIIT or MICT (involving 12 wk of training, three sessions per week) or a control group (CON) (n = 10 per group). Ad libitum energy intake from a laboratory test meal was assessed after both a low-energy (847 kJ) and a high-energy preload (2438 kJ) before and after the intervention. Perceived appetite and appetite-related blood variables were also measured. Results: There was no significant effect of the intervention period on energy intake at the test meal after the two different preloads (P Q 0.05). However, the 95% confidence interval indicated a clinically meaningful decrease in energy intake after the high-energy preload compared with the lowenergy preload in response to HIIT (516 T 395 kJ decrease), but not for MICT or CON, suggesting improved appetite regulation. This was not associated with alterations in the perception of appetite or the circulating concentration of a number of appetite-related peptides or metabolites, although insulin sensitivity was enhanced with HIIT only (P = 0.003). Conclusions: HIIT seems to benefit appetite regulation in overweight men. The mechanisms for this remain to be elucidated. Key Words: ENERGY INTAKE, INSULIN SENSITIVITY, APPETITE-RELATED HORMONES, PRELOAD, OVERWEIGHT, INACTIVE
individuals by promoting more sensitive eating behavior in response to previous energy intake. Similar improvements in appetite regulation have been reported in inactive overweight participants in response to 12 wk of aerobic exercise training (five sessions per week at approximately 75% of HRmax) (24). However, there is evidence that the benefits of exercise training for appetite regulation may be optimized by manipulating the specific type of exercise used. For instance, Guelfi et al. (9) found that 12 wk (three sessions per week) of aerobic-based exercise training (stationary cycling and elliptical cross training at approximately 70%–80% of HRmax) increased both fasting and postprandial ratings of perceived fullness whereas an equivalent period of resistance training (machine and free weights) did not. Another important aspect of exercise prescription that may influence appetite regulation is the intensity of training. Support for this notion comes from a recent study by our laboratory showing that an acute bout of intermittent highintensity exercise (consisting of repeated bouts of 15 s at ˙ O2peak with an active recovery period approximately 170% V ˙ O2peak) attenuated energy of 60 s at approximately 32% V intake in the postexercise meal compared with a bout of continuous moderate-intensity exercise (approximately 60% ˙ O2peak) of matched total work and a resting control in V overweight and inactive men (30). The lower energy intake after intermittent exercise was associated with reduced active
Address for correspondence: Aaron Sim, Ph.D., School of Sport Science, Exercise and Health, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia; E-mail: [email protected]. Submitted for publication November 2014. Accepted for publication April 2015. 0195-9131/15/4711-2441/0 MEDICINE & SCIENCE IN SPORTS & EXERCISEÒ Copyright Ó 2015 by the American College of Sports Medicine DOI: 10.1249/MSS.0000000000000687
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A
growing body of research has demonstrated a link between exercise and the physiological mechanisms controlling appetite and energy intake, with inactivity potentially contributing to a positive energy balance and subsequent weight gain (18,22,31). Conversely, it is widely acknowledged that exercise plays a prominent role in weight management by 1) contributing to a negative energy balance by increasing energy expenditure (3,4,27) and 2) having a favorable influence on the sensitivity of appetite regulation (25), the total amount of energy consumed (30), feelings of hunger and fullness (3,9), and the circulating levels of a number of appetite-related hormones (1,3). More specifically, Martins et al. (25) demonstrated that 6 wk of moderate-intensity aerobic exercise training (four sessions per week at approximately 65%–75% of HRmax) improved appetite regulation in previously inactive normal-weight
ghrelin, together with elevated blood lactate and glucose. In addition, free-living energy intake in the 48 h after leaving the laboratory remained lower after the intermittent exercise compared with moderate continuous exercise and control. Whether these acute benefits of intermittent high-intensity exercise translate to differences in long-term appetite regulation and weight loss remains to be determined. Therefore, the purpose of this study was to examine the effect of 12 wk of supervised exercise (high-intensity intermittent exercise training (HIIT) compared with continuous moderate-intensity training (MICT) and a no-exercise control) on appetite regulation (using the high-energy vs low-energy preload test meal paradigm), perceptions of appetite and the circulating concentrations of appetite-related hormones (particularly active ghrelin, leptin, insulin, pancreatic peptide (PP), and peptide tyrosine tyrosine (PYY)) in the fasted state and in response to caloric consumption in previously inactive overweight men. It was hypothesized that 12 wk of supervised exercise would improve appetite regulation (i.e., promote more sensitive eating behavior) compared with a no-exercise control but that the improvement would be to a greater extent in response to HIIT compared with MICT.
