The influence of vigorous running and cycling exercise on hunger perceptions and plasma acylated ghrelin concentrations in lean young men

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Vigorous running suppresses plasma acylated ghrelin concentrations but the limited literature on cycling suggests that acylated ghrelin is unchanged, perhaps because body mass is supported during cycling. It is important from a research and applied perspective to determine whether acylated ghrelin and hunger responses are exercise-mode specific. This study sought to examine this. Eleven recreationally active males fasted overnight and completed three 4-h trials: control, running, and cycling, in a random order. Participants rested throughout the control trial and ran or cycled at 70% of mode-specific maximal oxygen uptake for the first hour during exercise trials, resting thereafter. Hunger was measured every 0.5 h using visual analogue scales. Eight venous blood samples were collected to determine acylated ghrelin concentrations and a standardised meal was consumed at 3 h. Compared with the control trial, acylated ghrelin concentrations were suppressed to a similar extent at 0.5 and 1 h during the running (p < 0.005) and cycling (p < 0.001) trials. Area under the curve values for ghrelin concentration over time were lower during exercise trials versus control (Control: 606 [+ or -] 379; Running: 455 [+ or -] 356; Cycling: 448 [+ or -] 315 pg x [mL.sup.-1] x 4 [h.sup.-1]; mean [+ or -] SD, p < 0.05). Hunger values did not differ significantly between trials but an interaction effect (p < 0.05) indicated a tendency for hunger to be suppressed during exercise. Thus, at similar relative exercise intensities, plasma acylated ghrelin concentrations are suppressed to a similar extent during running and cycling.

Key words: exercise mode, acylated ghrelin, gut hormones, appetite.

La course d'intensite vigoureuse fait disparaitre la concentration plasmatique de ghreline acylee; cependant, le peu d'etudes sur le sujet indique que la concentration ne change pas dans l'exercice a velo, et ce, probablement parce que le poids du corps est supporte. Selon des perspectives scientifique et appliquee, il est important de determiner si les variations de la ghreline acylee et de la faim sont specifiques au type d'exercice. C'est le but de cette etude. Onze sujets masculins physiquement actifs a titre recreatif participent apres une nuit de jeune a trois essais d'une duree de4het presentes de fa^on aleatoire: controle, course et cyclisme. Dans la condition de controle, les sujets se reposent tout au long de l'essai, mais dans les deux autres conditions, ils courent ou pedalent a une intensite sollicitant 70 % de leur consommation maximale d'oxygene puis se reposent. Toutes les 30 min, on evalue la faim au moyen d'une echelle visuelle analogue. On preleve huit echantillons de sang veineux pour analyser la concentration de ghreline acylee et on sert un repas standard a la 3e heure. Comparativement a la condition de controle, on observe a la 30e minute et a la [60.sup.e] minute une disparition similaire de la concentration de ghreline acylee a la course (p < 0,005) et a velo (p < 0,001). La surface sous la courbe de concentration de ghreline acylee est plus petite au cours des seances d'exercice comparativement a la condition de controle (controle: 606 [+ or -] 379; course: 455 [+ or -] 356; velo: 448 [+ or -] 315 pg x [mL.sup.-1] par 4 h; moyenne [+ or -] ecart type, p < 0,05). La faim ne varie pas significativement d'un essai a l'autre, mais l'analyse revele une interaction significative (p < 0,05), ce qui indique une tendance a la suppression de la faim au cours de l'exercice. En conclusion, la concentration plasmatique de ghreline acylee est abaissee de fa^on similaire a une meme intensite relative d'effort a la course et a velo. [Traduit par la Redaction]

Mots-cles : type d'exercice, ghreline acylee, hormones gastro-intestinales, appetit.

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The last few decades have seen the identification of numerous gastrointestinal hormones that play a vital role in energy homeostasis by acting on the brain to regulate appetite and food intake (Chaudhri et al. 2006). Research is now being undertaken to determine how exercise affects concentrations of these hormones and whether any alterations lead to compensatory changes in appetite and energy intake in the hours after exercise (Martins et al. 2007; Ueda et al. 2009b; King et al. 2010a).

Vigorous running and cycling exercise can induce a temporary suppression of appetite, termed "exercise-induced anorexia" (Thompson et al. 1988; King et al. 1994; King and Blundell 1995). A potential role for the orexigenic gut hormone ghrelin in mediating this effect has been proposed (Burns et al. 2007), although early studies showed increases (Christ et al. 2006; Erdmann et al. 2007), decreases (Toshinai et al. 2007; Vestergaard et al. 2007), and no change (Burns et al. 2007; Martins et al. 2007) in circulating total ghrelin levels during exercise, suggesting that ghrelin is not involved in exercise-induced anorexia. However, ghrelin is acylated with octanoate by the enzyme ghrelin O-acyltransferase (Yang et al. 2008; Gutierrez et al. 2008) and this acylation is thought to be essential for its role in appetite stimulation (Broglio et al. 2004). The importance of measuring the acylated form of ghrelin is made evident by Marzullo and colleagues (2008), who demonstrate a suppression of acylated ghrelin concentrations in lean and obese participants in response to exercise despite no change in total ghrelin levels.

