There is a prevailing view that “exercise generally results in less weight loss than expected and it is frequently observed that men and women do not respond equally to exercise for weight loss” (11, p1). This statement is based partly on previous reports demonstrating that females lose less body weight in response to exercise than males do. Després et al. (9) found that, after a 20-wk exercise intervention, males lost body mass (BM), whereas females did not. A further long-term study (44 wk) undertaken by Westerterp et al. (37) demonstrated that men lost more fat mass (FM) in response to supervised exercise training than women did (4.2 vs 2.2 kg) and concluded that females tend to preserve their FM more strongly than males do through an increase in food intake in response to long-term exercise training (although neither energy expenditure [EE] or energy intake [EI] was not measured).
The strongest evidence for a different sex-based response to exercise was demonstrated by Donnelly et al. (10). Participants were enrolled in a 64-wk exercise program designed to expend 8.4 MJ·wk−1. Each exercise session was supervised, and the EE of the exercise was recorded. After the intervention, males lost on average 5.2 kg, whereas females gained 0.6 kg. However, it was found that males expended a much greater amount of energy per week (∼4.2 MJ) compared to females. Therefore, the difference in weight loss could be accounted for by the additional EE in males. Using an energy equivalent of 32 MJ·kg−1 of body tissue, this 267.5-MJ difference equated to an additional 8.3 kg in body weight (5). Even using the more recent and conservative calculations of Hall et al. (23), this additional EE resulted in an additional weight loss of 7.1 kg for the males compared to the females (23). One possibility is that the exercise suppressed EI in males but generated a compensatory increase in appetite in females. However, self-reported EI were not found to change in response to the exercise in either males or females. In contrast to this, a randomized control trial conducted by McTiernan et al. (31) demonstrated that when the exercise was supervised and males and females expended similar amounts of energy, there were comparable effects on body composition changes in response to the 12-month exercise intervention in males and females. This suggests that there were no sex differences in energy compensation, although food intake was not objectively measured, and any effect of exercise on food intake was not reported in the article.
The smaller reductions in FM and BM reported in females are often attributed to a stronger defense of the body’s energy stores in females and a stronger compensatory increase in EI to maintain energy balance. A series of short studies carried out by Stubbs et al. investigated EI response to exercise in males and females. This research demonstrated that, in the short term (after 7 d), females partially compensated (25%–30%) for energy expended through exercise by increasing food intake (36), whereas males did not (35). In these studies, the exercise was measured and carried out in the laboratory, and males and females expended the same energy through exercise. Surprisingly, when this study was replicated for a longer period of 14 d, males compensated for the increase in EE through the exercise, whereas the females did not (38). However, in these studies, the individuals were of normal weight, and the number of participants was small, perhaps partly explaining the inconclusive outcomes.
Consequently, there is currently no clear conclusion to indicate whether males and females show equivalent weight loss in response to exercise. To do so, there seems to be five main methodological issues to consider. First, if exercise is prescribed but not supervised then it cannot be guaranteed that the exercise has been performed or has met the required intensity or duration. The exercise may be prescribed but not carried out. Second, if EE from exercise is not measured, it cannot be assumed that males and females (varying in body size and body composition) would expend equivalent amounts of energy for what seem to be equal exercise prescriptions. It should be noted that differences in body composition would affect exercise EE not only between the sexes but also between individuals. Third, differences in weight loss could be explained by variations in EI, reflecting an appetite compensation for the energy expended. This means that EI should be objectively measured. Fourth, if body composition were not measured, then changes in body weight would fail to reveal important changes in body fat or fat-free mass (FFM) that could influence the interpretation. Finally, the temporal factor is important because acute or persistent exercise will place different demands on the regulation of energy balance, with long-term exercise creating a greater cumulative energy deficit, which we infer would create a stronger stimulus for compensation and therefore an increased likelihood of eliciting an increase in EI.
The present study sought to extend the literature examining sex-based differences in body weight and appetite responses to exercise in overweight and obese adults. We hypothesized that, when exercise is supervised, EE is fixed and equivalent between males and premenopausal females, then the resultant body composition changes will be comparable.