METHODS
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Participants Thirty overweight, physically inactive men (age, 31T 8 yr; ˙ O2peak, 35.3 T body mass index (BMI), 27.2 T 1.3 kgImj2; V j1 j1 5.3 mLIkg Imin ) were recruited from the local community. Physical inactivity was defined as not engaging in moderate-intensity exercise for more than 75 minIwkj1 (35). To minimize any influence of dietary restraint on the results, participants were excluded if they scored Q3.5 on the restraint scale of the Dutch Eating Behavior Questionnaire (33). Ethics approval was granted by the human research ethics committee at the University of Western Australia, and a written consent was obtained from all participants. Study Design Participants were randomly allocated (using a random number generator software (32) into one of the following three experimental groups: 1) HIIT, 2) MICT, or 3) no exercise training control (CON). Appetite regulation was assessed before and after the intervention on the basis of a preload-test meal paradigm, originally introduced by Schachter et al. (29) (involving the assessment of ad libitum energy intake in response to previous energy intake of differing caloric contents). The effect of the intervention period on perceived appetite, appetite-related blood variables, free-living energy intake, physical activity levels, anthropometric measures, aerobic fitness, dietary restraint, and physical activity enjoyment were also assessed. Baseline testing and familiarization. Participants completed an initial baseline testing and familiarization session. This included the assessment of 1) body composition
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using dual-energy x-ray absorptiometry (GE Lunar Prodigy Vision; GE Medical Systems, Madison, WI), 2) peak aero˙ O2peak) using a continuous incremental bic capacity (V exercise test performed on an air-braked cycle ergometer as previously described (30), 3) dietary restraint via the Dutch Eating Behavior Questionnaire (33), and 4) whether they were regular breakfast consumers (Q5 times per week). Familiarization with the questionnaires and protocols to be used for the subsequent assessment of pre- and postintervention outcome measures (i.e., blood sampling, laboratory test meal) was also performed during this session to minimize the novelty of these tasks. Body compo˙ O2peak, and dietary restraint were reassessed at the sition, V end of the study period. Pre- and postintervention testing. Participants attended the laboratory at approximately 0700 h, having fasted for 10–12 h, on two separate occasions both before and after intervention (i.e., four visits in total) for the assessment of outcomes measures. In the 24 h before the first visit, participants were required to document their food and drink consumption and to refrain from vigorous physical activity. The documented dietary information was reviewed by the investigator upon arrival at the laboratory, and participants were instructed to replicate their food and drink intake before each subsequent visit, with compliance confirmed by the inspection of the records upon arrival to the laboratory and later nutritional analyses. All postintervention testing was conducted within the week and at least 48 h after the last training session. Enjoyment of physical activity was assessed before and after intervention (i.e., first and final exercise training session) via the Physical Activity Enjoyment Scale (16). Preload test meal. Upon arrival at the laboratory, participants were provided with either a high-energy preload (HEP, 2438 kJ) or low-energy preload (LEP, 847 kJ) in a counterbalanced, single-blind design (preloads were of similar volume and sensory properties for consumption). The HEP consisted of 250 mL of UP&GOÒ liquid breakfast (Sanitariumi; Berkeley Vale, New South Wales, Australia), 100 g of maltodextrin (Poly-JouleÒ; Nutricia, Macquarie Park, New South Wales, Australia), and approximately 100 mL of water to make a total volume of 450 mL, whereas the LEP consisted of 250-mL UP&GOÒ liquid breakfast, 2 g of ResourceÒ ThickenUpi Clear (Nestle´, Notting Hill, Victoria, Australia), 5-mL SugarlessÒ Liquid Sweetener, (Sugarlessi, Chipping Norton, New South Wales, Australia), and approximately 193-mL water to make a total volume of 450 mL. Participants remained seated for 70 min after consuming the preload, at which point they were given access to a laboratory test meal for 20 min, during which time they were instructed to consume ad libitum until they felt ‘‘comfortably full.’’ The test meal consisted of porridge made from a mixture of instant oats (Oats Quick Sachet—Creamy Honey; Uncle TobysÒ, Nestle´, Rhodes, New South Wales, Australia) and milk (HiLo Milk; PuraÒ, Melbourne, Victoria, Australia) of known quantity and nutrition content. In favor of external