It is now well established that acylated ghrelin concentrations are transiently suppressed during vigorous (>68% maximal oxygen uptake ([??][O.sub.2max])) treadmill running (Broom et al. 2007, 2009; King et al. 2010a) and this suppression may be implicated in exercise-induced anorexia. Limited evidence is available about the effects of cycling exercise on acylated ghrelin. It is possible that responses differ between running and cycling exercise because running is weight-bearing and cycling is weight-supported and involves a smaller muscle mass than running (Millet et al. 2009). Moreover, gastrointestinal distress is more commonly reported amongst runners than cyclists (Brouns et al. 1987). Given that ghrelin is produced mainly in the stomach (Ariyasu et al. 2001), it is possible that the jostling of the abdomen that occurs during running but not cycling could interfere with the production or secretion of acylated ghrelin when running. Recent studies have failed to detect a suppression of acylated ghrelin in response to cycling at 50% (Morris et al. 2010) and 60% (Ueda et al. 2009a)of [??][O.sub.2max]. However, this may be due to the moderate exercise intensities examined because another study has observed suppressed concentrations of acylated ghrelin during peak cycling exercise (Marzullo et al. 2008).

The effects of these 2 modes of exercise on plasma acylated ghrelin concentrations need to be clarified because they are the most commonly used modes of aerobic exercise in studies that investigated the effect of exercise on gut hormones and the subsequent impact on energy balance. To date no studies have directly compared acylated ghrelin responses with running versus cycling exercise. Thus, using a within-subjects design, we sought to examine whether the discrepancies in the literature are true physiological differences or are simply due to methodological differences between studies. First, from a research perspective this will enable comparisons to be made between studies that evaluate the impact of exercise on changes in the orexigenic gut peptide, acylated ghrelin, and how this may affect subsequent energy intake. Second, if running and cycling elicit similar effects, because cycling is a low impact form of exercise, it may be a more acceptable form of exercise to use in research of this kind when involving population groups, such as overweight and obese, who are less likely to tolerate treadmill running. From an applied perspective, this research may aid with the understanding of the appetite suppression reported by athletes undertaking vigorous exercise. Therefore, the purpose of this study was to compare the effects of running and cycling exercise at equal relative intensities on plasma acylated ghrelin concentrations and ratings of perceived hunger.

Materials and methods


Twelve healthy, recreationally active males aged 19-26 years from the student and staff population at Loughborough University volunteered to participate in this study, which was reviewed and approved by the Loughborough University Ethical Advisory Committee. One participant completed 2 of the 3 visits but subsequently dropped out because of an injury unrelated to study involvement and, therefore, was not included in final analyses. Eleven participants completed all 3 visits, Table 1 shows their characteristics.


Each participant attended the laboratory for 2 preliminary visits. During the first visit participants completed a health screen questionnaire and gave their written informed consent to participate. Anthropometric data were collected: height was measured using a stadiometer (Seca, Hamburg, Germany) to the nearest 0.1 cm; body mass was measured to the nearest 0.01 kg using a balance beam scale (Avery, Birmingham, UK); and skin-fold thicknesses at the tricep, bicep, subscapular, and suprailiac on the right side of the body were measured using callipers (Harpenden, Burgess Hill, UK). Participants then completed a submaximal incremental treadmill running test (RunRace, Technogym, Gambettola, Italy) and after sufficient rest, a [??][O.sub.2max] treadmill running test, as described previously (Broom et al. 2007). After allowing several days for recovery, participants returned to the laboratory for a second visit and completed a submaximal incremental cycling test on a cycle ergometer (Monark Ergomedic 874E, Vansbro, Sweden), followed by a cycling [??][O.sub.2max] test using a similar protocol to that used for running (i.e., 3-min stages until voluntary exhaustion).

After completion of the preliminary visits, participants completed 3 experimental trials, each lasting 4 h. These trials consisted of a resting control trial, a running trial, and a cycling trial. Trials were undertaken in a randomised crossover design with at least 7 days between each trial.

During the 24 h prior to the first experimental trial, participants weighed and recorded their food intake and they replicated this before each subsequent main trial. During this time, participants refrained from consuming alcohol and from participating in vigorous physical activity. On the morning of each trial, participants arrived at the laboratory at approximately 0830 h after a 10-h overnight fast. Upon arrival, the body mass of each participant was obtained and they then rested in a semi-supine position whilst a cannula was inserted into an antecubital vein to enable venous blood collection. After this, during exercise trials, participants either ran on a treadmill or cycled on a cycle ergometer (treadmill and cycle ergometer as described above) for 1 h at an intensity predicted to elicit 70% of mode-specific [??][O.sub.2max]. Exercise was performed in a fasted state for consistency with our previous work (e.g., Broom et al. 2007, 2009). The rationale for this aspect is that ghrelin concentrations are likely to be elevated in the fasted state, hence increasing the chances of detecting any exercise induced suppression of ghrelin if it occurs.