A total of 107 overweight and obese males (n = 35, body mass index [BMI] = 30.5 ± 8.6 kg·m−2, age = 41.3 ± 8.6 yr) and premenopausal females (n = 72, 31.8 ± 4.3 kg·m−2, age = 40.6 ± 9.5 yr) completed a 12-wk exercise program. The participants’ baseline characteristics are shown in Table 1. Participants were recruited from the University of Leeds, United Kingdom, and surrounding area using poster advertisements and recruitment e-mails. Participants were excluded if their weight had changed by >3 kg in the previous 3 months, if they were smokers, if they had any health issues, if they were taking medication that would affect their appetite or metabolism, or if they took part in regular physical activity (more than one session per week). Participants gave their written informed consent form before taking part in the research. The research was granted ethical permission by the NHS Research Ethics Committee (Leeds West) number 09/H1307/7. The project was registered under International Standard Randomised Controlled Trial Registry authorization (ISRCTN47291569) in compliance with guidelines from the World Health Organization and CONSORT.
Participants completed a 12-wk supervised exercise intervention designed to expend ∼10.5 MJ·wk−1. Dependent variables were measured at week 0 (before the exercise intervention) and at week 12 (after the intervention was completed). Data collected at intermittent time points are not reported here. These measured variables are detailed further below and also more comprehensively in Caudwell et al. (7).
Exercise program and cardiovascular fitness
Participants exercised five times per week for 12 wk. The exercise was aerobic and participants were free to choose the mode of exercise—treadmill, cross trainer, rowing-ergometer, and cycle-ergometer. Each exercise session was individually calibrated to expend approximately 2.1 MJ at a moderate and fixed intensity of 70% HRmax. The exercise EE was calibrated at week 0 to determine the duration required to meet the prescribed 2.1 MJ. The exercise duration was recalibrated at weeks 4, 6, and 8 to adjust the exercise prescription taking into account changing levels of fitness. The calibration of exercise EE was carried out using indirect calorimetry (V˙max encore; SensorMedics, USA) and HR monitors (Polar, Finland). Each exercise session was supervised, and participants wore HR monitors to record the intensity and duration of each session.
Cardiovascular fitness was measured after an overnight fast using a maximal graded exercise test to volitional exhaustion. This was carried out on a treadmill using an adapted version of the Bruce walking protocol. Inspired and expired air was recorded alongside HR continually throughout the protocol using an automated system (V˙max encore; SenorMedics, USA). The gas analyzers were calibrated using known concentrations of oxygen and carbon dioxide before every test. The last 30 s of expired air was analyzed, and this volume of oxygen was taken as the V˙O2max.
Body weight and body composition were measured using air displacement plethysmography (BodPod, Concord, CA). This technique has been validated in both normal weight (14) and obese adults (19) against under water weighing. The procedure took place in the laboratory after an overnight fast. Subjects wore a bathing suit and swim cap and were weighed to the nearest 0.01 kg before being seated in the BodPod. The BodPod uses air displacement to measure body volume, and body density is calculated by body weight / whole body volume. Once the overall body density was calculated, the proportions of fat and fat-free tissue were determined using the equations of Siri (34). Waist circumference was measured following standardized procedures outlined by the International Society for the Advancement of Kinanthropometry (28).
This was measured after an overnight fast using an indirect calorimeter fitted with a ventilated hood (GEM, Nutren Technology Ltd., Cheshire, UK). Participants were to remain awake but motionless in a supine position for 45 min, with RMR calculated from respiratory data averaged during the final 30 min of assessment. V˙O2 and V˙CO2 were calculated from O2 and CO2 concentrations in inspired and expired air, diluted in a constant airflow of ≈40 L·min−1 (individually calibrated for each participant) and averaged during 30-s intervals.
The 24-h EI was measured using a test meal design. Participants arrived at the laboratory after an overnight fast and meals were given at four hourly intervals. After an individualized fixed-energy breakfast (ad libitum on the first visit), participants were provided with a fixed-energy lunch, an ad libitum dinner meal, and a snack box for the evening. Participants were instructed to refrain from eating between meals; water was available ad libitum throughout the day. Food intake was assessed at weeks 0 and 12 on probe days within the laboratory. Therefore, an objective measure of total daily EI was compiled from the meals provided throughout the day. At week 0, all participants selected their own preferred breakfast from a limited range of foods, to generate comfortable fullness. This same breakfast was presented at week 12. Therefore, total daily EI was compiled from three self-determined eating episodes (breakfast, dinner, and snack box) and one fixed meal (lunch). We have previously demonstrated that this procedure is consistent with natural eating patterns (26). The test meal probe day procedure provides objective measurement of EI that is more sensitive and accurate than self-report.