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EXERCISE TRAINING AND APPETITE REGULATION
activity based on accelerometry were determined using ActiLife software (ActiGraph, Pensacola, FL). Exercise intervention. Both exercise training groups (HIIT and MICT) were required to participate in three training sessions each week over 12 wk. All training was conducted on calibrated front-access air-braked cycle ergometers (model EX-10; Repco Cycle, Huntingdale, Victoria, Australia) that were interfaced with a customized software program (Cyclemax; School of Sport Science, Exercise and Health, University of Western Australia, Perth, Western Australia, Australia). Participants randomized to HIIT were required to complete repeated bouts of high-intensity exercise (15 s at a power output equivalent to approximately ˙ O2peak) with an active recovery period (60 s at a power 170% V ˙ O2peak) between efforts. This output approximately 32% V protocol was intended to replicate the intensity and duration of intervals (and corresponding work-to-recovery ratio) shown to attenuate short-term ad libitum energy intake in our previous study (30). Participants allocated to MICT exercised ˙ O2peak continuously for at a power output equivalent to 60% V the duration of each training session. Relative total work was matched between exercise protocols, and the workload for each participant was determined using their individual base˙ O2peak results. line V All training sessions were fully supervised by an exercise physiologist (A.Y.S.). Training sessions commenced with a 5-min warm-up that involved easy pedaling followed by light static/dynamic stretching of the lower limbs. Heart rate (HR) and rating of perceived exertion (RPE) were measured during each exercise session. To accommodate for an increase in fitness throughout the intervention period, the workload and duration of the training sessions were progressively increased. Training workloads were adjusted on the basis of a conservative 1% improvement in aerobic capacity per week, whereas duration progressed as follows: weeks 1–3 (30 min), weeks 4–6 (35 min), weeks 7–9 ˙ O2peak (40 min), and weeks 10–12 (45 min). In addition, the V test was repeated during week 6 of the intervention and training workloads were further adjusted accordingly. Statistical Analysis Insulin sensitivity was calculated using the homeostatic model assessment (HOMA-IR) index (based on fasting blood glucose and insulin concentration) (34). Repeated-measures ANOVA were used to compare the estimated energy intake and energy expenditure for the 24 h before each laboratory visit for the assessment of outcome measures to confirm that these factors were well matched. Mixed-model ANOVA was applied to determine treatment effects for each outcome variable, as follows: 1) two-way (pre- vs postintervention condition (HIIT, MICT, and CON)) for aerobic fitness, anthropometric measures, physical activity enjoyment, and dietary restraint, 2) three-way (pre- vs postintervention preload (HEP vs LEP) condition) for energy intake at the laboratory test meal and 24-h cumulative energy intake, 3)