To monitor the exercise intensity, samples of expired air were collected into Douglas bags every 15 min and immediately analysed for oxygen consumption and carbon dioxide production. If oxygen consumption was higher or lower than the predicted value of 70% of [??][O.sub.2max], running speed (running trial) or the mass applied to the basket on the cycle ergometer (cycling trial) was adjusted accordingly. Heart rate and ratings of perceived exertion (Borg scale (Borg 1973)) were recorded during expired air collections in the running and cycling trials. During the expired air collection in the cycling trial, flywheel revolutions were also recorded so that work rate could be calculated. After completion of the exercise bout, participants rested in the laboratory for the remainder of the 4-h trial where they were free to work, read, or watch DVDs. During control trials, the protocol was identical with the exception that participants rested for the entire 4-h trial duration. In all 3 trials participants were fed a standardised meal at 3 h (see below).

Blood sampling and analysis

Venous blood samples were collected into pre-cooled EDTA monovettes at 0 (baseline), 0.5, 1, 1.5, 2, 3, 3.5, and 4 h for the determination of plasma glucose. Separate venous blood samples were drawn into pre-cooled and pre-treated 4.9-mL EDTA monovettes for the determination of plasma acylated ghrelin concentrations (as described previously (Broom et al. 2007)). During the control trial, all blood samples were taken with the participant in a semi-supine position. In the exercise trials, blood samples were collected with the participant in the semi-supine position with the exception of the sample at the 0.5-h timepoint, which was collected whilst the participant straddled the treadmill in the running trial and with the participant seated, but not pedalling, on the cycle ergometer during the cycling trial.

Immediately after collection, blood samples for plasma glucose analysis were centrifuged at 3500 r x [min.sup.-1] (1681g) for 10 min at 4 [degrees]C (Heraeus Labofuge 400 R, Thermo Fisher Scientific Inc., UK). The plasma supernatant was then aliquoted into separate Eppendorf tubes for storage at -20 [degrees]C prior to analysis. The 4.9-mL EDTA monovettes for determination of plasma acylated ghrelin were immediately centrifuged for 10 min at 3500 r x [min.sup.-1] (1287g) at 4[degrees]C (GS-15 R Centrifuge, Beckman Coulter, Fullerton, USA). The plasma was dispensed into plain storage tubes and 100 [micro]L of 1 mol x [L.sup.-1] hydrochloric acid (HCl) was added per 1 mL of plasma. These samples were centrifuged at 3500 r x [min.sup.-1] (1287g) for 5 min at 4 [degrees]C before being transferred into Eppendorf tubes and immediately stored at -20 [degrees]C until analysis of acylated ghrelin concentrations.

Prior to centrifugation of venous blood samples, blood was collected in triplicate into 20 [micro]L heparinised microhaematocrit tubes for the determination of haematocrit, and in duplicate into micropippetes for the measurement of haemoglobin concentration. This enabled calculation of plasma volume changes (Dill and Costill 1974).

Hunger and standardised meal

Hunger was assessed at baseline and every 30 min thereafter by using a validated 100-mm visual analogue scale, which was anchored on the left with "not at all hungry" and on the right with "very hungry" (Flint et al. 2000). Participants indicated with a mark along the 100-mm line how hungry they were.

A standardised high-fat meal was consumed by all participants at 3 h. The meal was not designed to replicate that either commonly consumed by an individual at a typical meal, nor one that should be recommended as a healthy balanced meal. High-fat meals are commonly used in our laboratory when conducting studies of postprandial lipaemia. We employed this meal for consistency with our previous work (e.g., Broom et al. 2007) and because the sole purpose of the meal was to confirm suppression of acylated ghrelin after feeding. The meal consisted of white bread, cheese, butter, full fat mayonnaise, salted potato crisps, and a full fat strawberry milkshake. The meal provided 46.1 kJ x [kg.sup.-1] of body mass and the macronutrient content of the meal was 0.69 g of fat, 0.30 g of protein, and 0.91 g carbohydrate * kg body [mass.sup.-1]. This provided 56% of the calories as fat, 11% as protein, and 33% as carbohydrate. Participants consumed the standardised meal within 15 min and the start and finish times were recorded and replicated for subsequent trials. The quantity of food provided to each participant was based on their body weight at the start of the first trial and identical quantities provided at each subsequent trial. Participants were free to consume water ad libitum throughout the trials and the volume consumed was recorded.

Blood biochemistry

Plasma acylated ghrelin concentrations were determined by enzyme immunoassay (SPI BIO, Montigny le Bretonneux, France). Plasma samples were analysed for glucose concentrations via colorimetric methods with reagents from ABX Diagnostics (Montpellier, France) by using a Pentra 400 automated analyser (Horiba ABX Diagnostics, France). To eliminate inter assay variation, samples from each participant were analysed in the same run. The within-batch coefficients of variation for the assays were as follows: acylated ghrelin 7.2%, glucose 0.4%.

