Walking can provide many health benefits, lessening the risk of a range of chronic health conditions, particularly those relating to cardiovascular disease and type 2 diabetes mellitus (7,28,31). Less clear is the influence of walking on energy balance and weight control (31). This is a concern, given the rising global prevalence of overweight and obesity (20). Enhancing levels of physical activity within the population have been highlighted as important in combating present trends (12), and because walking is the most popular modality of physical activity undertaken on this scale, a definitive understanding of its influence on energy balance and weight control is necessary.
Consistent with any form of physical exertion, walking induces the expenditure of energy. Therefore, if performed frequently, walking should make an important contribution to successful energy balance. This account may be too simplistic, however, as the consensus of evidence fails to demonstrate a consistent effect of walking on indices of weight control (31). Compensatory responses after exercise may be implicit in this regard (23). In particular, it is possible that an augmentation of appetite and energy intake may occur after the expenditure of energy through physical activity (23). It is foreseeable that an increase in energy intake after exercise could negate the energy expended during an acute bout of walking. Variability in appetite and energy intake responses after both discrete and chronic episodes of walking may explain the inconsistent findings reported previously (31).
Studies examining the effect of exercise on both appetite and energy intake typically demonstrate a lack of influence in the short term (2). Studies examining the specific influence of walking on appetite (19) and energy intake (18,19,33) typically confirm this finding, although one study has found a suppression of hunger after 20 min of brisk walking (39).
The regulation of appetite and energy intake is under complex neuroendocrine control involving both centrally and peripherally mediated systems (32). Gut peptides within the enteric endocrine system are integral to this process, and efforts seeking to define how these peptides respond to exercise have recently begun (26,29). Of the gut peptides regulating energy homeostasis, ghrelin remains unique as the only known circulating orexigen (25). The influence of acute exercise on plasma total ghrelin is contentious, however, as studies have reported no change in ghrelin during or after exercise (6,27) in addition to both increases (8,15,34) and decreases (38,40). Acylation of ghrelin is thought to be essential for appetite regulation; therefore, assessment of total ghrelin may mask important changes in acylated ghrelin. Indeed, after a cycling stimulus, Marzullo et al. (30) recently found no change in plasma concentrations of total ghrelin despite acylated ghrelin being suppressed. Furthermore, concomitant suppressions of acylated ghrelin and hunger have been reported after high-intensity bouts of running and resistance exercise (4,5). Despite this, how acylated ghrelin responds to low-intensity exercise such as walking remains unknown. In addition to this, the question of whether exercise-induced changes in acylated ghrelin have implications for actual food intake is yet to receive attention.
The purpose of the present study was to examine the appetite, energy intake, and the plasma acylated ghrelin response for an extended period after an acute bout of exercise. Specifically, the response of these variables during and for several hours after a 60-min bout of brisk walking was examined. We sought to assess both the immediate and the prolonged influence of walking on acylated ghrelin, appetite, and energy intake. The findings reported here may have implications concerning the promotion of walking for successful weight control.
After ethical advisory committee approval, 14 healthy males (18-26 yr) gave their written informed consent to participate. Participants were nonsmokers, had no known history of cardiovascular/metabolic disease, were not dieting or taking medication, and were not obese (body mass index (BMI) ≤29.9 kg·m−2) or hypertensive (resting blood pressure <140/90 mm Hg). Table 1 details the participant characteristics.
Screening and familiarization.
Before partaking in the main trials, participants visited the laboratory to undergo screening, familiarization, and preliminary anthropometric and exercise testing. Questionnaires were completed to assess health status, physical activity habits, and food preferences. Height was measured to the nearest 0.1 cm using a stadiometer (Seca Ltd., Germany), and body weight was measured to the nearest 0.01 kg using a balance beam scale (Avery Industrial Ltd., Leicester, United Kingdom). BMI was then calculated. Waist circumference was determined as the narrowest part of the torso (above the umbilicus and below the xiphoid process). Body density was estimated via subcutaneous fat measurements (13) taken using skinfold calipers (Baty International, West Sussex, United Kingdom), and body fat percentage was ascertained (35).