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validity (i.e., there is typically free access to water intake when consuming a meal), a standardized bottle of plain drinking water (approximately 1000 mL) was also available for ad libitum consumption. The porridge and drinking water were weighed before and after consumption. Measures were taken to minimize the influence of environmental factors on eating behavior as previously described (30). Assessment of perceptions of appetite. Subjective perceptions of appetite (fullness, hunger, satiation, desire to eat, and prospective food consumption) were assessed using a 100-mm visual analog scale (13) in the fasted state (before preload consumption) and in response to caloric consumption (immediately and 30, 60, and 90 min after preload). Assessment of appetite-related blood variables. Blood was sampled in the fasted state (before preload consumption) and in response to caloric consumption (30 and 60 min after preload). To prepare the sampling site, the entire hand was placed into a box heated with warm air (approximately 60-C). Capillary blood (535 KL) was then collected from the warmed fingertip using a sterile lancet (Unistik 2 Normal; Owen Mumford, Oxford, United Kingdom). Blood glucose concentration was measured using a blood gas analyzer (35-KL ABL 735; Radiometer, Copenhagen, Denmark). The remaining blood was treated with EDTA (Microtainer Tubes with K2E (K2EDTA); BD Microtainer, Franklin Lakes, NJ) and serine protease inhibitor (20 KL per 500 KL of blood; Pefabloc SC, Roche Diagnostics, Sydney, New South Wales, Australia) before being centrifuged at 1020g for 10 min. Plasma obtained was stored at approximately j80-C, and samples from the HEP condition only were later analyzed for a range of appetiterelated hormones leptin, insulin, active ghrelin, PP, and PYY using a commercially available assay kit (Milliplex Map Human Metabolic Hormone Magnetic Bead Panel; Millipore Corporation, Billerica, MA). The minimum detectable concentrations of the respective peptides are as follows: ghrelin, 1.8 pgImLj1; leptin, 157.2 pgImLj1; PP, 2.4 pgImLj1; PYY, 8.4 pgImLj1; insulin, 44.5 pgImLj1. The intraassay variation (%coefficient of variation) of the Milliplex multiplex assay is G11%. Assessment of free-living energy intake and physical activity levels. Free-living energy intake and physical activity levels in the 24 h before and for the remainder of the day after leaving the laboratory sessions were assessed using a self-recorded food diary and accelerometry (GT1M Activity Monitor; ActiGraph, Pensacola, FL), respectively. The food diary required participants to record the portion size (weighing scales were provided to assist) and describe the food consumed. Detailed instructions on the use of the food diary and the necessity for timely and accurate recordings after food and drink consumption were emphasized. Energy intake from food records was calculated using a commercially available software program (Foodworks; Xyris Software, Queensland, Australia). The total number of steps and estimated energy expenditure from physical
TABLE 1. Aerobic fitness and body composition before and after 12 wk of HIIT (n = 10), MICT (n = 10), or no exercise training control (CON, n = 10). HIIT V˙O2peak (mLIkgj1Iminj1) Body mass (kg) BMI (kgImj2) Body fat percentage (%)
Preintervention Postintervention Preintervention Postintervention Preintervention Postintervention Preintervention Postintervention
34.8 40.4 87.4 86.6 27.4 27.1 32.0 30.9
T 4.5 T 4.4*,** T 7.7 T 7.5 T 1.6 T 1.4 T 2.9 T 2.7
MICT 34.8 T 39.7 T 86.5 T 85.9 T 27.2 T 27.0 T 31.1 T 30.2 T
CON
6.2 6.9*,** 8.6 8.5 1.5 2.3 5.0 6.5
36.3 35.8 85.6 87.1 27.0 27.5 32.2 32.5
T 5.6 T 5.5 T 6.4 T 6.7 T 0.9 T 0.9** T 3.9 T 3.9
Values are presented as mean T SD. *Indicates significant difference from preintervention (P e 0.050). **Indicates moderate-to-large Cohen d effect size from preintervention.
APPLIED SCIENCES
four-way (pre- vs postintervention preload time (0 min, immediately after preload, 30 min after preload, 60 min after preload, and 90 min post-preload) condition) for perceived appetite, and 4) three-way (pre-vs postintervention time (0 min, 30 min after preload, and 60 min after preload) condition) for appetite-related hormone concentration in response to caloric intake. The effect of the intervention and condition (HIIT, MICT, and CON) on HR and RPE was assessed using a mixed-model ANOVA. Post hoc comparisons were conducted where appropriate. Statistical significance was accepted at P e 0.050 (SPSS version 20; IBM Corporation, Armonk, NY). In addition, 95% confidence intervals (CI) were presented as follows: lower bound value–upper bound value. Furthermore, Cohen d effect sizes (d) were also calculated for pairwise comparisons; only moderate (0.50–0.79) and large (90.80) effect sizes are reported. All results are presented as mean T SD, unless otherwise indicated.