Statistical analyses

Data were analysed using the Statistical Package for the Social Sciences (SPSS) software, version 17.0 for Windows (SPSS Inc., Chicago, Ill., USA). Area under the curve (AUC) values were calculated for acylated ghrelin and hunger by using the trapezoidal rule. Repeated measures ANOVA was used to assess differences in AUC between the trials as well as differences between fasting measures of acylated ghrelin, hunger, and glucose. Two-factor repeated measures ANOVA was used to examine differences between the trials over time for acylated ghrelin, hunger, and glucose. Where there were significant main effects, post hoc analysis by using the Bonferroni correction for multiple comparisons were performed. The Pearson product moment correlation coefficient was used to examine relationships between variables. Statistical significance was accepted at the 5% level. When plasma volume changes were adjusted for, statistical findings were not altered, hence unadjusted values are reported. Results are displayed as means [+ or -] SD in the text and tables and as means [+ or -] SE in the figures for clarity.


Responses to running and cycling exercise

During preliminary trials, participants achieved a lower [??][O.sub.2max] when they cycled compared with running on the treadmill (Table 1). During the main trials, participants expended more energy during the running trial compared with the cycling trial (p < 0.001). Table 2 shows the physiological responses to the running and cycling bouts.

Plasma acylated ghrelin concentrations

Fasting plasma acylated ghrelin concentrations did not differ significantly at baseline (p = 0.420) between the control (173 [+ or -] 127 pg x [mL.sup.-1]), running (158 [+ or -] 109 pg x [mL.sup.-1]), and cycling (170 [+ or -] 126 pg x [mL.sup.-1]) trials. There was a main effect of trial (p < 0.05), time (p < 0.005), and a trial x time interaction (p < 0.005) for plasma acylated ghrelin (Fig. 1a). Post hoc analysis showed that compared with the control trial, plasma acylated ghrelin concentrations were significantly lower during the cycling trial (p = 0.04) and tended to be lower during the running trial (p = 0.06). There were significant differences between trials at 0.5 and 1 h, indicating suppressed acylated ghrelin concentrations during the running (p < 0.005) and cycling trials (p < 0.001) compared with the control trial.

Differences between the trials in plasma acylated ghrelin concentrations were also assessed using AUC values (Table 3). AUC values differed during the exercise period (0-1 h; p < 0.05). Post hoc analysis revealed acylated ghrelin AUC was lower in the running and cycling trials compared with the control trial (p = 0.04). Preprandial (0-3 h) AUC values were significantly different between trials (p = 0.007) and post hoc analysis indicated that compared with the control trial, AUC values were lower during the running (p = 0.02) and cycling trials (p = 0.01). Finally, there was a significant difference in acylated ghrelin AUC values for the total trial duration (0-4 h; p = 0.01), with values for the running and cycling trials being lower than the control trial (p < 0.05).

Subjective ratings of hunger

Fasting ratings of hunger did not differ at baseline between trials (p = 0.263). There was a main effect of time (p < 0.001), indicating that hunger was suppressed in response to the standardised meal. There was a trial x time interaction (p < 0.05; Fig. 1b), indicating that hunger responses differed over time between the control, running, and cycling trials. However, post hoc analysis using the Bonferroni method revealed no differences in hunger between the trials at any point. Differences in hunger ratings between the trials were also analysed by using AUC values for the entire 4-h trial duration, during the exercise bout (0-1 h), and for the pre-meal interval (0-3 h). There were no differences for any of the time intervals assessed.

Plasma glucose concentrations

Fasting plasma glucose concentrations did not differ significantly at baseline (control 4.6 [+ or -] 0.1 mmol x [L.sup.-1], running 4.5 [+ or -] 0.2 mmol x [L.sup.-1], cycling 4.6 [+ or -] 0.1 mmol x [L.sup.-1]; p = 0.563). There was a main effect of time (p < 0.001) and a trial x time interaction for plasma glucose (p < 0.001; Fig. 1c). Post hoc analysis indicated that plasma glucose concentrations were elevated in the running and cycling trials compared with the control trial at 4 h (p < 0.001).

Correlations between variables

Fasting plasma acylated ghrelin concentrations at baseline were not correlated with baseline hunger ratings in any trial. Similarly, acylated ghrelin was not correlated with hunger at subsequent times during the trials. There were no correlations between fasting plasma acylated ghrelin concentrations and body mass index, body mass, percentage body fat, [??][O.sub.2max] (running and cycling), or fasting plasma glucose concentrations.


The main finding that arose from this investigation was that plasma acylated ghrelin concentrations were suppressed in response to vigorous cycling exercise and the degree of suppression was similar to that observed with a bout of vigorous treadmill running that was equivalent in duration and intensity.