Subjective appetite sensations
During laboratory probe days, participants’ subjective appetite sensations were measured using visual analog scales on a validated electronic appetite ratings system (16). The reliability and validity of these scales has been confirmed (15,17). Ratings were recorded immediately before and after each meal and at hourly intervals throughout the test meal days. The scales were used to assess hunger, fullness, and desire to eat (33).
The satiety quotient (SQ) is a measure of the strength of the suppression of hunger generated by the energy ingested from food (20) and has been used previously to map the potency of satiety after drug administration (8) and nutritional loads (4). In this study, the SQ was calculated from the breakfast test meal in relation to the profile of hunger ratings after the meal. This variable therefore can be used to compare satiety in males and females.
The following formula was used to calculate SQ:
Data are reported as the mean ± SD unless otherwise stated. Data were analyzed using SPSS version 19. Body composition, EI, and cardiovascular fitness were analyzed using a mixed-model ANOVA with sex (male or female) as a between-subject factor and week (weeks 0 and 12) as a within-subject factor to assess group differences, changes in outcome variables across the 12-wk intervention, and group-by-week interactions. Changes in satiety (SQ) were compared over time (baseline to after breakfast, +1 h, +2 h, +3 h, and +4 h) and across the intervention (weeks 0 and 12) using repeated-measures ANOVA. An independent t-test was used to assess differences in exercise EE during the intervention between males and females. AUC hunger levels (calculated using the trapezoid method) and fasting hunger (measured before the breakfast test meal) were examined using mixed-model ANOVA. Where appropriate, Greenhouse–Geisser probability levels were used to adjust for violations of sphericity. Results were considered statistically significant at P < 0.05.
Exercise EE and Exercise Duration
Calculations made during the supervised exercise sessions demonstrated that total energy expended during the exercise was 122.8 ± 20.9 MJ for the males and 115.3 ± 15.1 MJ for the females (t = 1.82, df = 105, P = 0.075). The lack of any significant difference between males and females was anticipated and was an explicit aim of the study design. Because the intensity and EE of the exercise was fixed, duration varied to meet the required EE. Therefore, the females exercised for a longer duration than the males did to meet the required energy cost of the exercise sessions. The average exercise session for women was 54 ± 10.2 min and that for men was 43 ± 8.7 min. This resulted in the women exercising for a significantly longer duration than the men during 12-wk exercise period (3097.6 ± 671.9 compared to 2505.2 ± 497.6 min; t = −5.5, df = 105, P < 0.0001).
Participants’ cardiovascular fitness levels were generally low at the start of the exercise intervention (males [M] = 34.9 ± 6.9 mL·kg·min−1, females [F] = 29.1 ± 6.5 mL·kg·min−1). The exercise led to significant improvements in V˙O2max·kilogram of BM for males (+8.4 ± 6.9 mL·kg·min−1) and females (+6.0 ± 5.5 mL·kg·min−1). There was a significant effect of week (F1,105 = 121.8, P < 0.0001) but no significant interaction between week and sex (F1,105 = 3.6, P = 0.061). There was, however, a significant main effect of sex (F1,105 = 33.9, P < 0.0001); males had higher fitness levels than females did before and after the intervention. When V˙O2max levels were calculated per kilogram of FFM, males and females demonstrated comparable fitness levels (F1,105 = 1.57, P = 0.213).