RESULTS There were no dropouts in any of the treatment groups, with every participant in the study completing all the required testing sessions. Furthermore, training attendance was similar between groups (P = 0.712), with 98% T 3% (mean, 35 of 36 sessions; minimum, 33 sessions) compliance for HIIT and 97% T 4% (mean, 35 of 36; minimum, 33 sessions) for MICT. Training intervention. A main effect of condition revealed higher average HR (P G 0.001) and RPE (P = 0.034) during HIIT (HR, 158 T 3 bpm; RPE, 14 T 1) compared with MICT (HR, 133 T 5 bpm; RPE, 13 T 1). A main effect of training time point showed that average HR (P G 0.001) and
RPE (P G 0.001) increased through the course of both training interventions. ˙ O2peak was improved in After the 12-wk study period, V both the HIIT and MICT groups (P G 0.001) (Table 1) to a similar extent but remained unchanged in the CON group. There were no significant changes in anthropometric measures (body mass, P = 0.234; BMI, P = 0.204; body fat, P = 0.187) in response to the interventions (Table 1). With respect to the enjoyment of exercise, there was a main effect of the exercise intervention period (P = 0.006), with an increase in enjoyment after intervention compared with baseline (preintervention, 93 T 15; postintervention, 102 T 13; d = 0.64); however, there was no difference between HIIT and MICT (P = 0.172). Furthermore, there was no interaction effect of pre- vs postintervention condition on dietary restraint (pre- vs postintervention, HIIT: 2.7 T 0.4 vs 2.6 T 0.5; MICT, 2.4 T 0.6 vs. 2.5 T 0.8; CON, 2.2 T 0.5 vs 2.4 T 0.5; P = 0.829). Ad libitum energy intake at the laboratory test meal. Energy intake and energy expenditure from physical activity in the 24 h before each preload test session were well-matched (energy intake = 8327 T 2191 kJ, P = 0.416; energy expenditure = 1905 T 573 kJ, P = 0.768). Likewise, the environmental conditions were consistent during the preload test sessions (temperature = 21.3-C T 0.9-C, P = 0.996; humidity = 52.6% T 7.2 %, P = 0.700). Absolute ad libitum energy intake during the laboratory test meal after the HEP and LEP assessed pre- and postintervention is shown in Figure 1, with differences in energy intake pre- and postintervention displayed in Table 2. Energy intake during the test meal after the two different preloads was similar at baseline in all groups (P = 0.396),
FIGURE 1—Mean (T SE) ad libitum energy intake at laboratory test meal after HEP and LEP before (preintervention) and after (postintervention) 12 wk of HIIT, MICT, or no exercise training (CON) (n = 10 in each group).
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TABLE 2. Difference in ad libitum energy intake from a laboratory test meal and cumulative 24-h energy intake (kJ) after HEP and LEP before and after 12 wk of HIIT, MICT, or no exercise training (CON; n = 10 in each group). Study Time Point/Preload $ Energy intake at test meal (i.e., HEP j LEP) $ 24-h energy intake (i.e., HEP j LEP) $ Energy intake at test meal (i.e., preintervention j postintervention) $ 24-h energy intake (i.e., preintervention j postintervention)
Preintervention Postintervention Preintervention Postintervention HEP LEP HEP LEP
HIIT x¯ T SD (95% CI) j43 j516 402 186 517 43 928 712
T 585 (320, j406) T 395 (j271, j762) T 1597 (1392, j588) T 1108 (873, j500) T 736 (61, 973) T 640 (j354, 439) T 1590 (j58, 1913) T 1241 (j57, 1481)
MICT x¯ T SD (95% CI) 219 j68 649 j617 199 j89 758 j509
T 523 (544, j105) T 677 (351, j488) T 2103 (1953, j654) T 2445 (898, j2133) T 1043 (j447, 845) T 783 (j574, 397) T 1917 (j430, 1946) T 1265 (j1293, 275)
CON x¯ T SD (95% CI) j88 T j66 T j204 T 265 T j223 T j202 T j199 T 104 T
494 (218, j394) 688 (360, j493) 1054 (449, j857) 1345 (1099, j569) 628 (j612, 166) 736 (j658, 254) 648 (j601, 203) 1354 (j735, 943)
Values are presented as mean (x¯) and 95% CI for preintervention energy intake minus postintervention energy intake (lower bound, upper bound). Where the 95% CI does not cross zero, the value was set in bold.