Unlike the transient suppression of acylated ghrelin concentrations observed in response to intense bouts of treadmill running (Broom et al. 2007, 2009; King et al. 2010a), current evidence regarding the effects of cycling exercise on concentrations of plasma acylated ghrelin is inconclusive and it is possible that the conflicting findings reported in the literature between running and cycling are due to the different exercise modes. During cycling the upper body is relatively static and the body mass is supported, thus gastrointestinal disturbances are minimised, whereas during running intestinal jarring occurs and this could affect the secretion of ghrelin from the stomach. Rehrer and Meijer (1991) measured the mechanical vibration of the body during exercise and found that acceleration-deceleration was more than doubled in running compared with cycling. Although we did not measure this we can presume there was a lower mechanical vibration of the body during vigorous cycling and despite this, acylated ghrelin was suppressed to a similar extent as with vigorous running. Thus, the exercise-induced response of acylated ghrelin did not appear to be specific to the mode of exercise. This is further supported by studies that demonstrated a transient suppression of acylated ghrelin during swimming (King et al. 2011) and resistance exercise (Broom et al. 2009). It is likely that methodological differences--including feeding prior to exercise, the time of day that exercise was performed, and intensity of the exercise bout-- explains the lack of suppression of acylated ghrelin during cycling exercise that has previously been reported in the literature (Ueda et al. 2009a; Morris et al. 2010).

Ghrelin plays an important role in the acute regulation of energy balance and contributes to mealtime hunger and meal initiation (Cummings 2006). The caloric load of a meal determines the extent of ghrelin suppression (Callahan et al. 2004; le Roux et al. 2005) and the preprandial increase in circulating ghrelin is determined by the energy content of the preceding meals (Leidy and Williams 2006). In response to chronic caloric deprivation, peak Ghrelin concentrations are elevated prior to meals (Leidy et al. 2007). Collectively, these findings suggest ghrelin is highly sensitive to changes in energy balance and acts to restore it by compensatory alterations in circulating concentrations. It may therefore be expected that after a large amount of energy is expended during exercise, compensatory increases in ghrelin would occur in the hours after exercise to stimulate appetite and restore energy balance. However, in the present study, compared with the control trial, preprandial (0-3 h) AUC values for ghrelin were suppressed by approximately 26% and 28% in the running and cycling trials, respectively, indicating that at least in the short term, acylated ghrelin is not stimulated after an acute bout of exercise. Similarly, King et al (2010a) observed acylated ghrelin AUC values to be significantly suppressed over a 10-h trial when 90 min of prolonged treadmill running was undertaken compared with a resting control condition. Furthermore, they observed no change in energy intake over a 22.5-h period after exercise compared with control. In the present study, participants were fed a standardised meal; thus, it is not possible to assess the effect of this sustained suppression of acylated ghrelin on spontaneous energy intake.

Given the well-documented transient suppression of hunger in response to moderate- to high-intensity bouts of physical activity (Thompson et al. 1988; King et al. 1994; King and Blundell 1995; Broom et al. 2007, 2009; King et al. 2010a), it was surprising that hunger was unaffected by running and cycling exercise in the present study. Exercise intensity and duration are important determinants of exercise-induced anorexia (Thompson et al. 1988; King et al. 1994). In the present study, the intensity and duration of exercise were similar or greater than the intensity and duration of exercise examined in previous studies that have observed a suppression of hunger. It is therefore unlikely that the apparent lack of change in hunger is due to inadequate exercise intensity, although it is important to highlight that a significant interaction effect was observed and although the post hoc tests were not significant, the trends indicated a small suppression of hunger during exercise. The present findings are in agreement with some other research that does not demonstrate a suppression of appetite with moderate to high intensity exercise (King et al. 1996; Maraki et al. 2005; Morris et al. 2010; Ueda et al. 2009a). However, because these studies differ with respect to the sex of the participants, the timing of appetite assessment after exercise, the time of day when exercise was performed, and (or) the feeding status of the participants, the reason for a lack of exercise-induced anorexia in the present study remains unclear.

The mechanisms responsible for alterations in appetite with exercise are not fully established. Given the role of the gut hormones in the regulation of appetite, the effect of exercise on circulating concentrations of many of these hormones has become the focus of attention (Broom et al. 2007, 2009; Martins et al. 2007). Broom and colleagues (2007) postulated that a suppression of the orexigenic hormone acylated ghrelin mediated the transient suppression of hunger with treadmill running. Suppressed hunger and acylated ghrelin concentrations have also been observed with swimming and resistance exercise (Broom et al. 2009; King et al. 2011). The findings from the present study are therefore surprising in that although acylated ghrelin concentrations were suppressed with running and cycling exercise, hunger was unaffected. Hunger is regulated by many gut hormones, but how these hormones interact in response to exercise is complex and is still not fully clear. Alterations in concentrations of anorexigenic (appetite suppressing) gut peptides that were not measured in this study may also influence the appetite response and could override any inhibitory influence of suppressed acylated ghrelin concentrations. Conversely, although its role in appetite regulation and meal initiation is well established (Cummings 2006), acylated ghrelin may not be involved in the control of appetite in response to exercise. Ueda and colleagues (2009b) suggest that in response to different modes and intensities of exercise, each gut hormone may display its own specific kinetics in the blood and that each hormone may play a different role in the appetite regulatory process after a bout of exercise.