Effect of Exercise Intervention on Anthropometric Variables in Males and Females
Comparison of males and females at baseline (Table 1) indicated that males were significantly heavier than females (F1,105 = 17.1, P < 0.0001); females also had greater levels of FM (F1,105 = 6.85, P = 0.010) and percent FM (F1,105 = 85.7, P < 0.0001). Changes in the anthropometric variables (from before to after intervention) are shown in Figure 1. The 12-wk exercise intervention resulted in significant reductions in BMI (−0.94 ± 1.1 and −0.86 ± 1.1 kg·m−2), BM (−3.03 ± 3.3 and −2.3 ± 3.1 kg), FM (−3.14 ± 3.8 and −3.02 ± 3.0 kg), and waist circumference (−4.6 ± 3.4 and −4.3 ± 3.2 cm) for males and females, respectively (all P < 0.0001). The mean reduction in percent FM was identical between males and females (−2.45% ± 3.27% and −2.45% ± 2.16%, F1,105 = 85.7, P < 0.0001). There were no significant interactions between sex and week, demonstrating that males and females did not lose differing amounts of body weight or body fat and showed similar reductions in waist circumference.
A significant increase in absolute FFM was observed in females between weeks 0 and 12 (+0.60 ± 1.3 kg) but not in males (+0.13 ± 1.9 kg), confirmed by a significant sex-by-week interaction (F1,105 = 3.53, P = 0.006). When FFM was expressed as a percent of BM, it revealed a significant increase in both males and females (2.47% ± 3.2% and 2.50% ± 2.2%, F1,105 = 85.7, P < 0.0001) and no significant week-by-sex interaction (F1,105 = 0.004, P = 0.953). There was also no difference in the percent change in FFM (week 0 − week 12) between males and females (M = 0.32% and F = 1.33%; t = −1.79, df = 105, P = 0.078).
Within both sexes, there was large variability in the body composition response to the exercise intervention. Males demonstrated a range of BM change from a loss of 14.7 kg to a gain of 2.0 kg (percent BM change = −17.1% to −2.1%). Females demonstrated similar variability ranging from a loss of 10.0 kg to a gain of 4 kg (percent BM change = −10.6% to −5.0%). Figure 2 illustrates the individual variability in body composition change in males and females.
Effect of Exercise on RMR in Males and Females
Table 2 lists the RMR values for the males and females at weeks 0 and 12 expressed in absolute terms and relative to FFM. There was no significant change in RMR between weeks 0 and 12 for either males or females either expressed in absolute energy terms (F1,105 = 0.213 P = 0.646) or expressed relative to FFM (F1,105 = 0.107, P = 0.74). There were no significant interactions between week and sex, demonstrating that the RMR response to exercise was equivalent in males and females. There was a significant effect of sex, with males demonstrating a higher RMR than females do when RMR was expressed in absolute energy terms (F1,105 = 49.5, P < 0.0001). In contrast, when RMR was expressed per kilogram of FFM, females demonstrated a significantly higher RMR than males did (F1,105 = 14.7, P < 0.0001). Regression analysis demonstrated that both FFM and FM were independent factors that account for a significant amount of the variance in RMR (FFM: β = 0.626, P < 0.0001; FM: β = 0.234, P = 0.002). After controlling for FFM and FM in the regression model, there was no main effect of sex (β = −0.201, P = 0.105) on RMR.
Effect of Exercise on EI in Males and Females
Table 2 details the daily EI for males and females at weeks 0 and 12. At week 0, males consumed 12,074.3 ± 2439.8 kJ·d−1 and females consumed 10,336.8 ± 2692.7 kJ·d−1. There was no significant change in total daily EI assessed by test meals within the laboratory for either males or females (M = 199.2 ± 2418.1 kJ and F = −131.6 ± 1912.0 kJ, F1,105 = 0.025, P = 0.876). There was no difference between the percent change in EI for males and females (M = +3.3% ± 20.7% and F = +0.22% ± 20.3%, t = 0.733, df = 105, P = 0.465). Males consumed significantly more calories than females at both measurement time points (F1,105 = 13.9, P < 0.0001). Males also consumed more food within separate test meals (F1,105 = 5.1, P = 0.027) and the snack box (F1,105 = 16.3, P < 0.0001). However, when food intake was expressed relative to resting EE (EI/RMR), males and females consumed the same amount of energy (1.44 vs 1.45 kcal per RMR, F1,105 = 0.091, P = 0.763).