Appetite-related blood variables. An interaction effect of pre- versus postintervention time condition was observed for insulin (P = 0.050) (Fig. 3A), with post hoc analysis revealing lower insulin concentration in a fasted state after HIIT (P = 0.003, d = 0.60) and 60 min after caloric consumption in MICT (P = 0.010, d = 0.77) compared with preintervention. There was an interaction effect of preversus postintervention condition on leptin (P = 0.017) (Fig. 3B), revealing lower leptin concentration after HIIT but not after MICT and CON. There were no interaction effects observed for active ghrelin (P = 0.736) (Fig. 4A), PP (P = 0.060) (Fig. 4B), PYY (P = 0.077) (Fig. 4C), or blood glucose (P = 0.926) (Fig. 4D). However, there was a main effect of test session time (P e 0.001) for each of these blood variables, with increased PP, PYY, insulin, and blood glucose in response to caloric consumption, whereas active ghrelin and leptin decreased over time. HOMA-IR was similar between groups at baseline (P = 0.48). There was an interaction effect of pre- versus postintervention condition on HOMA-IR (P = 0.016), with post hoc analysis revealing significantly lower HOMA-IR after HIIT (pre, 3.8 T 1.9; post, 2.9 T 1.6; P = 0.018; d = 0.61) but not for MICT and CON.
DISCUSSION The main aim of the present study was to compare the effects of 12 wk of HIIT with an equivalent period of MICT or inactivity on appetite regulation in previously inactive overweight men. There were no statistically significant
FIGURE 2—Mean (T SE) cumulative 24-h energy intake after HEP and LEP before (preintervention) and after (postintervention) 12 wk of HIIT, MICT, or no exercise training (CON) (n = 10 in each group).
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suggesting a lack of appropriate compensation for previous energy intake. With respect to the effect of the intervention period on energy intake from the test meals, there was no significant interaction of pre- versus postintervention preload condition (P = 0.333); however, the 95% CI indicated a decrease in energy intake after the HEP after 12 wk of HIIT compared with the LEP postintervention (Table 2), suggesting a tendency for enhanced appetite regulation based on more appropriate adjustment for previous energy intake. There was no difference in ad libitum water intake at the laboratory test meal between trials (P = 0.601). Cumulative 24-h energy intake. Cumulative energy intake for the remainder of the day after the ad libitum laboratory meal is shown in Figure 2, and the differences in cumulative energy intake before to after intervention are presented in Table 2. Cumulative energy intake values after the two different preloads were similar at baseline in all groups (P = 0.644). The interaction effect of pre- versus postintervention preload condition on cumulative energy intake over 24 h was not significant (P = 0.082). Perception of appetite. There were no significant interactions of pre- versus postintervention preload time condition on perceived hunger (P = 0.691), fullness (P = 0.260), satiation (P = 0.352), desire to eat (P = 0.434), or prospective food consumption (P = 0.657; results not displayed). However, there was a main effect of time within each test session for each of these variables (P G 0.001), with increased feelings of fullness and satiation along with decreased hunger, desire to eat, and prospective food consumption after the test meal.
FIGURE 3—Mean (T SE) concentrations of insulin (A) and leptin (B) in the fasted state (time, 0 min) and in response to caloric consumption (indicated by an upward arrow, j) before (represented by black circles, ) and after (represented by white circles, )) 12 wk of HIIT, MICT, or no exercise training control (CON) (n = 10 in each group). #Significantly different from preintervention. *Significant interaction effect of pre- vs postintervention, test session time (0, 35, and 65 min), and condition (HIIT, MICT, and CON). †Significant main effect of test session time point (0, 35, and 65 min) is different from preintervention (P e 0.050).
the test meal after the HEP compared with LEP in response to HIIT but not for MICT or CON. The tendency for lower energy intake after HEP compared with LEP in response to HIIT suggests improved appetite regulation (based on a more appropriate adjustment of energy intake in response to
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differences in energy intake at the laboratory test meal or cumulative energy intake after leaving the laboratory as a result of the intervention period. However, the 95% CI indicated improved appetite regulation after HIIT on the basis of a clinically meaningful decrease (14) in energy intake at
FIGURE 4—Mean (T SE) concentrations of active ghrelin (A), PP (B), PYY (C), and glucose (D) in the fasted state (time, 0 min) and in response to caloric consumption (indicated by upward arrow, j) before (represented by black circles, ) and after (represented by white circles, )) 12 wk of HIIT, MICT, or no exercise training control (CON) (n = 10 in each group). †Significant main effect of test session time point (0, 35, and 65 min) is different from preintervention (P e 0.050).