A submaximal treadmill walking test was completed on a level-motorized treadmill to ascertain each participant's subjective brisk walking speed. Participants were told that brisk walking was defined as an exercise intensity yielding a mild shortening of breath yet still enabling the individual to converse. During the test, the treadmill speed was initially adjusted until a suitable pace was determined. Participants then maintained this speed for 5 min. In the final minute of the test, HR was measured using short-range telemetry (Sports Tester PE3000; Polar Electro, Finland), and RPE were recorded (3). After sufficient rest, maximum oxygen uptake was assessed via an incremental treadmill run to exhaustion on a level-motorized treadmill (36). One-minute samples of expired air were collected in the final minute of each stage. Final collections were taken when participants could continue for 1 min only.
Participants completed two main trials (brisk walking and control) in a randomized counterbalanced fashion. Trials were separated by at least 1 wk. Participants began main trials in the fasted state having consumed only water since 11:00 p.m. on the evening immediately before the main trials. Each trial commenced between 09:00 and 09:30 a.m. and lasted 8 h. On trial days, participants traveled to the laboratory via motorized transport; however, if this was not possible, it was ensured that any exertion before trials was minimal. The brisk walking trial commenced with a 60-min subjectively paced brisk walk on a level-motorized treadmill (Runrace; Technogym, Gambettola, Italy). The initial walking pace was that ascertained in the preliminary laboratory visit, although adjustments were made if discomfort was experienced. Samples of expired air were collected at 15-min intervals throughout to determine energy expenditure and substrate oxidation (17). HR and RPE were also assessed at these times. After the walk, participants rested for 7 h (sitting reading, writing, working at a computer, or watching television). Participants rested for the entire duration of the control trial. To estimate the net energy expenditure of brisk walking (gross energy expenditure of walking minus resting energy expenditure), samples of expired air were collected in the semisupine position during the first hour of the control trial to estimate resting metabolic rate. At baseline and at 0.5-h, 1-h, and 30-min intervals thereafter, ratings of appetite (hunger, satisfaction, fullness, and prospective food consumption (PFC)) were assessed using 100-mm visual analog scales (16). Environmental temperature and humidity were also measured at these times using a handheld hygrometer (Omega RH85, Manchester, United Kingdom). Figure 1 provides an overview of the protocol for the main trials. Further details of these trials are given in the paragraphs below.
Ad libitum buffet meals.
During the main trials, participants consumed food from an ad libitum buffet meal provided twice throughout (1.5-2 and 5-5.5 h). The buffet foods were identical before each meal (Appendix A) and provided diversity in protein, fat, and carbohydrate content to facilitate the detection of macronutrient preferences. Food was presented in excess of expected consumption. Participants were told to eat until satisfied and that additional food was available if desired. Participants consumed meals in isolation so that social influence did not constrain food selection. Food consumption was ascertained by weighing buffet items before and after each meal. The energy and macronutrient content of the items consumed was ascertained using manufacturer values. Before the main trials, acceptability of the buffet food items presented was ensured after completion of a food preference questionnaire. The questionnaire required participants to rate preselected food items on a scale ranging from 1 (dislike extremely) to 10 (like extremely). Questionnaires were examined to ensure that the food items available would be to the taste of each individual. Distaste for the buffet items (rating 4 items ≤ 4) resulted in participant noninclusion.
Physical activity and dietary standardization.
Participants completed a weighed food record of all items consumed within the 24 h preceding their first main trial. Alcohol and caffeine were not permitted during this period. This feeding pattern was replicated before subsequent trials. Participants also refrained from strenuous physical activity during this time.
A cannula (Venflon; Becton Dickinson, Helsingborg, Sweden) was inserted into an antecubital or a forearm vein while participants lay in a semisupine position approximately 30 min before the main trials commenced. Venous blood samples were taken into prechilled 4.9-mL monovettes (Sarstedt, Leicester, United Kingdom) at baseline, 0.5, 1, 1.5, 2, 2.5, 5, 5.5, 6, 7, and 8 h to measure plasma acylated ghrelin. To prevent the degradation of acylated ghrelin by protease, these monovettes contained EDTA and a 50-μL solution containing potassium phosphate buffer (0.1 M), p-hydroxymercuribenzoic acid (100 mM), and sodium hydroxide (10 M). Monovettes were spun at 1287g for 10 min in a refrigerated centrifuge at 4°C. The plasma supernatant was then dispensed into a storage tube, and 100 μL of hydrochloric acid (1 M) was added per milliliter of plasma. Thereafter, samples were spun at 1287g for 5 min in a refrigerated centrifuge before storage. Additional blood samples were collected into prechilled 9-mL EDTA monovettes (Sarstedt) at baseline, 0.5, 1, 1.5, 2, 2.25, 2.5, 3, 3.5, 5, 5.5, 5.75, 6, 6.5, 7, and 8 h for the determination of plasma glucose and triacylglycerol. Plasma insulin was determined from collections at 0, 1, 1.5, 2, 2.25, 2.5, 3.5, 5, 5.5, 5.75, 6, 7, and 8 h. These monovettes were spun at 1681g for 10 min in a refrigerated centrifuge (Bukard, Hertfordshire, United Kingdom) at 4°C. The plasma supernatant was then aliquoted into 2-mL Eppendorf tubes before storage for analysis later.