This study was limited by the sole measure of hunger using VAS during exercise. Although the use of VAS to assess hunger in appetite research is deemed valid and reproducible (Flint et al. 2000), there are other validated measures of appetite, including fullness, desire to eat, and prospective food consumption, that may also be quantified when using VAS. In the future it may be prudent to include these other measures, which would provide more comprehensive information about the appetite response to exercise. This study did not measure energy intake after exercise and future research should provide ad libitum test meals to establish whether there are exercise-mode specific differences in energy intake, which could have implications for energy balance and weight control. The measurement of anorexigenic gut peptides during exercise would be useful to aid the understanding of the appetite response to exercise.

In conclusion, this study shows that running and cycling exercise of equivalent duration and intensity suppress plasma acylated ghrelin concentrations to a similar extent. This suggests that the findings from studies that use running and cycling are directly comparable with respect to acylated ghrelin concentrations. More research is required to establish the true significance, if any, of exercise induced alterations in plasma acylated ghrelin.


The authors thank all of the study volunteers for participating in this study. We are also grateful to Miss Catherine Gibbons, Miss Charlotte Petra, Miss Joanna Ng, and Miss Beth Walker for their help with data collection.


Ariyasu, H., Takaya, K., Tagami, T., Ogawa, Y., Hosoda, K., Akamizu, T., et al. 2001. Stomach is a major source of circulating ghrelin, and feeding state determines plasma ghrelin-like immunoreactivity levels in humans. J. Clin. Endocrinol. Metab. 86(10): 4753-4758. doi:10.1210/jc.86.10.4753. PMID: 11600536.

Borg, G.A. 1973. Perceived exertion: note on "history" and methods. Med. Sci. Sports. 5(2): 90-93. PMID:4721012.

Broglio, F., Gottero, C., Prodam, F., Gauna, C., Mucciolo, G., Papotti, M., et al. 2004. Non-acylated ghrelin counteracts the metabolic but not the neuroendocrine response to acylated ghrelin in humans. J. Clin. Endocrinol. Metab 89(6): 3062-3065. doi:10.1210/jc.2003-031964. PMID:15181099.

Broom, D.R., Stensel, D.J., Bishop, N.C., Burns, S.F., and Miyashita, M. 2007. Exercise-induced suppression of acylated ghrelin in humans. J. Appl. Physiol. 102(6): 2165-2171. doi:10.1152/japplphysiol.00759.2006. PMID:17347386.

Broom, D.R., Batterham, R.L., King, J.A., and Stensel, D.J. 2009. The influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin and peptide YY in healthy males. Am. J. Physiol. Regul. Integr. Comp. Physiol 296(1): R29-R35. doi:10.1152/ajpregu.90706.2008. PMID:18987287.

Brouns, F., Saris, W.H., and Rehrer, N.J. 1987. Abdominal complaints and gastrointestinal function during long-lasting exercise. Int. J. Sports. Med. 8(3): 175189. doi:10.1055/s-2008-1025653. PMID:3305389.

Burns, S.F., Broom, D.R., Miyashita, M., Mundy, C., and Stensel, D.J. 2007. Asingle session of treadmill running has no effect on plasma total ghrelin concentrations. J. Sports. Sci. 25(6): 635-642. doi:10.1080/02640410600831856. PMID: 17454530.

Callahan, H.S., Cummings, D.E., Pepe, M.S., Breen, P.A., Matthys, C.C., and Weigle, D.S. 2004. Postprandial suppression of plasma ghrelin level is proportional to ingested caloric load but does not predict intermeal interval in humans. J. Clin. Endocrinol. Metab. 89(3): 1319-1324. doi:10.1210/jc.2003 031267. PMID:15001628.

Chaudhri, O., Small, C., and Bloom, S. 2006. Gastrointestinal hormones regulating appetite. Philos. Trans. R. Soc. Lond. B Biol. Sci. 361(1471): 1187-1209. doi:10.1098/rstb.2006.1856.

Christ, E.R., Zehnder, M., Boesch, C., Trepp, R., Mullis, P.E., Diem, P., et al. 2006. The effect of increased lipid intake on hormonal responses during aerobic exercise in endurance-trained men. Eur. J. Endocrinol. 154(3): 397-403. doi: 10.1530/eje.1.02106. PMID:16498052.

Cummings, D.E. 2006. Ghrelin and the short- and long-term regulation of appetite and body weight. Physiol. Behav. 89(1): 71-84. doi:10.1016/j.physbeh.2006. 05.022.

Dill, D.B., and Costill, D.L. 1974. Calculation of percentage changes in volumes of blood, plasma and red cells in dehydration. J. Appl. Physiol. 37(2): 247-248. PMID:4850854.

Erdmann, J., Tahbaz, R., Lippl, F., Wagenpfeil, S., and Schusdziarra, V. 2007. Plasma ghrelin levels during exercise-effects of intensity and duration. Regul. Pept. 143(1-3): 127-135. doi:10.1016/j.regpep.2007.05.002. PMID: 17570540.