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This is in contrast with the reported increases in fasting and postprandial feelings of fullness in the study by Guelfi et al. (9) after an aerobic exercise intervention of similar duration and frequency to that used here. With respect to the appetite-related blood variables, we observed attenuated insulin concentration in a fasted state after HIIT and in a postprandial state after MICT compared with preintervention. However, improved insulin sensitivity (based on the HOMA-IR index) was only noted after HIIT but not after MICT. Given that insulin sensitivity has been reported to have a negative relation with ad libitum energy intake during a test meal in an overweight population (8,12), the tendency for enhanced appetite regulation after HIIT may be mediated by improved insulin sensitivity. Our findings are in line with those of Matinhomaee et al. (26), who also reported that 12 wk of HIIT improved insulin sensitivity (HOMA-IR index). Importantly, the present study may lend further support to the role of aerobic exercise training as a first line of defense in the management of insulin resistance. The decrease in leptin concentration after HIIT may be associated with the fat loss (although not significant) observed in the HIIT group (19). In contrast, active ghrelin, PP, and PYY were not altered in response to the intervention period. The lack of response of these appetite-related hormones after aerobic exercise training is consistent with the study of Guelfi et al. (9), who reported no change in active ghrelin, PP, and PYY concentration in sedentary overweight/ obese men after 12 wk of aerobic exercise training (three times weekly at 70%–80% of HRmax). In contrast, Martins et al. (23) reported that 12 wk of aerobic training (five times per week at 75% of HRmax) resulted in a significant increase in fasting acylated ghrelin concentration, together with feelings of hunger in sedentary overweight/obese men and women. Reasons that may explain the discrepancy in outcomes between these studies include differences in the volume of exercise performed and the characteristics of the participants. For instance, the study by Martins et al. (23) involved exercise training five times per week compared with three times per week in the study of Guelfi et al. (9) and the present study. Furthermore, given that active ghrelin has been shown to respond differently to aerobic exercise training in men and women (higher active ghrelin concentration in women) (11), the inclusion of women in the study by Martins et al. (23) may partially explain the difference in findings. Regardless, this raises the question of the potential mechanisms besides appetite-related blood variables that may have contributed to the tendency for enhanced appetite regulation after HIIT. Firstly, it should be acknowledged that the range of appetite-related peptides measured in this present study was not exhaustive and other appetite-related hormones such as glucagon-like peptide 1, cholecystokinin, and obestatin also influence appetite regulation. Furthermore, a series of recent studies have suggested that exercise may have a dampening effect (attenuated neural activity) on the food reward pathways located in the brain, which is consistent with reduced general palatability of food, reduced anticipation to eat, and
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previous caloric consumption). No significant changes in the perception of appetite were noted as a result of the intervention, and the circulating concentrations of glucose, active ghrelin, PP, and PYY were not altered across the intervention period. However, insulin was lower after both exercise interventions (fasting—HIIT, postprandial—MICT) but unaltered in CON, whereas leptin was reduced after HIIT only. Both exercise interventions resulted in a significant increase in aerobic fitness. Previous research has demonstrated improved appetite regulation in response to a period of aerobic exercise training (24,25). However, to our knowledge, this is the first study that has compared the effect of different types of exercise training (specifically HIIT with MICT) on appetite regulation. Despite no significant interaction effects being observed in energy intake in response to the intervention, the reported 95% CI suggests (i.e., lower and upper bound values do not cross zero) that 12 wk of HIIT improved appetite regulation in response to previous energy intake of differing caloric content. Specifically, participants ate less at the test meal after HEP compared with that after LEP (by 516 T 395 kJ) after the HIIT intervention, whereas intake remained unaltered in the MICT and CON groups. When comparing the preintervention and postintervention energy intake at the test meals, it is evident that this compensation was related to a reduction in energy intake after the postintervention HEP test meal compared with preintervention in the HIIT group (517 T 736 kJ decrease). Considering that an energy deficit of 419 kJIdj1 and 795 kJIdj1 has been calculated to prevent weight gain (maintain weight loss) and achieve weight loss, respectively (14), the energy deficits presented previously may be considered a clinically meaningful and important consideration for weight management. However, it is important to note that despite the mentioned changes in energy intake in the meal directly after the HEP or LEP, there were no significant differences in cumulative energy intake for the remainder of the day between preloads or conditions. This may be related to the level of accuracy of assessing energy intake at a laboratory test meal compared with that obtained from self-reported food diaries, with the former being a more precise measure. The lack of improvement in appetite regulation (based on the similar energy intake after HEP vs LEP) observed after MICT in the present study is in contrast with previous research of similar duration (24,25). Martins et al. (24) reported a significant within-group improvement in 24-h cumulative energy compensation after 12 wk of MICT. This discrepancy between studies may be explained by differences in the volume of exercise performed. The study of Martins et al. (23) involved exercise training five times per week compared with three times per week in the present study. Of note, exercise intensities used in both studies were similar; Martins et al. ˙ (24), 75% HRmax, versus present study, 60% VO 2peak (21). In addition, it was surprising that the tendency for improved appetite regulation in response to HIIT in the present study was not accompanied by changes in perception of appetite.