All blood samples were taken in the semisupine position except for collections at 0.5 h during the brisk walking trial where subjects straddled the treadmill. To avoid sample dilution, residual saline was discarded using a 2-mL syringe before each collection. Patency of the cannula was maintained by flushing with nonheparinized saline (0.9% wt./vol. sodium chloride; Baxter Healthcare Ltd, Norfolk, United Kingdom). To estimate changes in plasma volume (11), duplicate 20-μL blood samples were collected into micropipettes, and triplicate 20-μL samples were collected into heparinized microhematocrit tubes to determine blood hemoglobin and hematocrit concentrations, respectively.
Enzyme immunoassays were used to determine concentrations of plasma acylated ghrelin (SPI BIO, Montigny le Bretonneux, France) and insulin (Mercodia, Uppsala, Sweden) with the aid of a plate reader (Expert Plus; ASYS Atlantis, Eugendorf, Austria). Plasma glucose and triacylglycerol concentrations were determined spectrophotometrically using a bench top analyzer (Pentra 400; HORIBA ABX Diagnostics, Montpellier, France). To eliminate interassay variation, samples from each participant were analyzed in the same run. The within-batch coefficients of variation for the assays were as follows: acylated ghrelin 7.8%, insulin 6.3%, glucose 0.4%, and triacylglycerol 2.7%.
Data were analyzed using the Statistical Package for the social Sciences (SPSS) software version 14.0 for Windows (SPSS, Inc., Chicago, IL). Area under the concentration versus time curve calculations were performed using the trapezoidal method. Student's t-tests for correlated data were used to assess differences between fasting and area under the curve (AUC) values for acylated ghrelin, glucose, insulin, triacylglycerol, temperature, humidity, and appetite between the control and brisk walking trials. Repeated-measures two-factor ANOVA was used to examine differences between the walking and control trials over time for body mass, appetite, energy and macronutrient intake, acylated ghrelin, glucose, insulin, and triacylglycerol. The Pearson product moment correlation coefficient was used to examine relationships between variables. Correction of values for changes in plasma volume did not alter the statistical significance of findings; therefore, for simplicity, the unadjusted values are presented. Statistical significance was accepted at the 5% level. Results are presented as mean ± SEM.
Brisk walking responses.
Participants completed the 60-min brisk walk at 7.0 ± 0.1 km·h−1. This elicited a mean oxygen consumption equivalent to 45.2 ± 2% of V˙O2max (range = 33.8%-55.5%) and generated an average HR and net (exercise minus resting) energy expenditure of 137 ± 6 bpm and 2008 ± 134 kJ, respectively. A mean nonprotein respiratory quotient of 0.89 ± 0.01 reflected the proportional contributions of carbohydrate and fat (61 ± 3% and 39 ± 3%) to energy provision. A median RPE value of 11 indicated that the intensity of the walk was perceived as "fairly light" (range = 10-12).
No between-trial differences existed at baseline in the plasma concentrations of acylated ghrelin, glucose, insulin, or triacylglycerol. Appetite perceptions were also no different at baseline (Table 2).
Appetite and energy intake.
Two-factor ANOVA revealed a main effect of time (P < 0.001), but no trial or interaction (trial × time) main effects for all appetite perceptions assessed (hunger, satisfaction, fullness, and PFC), indicating that these appetite perceptions changed significantly during the trials but were not influenced by brisk walking (Fig. 2). Two-factor ANOVA showed no trial or interaction (trial × meal) main effects for energy intake (P > 0.05). Thus, energy intake was not significantly different between the control and brisk walking trials. Moreover, energy intake was also no different between the morning meal and the afternoon meal during the control and brisk walking trials (Table 3). Examination of the relative energy intake (energy intake − (walking energy expenditure − resting energy expenditure)) showed that energy consumption was significantly reduced in the brisk walking trial compared with the control trial (P < 0.001). After adjusting for the energy expenditure of walking, there was an energy deficit of 1836 ± 130 kJ (439 ± 31 kcal) in the brisk walking trial compared with the control trial.