Flint, A., Raben, A., Blundell, J.E., and Astrup, A. 2000. Reproducibility, power and validity of visual analogue scales in assessment of appetite sensations in single test meal studies. Int. J. Obes. 24(1): 38-48. doi:10.1038/sj.ijo.0801083.

Gutierrez, J.A., Solenberg, P.J., Perkins, D.R., Willency, J.A., Knierman, M.D., Jin, Z., et al. 2008. Ghrelin octanoylation mediated by an orphan lipid transferase. Proc. Natl. Acad. Sci. U.S.A. 105(17): 6320-6325. doi:10.1073/pnas. 0800708105. PMID:18443287.

King, J.A., Miyashita, M., Wasse, L.K., and Stensel, D.J. 2010a. Influence of prolonged treadmill running on appetite, energy intake and circulating concentrations of acylated ghrelin. Appetite, 54(3): 492-498. doi:10.1016/j.appet.2010. 02.002. PMID:20152871.

King, J.A., Wasse, L.K., Broom, D.R., and Stensel, D.J. 2010b. Influence of brisk walking on appetite, energy intake, and plasma acylated ghrelin. Med. Sci. Sports. Exerc. 42(3): 485-492. doi:10.1249/MSS.0b013e3181ba10c4. PMID: 19952806.

King, J.A., Wasse, L.K., and Stensel, D.J. 2011. The acute effects of swimming on appetite, food intake, and plasma acylated ghrelin. J. Obes. 2011: pii: 351628. doi:10.1155/2011/351628. PMID:20953411.

King, N.A., and Blundell, J.E. 1995. High-fat foods overcome the energy expenditure induced by high-intensity cycling or running. Eur. J. Clin. Nutr. 49(2): 114-123. PMID:7743984.

King, N.A., Burley, V.J., and Blundell, J.E. 1994. Exercise-induced suppression of appetite: effects on food intake and implications for energy balance. Eur. J. Clin. Nutr. 48(10): 715-724. PMID:7835326.

King, N.A., Snell, L., Smith, R.D., and Blundell, J.E. 1996. Effects of short-term exercise on appetite responses in unrestrained females. Eur. J. Clin. Nutr. 50(10): 663-667. PMID:8909932.

le Roux, C.W., Patterson, M., Vincent, R.P., Hunt, C., Ghatei, M.A., and Bloom, S.R. 2005. Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects. J. Clin. Endo crinol. Metab. 90(2): 1068-1071. doi:10.1210/jc.2004-1216. PMID:15522935.

Leidy, H.J., and Williams, N.I. 2006. Meal energy content is related to features of meal-related ghrelin profiles across a typical day of eating in non-obese premenopausal women. Horm. Metab. Res. 38(5): 317-322. doi:10.1055/s-2006925397. PMID:16718628.

Leidy, H.J., Dougherty, K.A., Frye, B.R., Duke, K.M., and Williams, N.I. 2007. Twenty-four-hour ghrelin is elevated after calorie restriction and exercise training in non-obese women. Obesity, 15(2): 446-455. doi:10.1038/oby.2007. 542. PMID:17299118.

Maraki, M., Tsofliou, F., Pitsiladis, Y.P., Malkova, D., Mutrie, N., and Higgins, S. 2005. Acute effects of a single exercise class on appetite, energy intake and mood. Is there a time of day effect? Appetite, 45(3): 272-278. doi:10.1016/j. appet.2005.07.005. PMID:16157416.

Martins, C., Morgan, L.M., Bloom, S.R., and Robertson, M.D. 2007. Effects of exercise on gut peptides, energy intake and appetite. J. Endocrinol. 193(2): 251-258. doi:10.1677/JOE-06-0030. PMID:17470516.

Marzullo, P., Salvadori, A., Brunani, A., Verti, B., Walker, G.E., Fanari, P., et al. 2008. Acylated ghrelin decreases during acute exercise in the lean and obese state. Clin. Endocrinol. 69(6): 970-971. doi:10.1111/j.1365-2265.2008.03275.x.

Millet, G. 2009. Physiological differences between cycling and running. Rev. Med. Suisse, 5(212): 1564-1567. doi:10.2165/00007256-200939030-00002.

Morris, C.J., Fullick, S., Gregson, W., Clarke, N., Doran, D., MacLaren, D., and Atkinson, G. 2010. Paradoxical post-exercise responses of acylated ghrelin and leptin during a simulated night shift. Chronobiol. Int. 27(3): 590-605. doi:10.3109/07420521003663819. PMID:20524803.

Rehrer, N.J., and Meijer, G.A. 1991. Biomechanical vibration of the abdominal region during running and bicycling. J. Sports. Med. Phys. Fitness, 31(2): 231-234.

Thompson, D.A., Wolfe, L.A., and Eikelboom, R. 1988. Acute effects of exercise intensity on appetite in young men. Med. Sci. Sports. Exerc. 20(3): 222-227. doi:10.1249/00005768-198806000-00002. PMID:3386499.