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reduced food consumption (5–7). Specifically, Crabtree et al. (6) demonstrated that high-intensity exercise resulted in suppressed neural responses during the viewing of highcalorie foods. Another potential mechanism by which regular exercise training may enhance appetite regulation is via changes to substrate metabolism, particularly increased fatty acid oxidation, which may reduce energy intake via alterations to vagal afferent activity that report satiety signals to appetite centers in the brain (2). Furthermore, changes in psychological approaches to food may result from regular exercise. However, the lack of change in dietary restraint scores observed in the present study suggests minimal influence of eating attitudes on appetite regulation. Clearly, further research is required to determine the mechanisms through which exercise training may affect and improve appetite regulation. Average HR and RPE over the course of the intervention were found to be higher during HIIT compared with those during MICT. Considering the nature of the HIIT protocol (i.e., repeated short bouts of supramaximal high-intensity exercise), this was not unexpected. Despite this, physical activity enjoyment was not different between HIIT and MICT and enjoyment was greater after both training interventions. These findings are of importance, given that enjoyment of physical activity has been reported to be a key factor in physical activity performance and exercise adherence (10,28). The high attendance rate of study participants in both exercise groups seems to reflect the levels of enjoyment observed in the present study. Our study also demonstrated that 12 wk of aerobic exercise, regardless of exercise protocol, resulted in an increase in aerobic fitness. This is significant, given that improvement in aerobic fitness, independent of weight loss, has been associated with decreased mortality (20). Finally, it should be noted that even though HIIT may have resulted in a tendency for improved appetite regulation, the lack of significant alterations in anthropometric measures
(i.e., body mass and body fat) is consistent with previous literature reporting that exercise alone may not be the most effective method for weight loss (15). However, it is important to note that the magnitude of change in body fat after HIIT (d = 0.39) was comparable with previous studies that reported statistically significant body fat loss after aerobic exercise interventions of a similar duration, as follows: Martins et al. (24), d = 0.31; Guelfi et al. (9), d = 0.22. The lack of statistical significance in the present study may be related to the method of analysis used, with the present study comparing differences within (pre vs post) and between intervention/control groups, whereas Martins et al. (24) and Guelfi et al. (9) analyzed differences within (pre vs post) the intervention groups only. More studies with a larger sample size are needed to further investigate these findings. In summary, we found that HIIT resulted in clinically meaningful improvements in appetite regulation whereas an equivalent period of MICT and CON did not. The mechanisms behind this are unclear, with no alterations in the perception of appetite or a number of circulating appetiterelated peptides and metabolites in either the fasted or postprandial state, although insulin sensitivity was enhanced in response to HIIT only. Together with previous evidence suggesting the benefits of HIIT for various comorbidities of obesity (17), findings from the present study may have important implications for current exercise prescription guidelines for individuals exercising for weight loss/maintenance and the management of insulin sensitivity.
The hormone assays were carried out with the facilities at the Centre for Microscopy, Characterisation and Analysis, University of Western Australia, that are supported by the funding of the university, state, and federal government. T. J. F. is in receipt of a McCusker Charitable Foundation grant, which was used to help defray costs of the appetite hormone assays. The authors declare no conflict of interest. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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