Table 4 shows the energy derived from the macronutrients in the control and brisk walking trials. There was no significant difference between trials in the quantity of energy derived from fat (P = 0.396). Fat intake tended to be higher in the afternoon meal than in the morning meal (P = 0.053); however, this tendency was not different between trials (P = 0.495). Likewise, carbohydrate intake was not different between trials (P = 0.969). Neither was carbohydrate intake significantly different between the morning and afternoon meals (P = 0.628) in either the control or the brisk walking trial (P = 0.862). Consumption of protein was not different between trials (P = 0.358). Protein intake did not differ significantly between the morning and the afternoon meals (P = 0.461) in either the control or the brisk walking trial (trial × meal interaction, P = 0.290).
Plasma acylated ghrelin concentration changed significantly over time (two-factor ANOVA, P = 0.003). No trial (P = 0.922) or interaction (trial × time, P = 0.803) main effects were found. The plasma concentration of acylated ghrelin was suppressed after consumption of the morning meal (1.5-2 h) and then rose before the afternoon meal (5-5.5 h), although the concentration did not reach fasting values. The afternoon meal also induced a suppression of plasma acylated ghrelin concentrations (Fig. 3). Two-factor ANOVA revealed a main effect of time (all P < 0.001) but no trial or interaction (trial × time) main effects for plasma glucose, insulin, and triacylglycerol (Fig. 4).
Correlations between acylated ghrelin and other variables.
Fasting plasma acylated ghrelin concentration was not significantly correlated with body mass, BMI, waist circumference, percent body fat, maximum oxygen uptake, fasting insulin, fasting glucose, or fasting triacylglycerol concentration. In the brisk walking trial, acylated ghrelin and PFC AUC were positively correlated during the intermeal interval (1.5-5 h; r = 0.723, P = 0.028). In the brisk walking trial, acylated ghrelin and plasma triacylglycerol AUC were negatively correlated during the intermeal interval (1.5-5 h; r = −0.827, P = 0.006) and across the total trial (0-8 h; r = −0.694, P = 0.038). Acylated ghrelin and insulin AUC values tended to be negatively correlated across the total trial (0-8 h; r = −0.660, P = 0.053).
When examining correlations at individual time points, many significant relationships emerged. At 1 and 2 h during the control trial, acylated ghrelin was positively correlated with hunger and PFC. Correlation coefficients ranged from 0.672 to 0.809. During the control trial, acylated ghrelin was negatively correlated with fullness at 1 and 2 h, and with satisfaction at 1, 2, and 5.5 h. Correlation coefficients ranged from −0.716 to −0.898. Inverse relationships were observed between acylated ghrelin and plasma triacylglycerol at 2.5 h in the brisk walking trial (r = −0.714, P = 0.031) and with plasma insulin at 5 h in the brisk walking trial (r = −0.744, P = 0.022).
The purpose of this investigation was to examine the appetite, energy intake, and plasma acylated ghrelin response during and for several hours after a 60-min bout of brisk walking. The main finding arising from this study is that, despite inducing a moderate energy deficit, an acute bout of brisk walking did not modify appetite, energy intake, or the appetite-stimulating hormone-acylated ghrelin. These findings lend support for a role of brisk walking in weight control.
The finding of no difference in appetite (hunger, satiety, fullness, PFC) between the control and brisk walking trials is consistent with previous work that has failed to observe an immediate difference in appetite after an acute bout of exercise (2). The relatively moderate intensity of exertion and subsequent energy expenditure elicited through walking may explain this finding. Previous work has consistently observed a suppression of appetite during and briefly after intense bouts of activity (>60% of V˙O2max) (2). This response may therefore have been unanticipated in the present study because brisk walking provided a lesser physiological challenge to the relatively fit sample of participants examined.