Toshinai, K., Kawagoe, T., Shimbara, T., Tobina, T., Nishida, Y., Mondal, M.S., et al. 2007. Acute incremental exercise decreases plasma ghrelin level in healthy men. Horm. Metab. Res. 39(11): 849-851.

Ueda, S.-y., Yoshikawa, T., Katsura, Y., Usui, T., Nakao, H., and Fujimoto, S. 2009a. Changes in gut hormone levels and negative energy balance during aerobic exercise in obese young males. J. Endocrinol. 201(1): 151-159. doi:10.1677/JOE 08-0500. PMID:19158129.

Ueda, S.-y., Yoshikawa, T., Katsura, Y., Usui, T., and Fujimoto, S. 2009b. Comparable effects of moderate intensity exercise on changes in anorectic gut hormone levels and energy intake to high intensity exercise. J. Endocrinol. 203(3): 357-364. doi:10.1677/JOE-09-0190. PMID:19737911.

Vestergaard, E.T., Dall, R., Lange, K.H.W., Kjaer, M., Christiansen, J.S., and Jorgensen, J.O.L. 2007. The ghrelin response to exercise before and after growth hormone administration. J. Clin. Endocrinol. Metab. 92(1): 297-303. doi:10.1210/jc.2006-1435. PMID:17032714.

Yang, J., Zhao, T.-J., Goldstein, J.L., and Brown, M.S. 2008. Inhibition of ghrelin O-acyltransferase (GOAT) by octanoylated pentapaptides. Proc. Natl. Acad. Sci. U.S.A. 105(31): 10750-10755. doi:10.1073/pnas.0805353105. PMID: 18669668.

Lucy K. Wasse, Caroline Sunderland, James A. King, Masashi Miyashita, and David J. Stensel

L.K. Wasse *, J.A. King, and D.J. Stensel. School of Sport, Exercise, and Health Sciences, Loughborough University, Loughborough, LE113TU, UK.

C. Sunderland. Sport, Health, and Performance Enhancement (SHAPE) Research Group, School of Science and Technology, Nottingham Trent University, Nottingham, NG11 8NS, UK.

M. Miyashita. Department of Health and Sports Sciences, Tokyo Gakugei University, Koganei, 184-8501, Japan.

Corresponding author: David J. Stensel (e-mail:

* Present address: Gastrointestinal Centre, Institute of Inflammation and Repair, University of Manchester, Salford, M6 8HD.

Received 25 April 2012. Accepted 26 July 2012.

Table 1. Physical characteristics of the participants.

Characteristic              Mean[+ or -]SD

Age, y                      22.7[+ or -]2.3
Height, m                   1.79[+ or -]0.10
Body mass, kg               75.5[+ or -]12.7
BMI, kg x [m.sup.-2]        23.4[+ or -]2.4
Body fat, %                 18.6[+ or -]4.7
Running [??][O.sub.2max],   57.8[+ or -]9.9
  mL x [kg.sup.-1]
  x [min.sup.-1]
Cycling [??][O.sub.2max],   50.0[+ or -]9.5
  mL x [kg.sup.-1]
  x [min.sup.-1]

Note: Values are means [+ or -] SD (n = 11). [??][O.sub.2max].
maximal oxygen uptake.

Table 2. Physiological responses to 60-min running and cycling

                               Running             Cycling

Exercise intensity,            71.7[+ or -]2.5     70.3[+ or -]4.0
Energy expenditure, kJ         3843[+ or -]872 *   3258[+ or -]841
Energy expenditure, kcal       919[+ or -]208 *    779[+ or -]201
Heart rate, beats              171[+ or -]10 *     158[+ or -]11
  x [min.sup.-1]
Respiratory exchange ratio     0.93[+ or -]0.03    0.94[+ or -]0.04
Median RPE                     14 (12-16)          14 (13-16)
Energy from fat, %             24[+ or -]10        22[+ or -]12
Energy from carbohydrate, %    76[+ or -]10        78[+ or -]12

Note: Values are means [+ or -] SD (n = 11). Values in parentheses
represent ranges.

RPE, rate of perceived exertion.

* Significantly different from cycling trial (p < 0.05).

Table 3. Acylated ghrelin concentration versus time area under the
curve values in the control, running, and cycling trials.

           Exercise or rest   Preprandial        Total trial
           (0-1 h),           (0-3 h),           (0-4 h),
           pg x [mL.sup.-1]   pg x [mL.sup.-1]   pg x [mL.sup.-1]
           x 1 [h.sup.-1]     x 1 [h.sup.-1]     x 1 [h.sup.-1]


Control    165[+ or -]114     476[+ or -]291     606[+ or -]379
Running    119[+ or -]121 *   351[+ or -]280 *   455[+ or -]356 *
Cycling    119[+ or -]98 *    342[+ or -]233 *   448[+ or -]315 *

Note: Values are means [+ or -] SD (n = 11).

* Significantly lower than the control trial (p < 0.05).

Source Citation

Source Citation   

Gale Document Number: GALE|A319383074