Consistent with no change in appetite, brisk walking also failed to influence energy intake because, in both morning and afternoon meals, energy intake was highly congruent between trials. This observation confirms previous findings that have typically shown no difference in energy intake in the short term (1-2 d) after an acute exercise bout (2). Participants therefore failed to compensate for the exercise-induced energy expenditure. King et al. (22) have suggested that the relative postexercise energy intake response (absolute energy intake adjusted for the net exercise-induced energy expenditure) is of greater importance than the absolute amount of energy consumed. Using this formula, in the present study, brisk walking induced a relative deficit in energy in comparison with control (1836 kJ, 439 kcal). This finding suggests that brisk walking does not elicit an automatic compensation in energy intake in the immediate hours after exercise. Although a more delayed response remains a possibility, this initial finding lends support for the utility of brisk walking in successful body weight control.
No change in macronutrient preference was detected between the control and brisk walking trials because, in both the morning and afternoon meals, the distribution of energy was typical of a Western diet. This observation confirms results from the majority of previous laboratory interventions that have failed to show any consistent effect of exercise on food preferences (14). In this investigation, no change in macronutrient selection contributed to the lack of difference in energy intake observed between trials. Previous work has shown that switching from low-fat to high-fat food options completely reverses the energy deficit induced by previous exercise (21,24). It is therefore appealing that brisk walking did not stimulate an appetite for foods with a higher content of fat and therefore energy.
To the authors' knowledge, this study is the first to examine the acylated ghrelin response to brisk walking. Therefore, a novel finding is that plasma acylated ghrelin concentration is not affected during or for several hours after an acute bout of brisk walking. This finding is consistent with the lack of difference in appetite and energy intake observed between trials. Previously, a concomitant suppression of plasma acylated ghrelin and hunger has been observed during and briefly after an intense bout of treadmill running (4,5). Brisk walking did not affect hunger in the present study; therefore, given the role of ghrelin in appetite regulation, no change in acylated ghrelin is a logical outcome. The reduced physiological challenge imposed by walking compared with running may account for the difference in findings between studies. In particular, an attenuated gut disturbance and/or redistribution of splanchnic blood volume during walking may be implicative. This finding indicates that acylated ghrelin is not sensitive to moderate deficits in energy induced via low-intensity bouts of physical activity and holds positive implications for brisk walking in healthy body weight control.
In each trial, acylated ghrelin was suppressed after the consumption of the morning meal, rose during the intermeal interval, and declined again after the afternoon meal. This observation confirms previous findings regarding the temporal response of ghrelin to feeding (9,10). The postprandial acylated ghrelin response may be related to an increase in plasma insulin concentration (1). The inverse relationship observed between insulin and acylated ghrelin across the walking trial lends support to this hypothesis. Meals high in fat do not suppress acylated ghrelin as efficaciously as those high in protein and carbohydrate (37). The significant inverse associations found between acylated ghrelin and triacylglycerol were therefore an unexpected finding in the present investigation. Further work is needed to illuminate their relevance.
This study has two notable limitations. Firstly, the sample of participants was composed of a relatively homogenous population of young, healthy males; therefore, the findings may not generalize to clinical populations. The homogeneity of the sample may also have prevented the detection of significant relationships between important variables such as fasting acylated ghrelin and anthropometric parameters. Secondly, appetite, energy intake, and acylated ghrelin responses were observed merely for several hours after walking. Assessment of these variables during a longer period may be necessary to detect any compensatory responses.
In conclusion, this study demonstrates that an acute bout of brisk walking does not increase appetite, energy intake, or plasma acylated ghrelin concentrations, despite inducing a moderate deficit in energy. This finding lends support for a role of brisk walking in successful weight management. Further work is now required to examine responses during a longer period and in other important populations including the elderly and the obese. Such findings will contribute to a greater understanding of the influence of walking on energy homeostasis.
The authors thank the Ramblers' Association for funding this investigation. The authors also thank Mr. David Finney and Ms. Louise Watkins for their help with data collection and all of the volunteers for their participation in this study. J.A.K. recruited the participants, supervised the data collection, assisted with all aspects of the biochemistry, and performed the data analysis. D.R.B. and L.K.W. assisted with data collection and provided assistance with the biochemical analysis. D.J.S. obtained the funding and performed the venous cannulations. D.J.S. and J.A.K. conceived the study and wrote the manuscript.
None of the authors had any conflict of interest regarding any aspect of this study. The results of the present study do not constitute endorsement by the American College of Sports and Medicine.
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Appendix A: Items presented at buffet meals
Keywords:©2010The American College of Sports Medicine
EXERCISE; ENERGY BALANCE; GUT HORMONES; WEIGHT CONTROL