Effect of 12 wk of Exercise on Appetite Variables in Males and Females
There was a significant increase in fasting hunger levels between weeks 0 and 12 (F1,105 = 28.0, P < 0.0001), as shown in Figure 3. Males and females both demonstrated an increase in fasting hunger (M = 10.96 ± 3.7 mm and F = 14.0 ± 2.7 mm, 33% and 49.3%, F1,105 = 0.203, P = 0.653), but there was no sex-by-week interaction (F1,105 = 0.41, P = 0.524).
AUC hunger levels, computed from the daily appetite profiles, did not change across the 12-wk intervention (F1,105 = 3.2, P = 0.08) nor were there different responses to exercise in males and females (M = 1389.9 ± 5356.5 and F = 757.6 ± 5924.7, F1,105 = 0.277, P = 0.60). Males and females did not differ in AUC hunger levels at either measurement point (F1,105 = 0.562, P = 0.455).
Figure 4 shows the SQ profiles, after individualized fixed-energy breakfasts, for males and females at weeks 0 and 12. It was found that the exercise program improved satiety responses in both males and females (F1,105 = 23.7, P < 0.0001). There was, however, a difference according to sex (F1,105 = 6.25, P = 0.014). Females demonstrated a higher satiety response than males did before and after the intervention.
The main purpose of this research was to compare the body composition changes and compensatory responses to imposed exercise between males and premenopausal females when the expenditure was both supervised and measured. Indeed, the exercise EE was verified as similar for males and females. However, it should be noted that these conclusions are limited to premenopausal females until studies of older populations are completed. Average total daily EI (measured objectively from test meals in the research unit) did not change in response to the exercise intervention in males or females. Consequently, the exercise created a negative energy balance and participants lost body weight and body fat. These reductions in body fat were similar for males and females. In addition, response to exercise within both sexes was subject to sizeable individual differences in body weight and body fats, but the range of these differences was similar for males and females.
The 12-wk supervised exercise regimen did have an effect on appetite behavior, as reflected in measures of fasting hunger and SQ. Specifically, exercise increased fasting hunger levels and improved the satiating efficiency of food. However, these changes were similar in males and females.
There was no significant difference in the change in body weight and FM in response to the same dose of exercise between males and females. Males lost 3.0 kg, whereas females lost 2.3 kg. This slight difference in BM change between males and females was accounted for by a small but interesting increase in FFM observed in females (+0.6 kg). This outcome is in contrast to the many previous studies, which suggest that exercise alone results in a small amount of fat loss and that females lose less weight than males do after prolonged exercise (3). However, in most of these studies, males were able to expend significantly more calories than females did. It therefore follows that the males were likely to lose more weight than females did, rather than females having a greater compensatory response to exercise than males do. It should be noted, however, that the females in this study had to exercise for a significantly longer duration (F = 54 ± 10.2 vs M = 43 ± 8.7 min per session) than the males did to expend comparable amounts of energy through exercise.
Moreover, a smaller amount of weight loss in females is often attributed to a sex-specific stronger defense of body fat and a stronger compensatory increase in EI to maintain energy balance (37). However, there is little evidence to demonstrate this phenomenon when objective measurements of food intake have been carried out alongside the exercise regimen. In the present study, neither males nor females significantly changed EI in response to the increased EE through exercise (M = +199.2 ± 2418.1 kJ and F = −131.6 ± 1912.0 kJ).
Another interesting issue is the possible contribution of RMR to weight loss. In this study, exercise did not significantly change RMR in either males or females. However, as noted in the Results section, females demonstrated a higher RMR relative to FFM than the males did. This can be compared with some opposite effects found in the literature (2,6). We feel that this is probably due to our use of obese women who have a higher proportion of FM, which makes an independent contribution to RMR. Indeed, when FM and FFM were accounted for using regression analysis, there was no significant difference in RMR between males and females. It has also been demonstrated that using the ratio method to compare RMR between males and females can be misleading (32).
It was found that the 12-wk exercise regimen did have an effect on sensations of appetite. There was an increase in fasting hunger after the intervention, a phenomenon that has been reported previously (25,29). It may be questioned why this increase in hunger motivation did not lead to an increase in food intake. One explanation could be the simultaneous effect of prolonged exercise on sensitizing the satiety signaling system. This has been proposed as the “dual action” of exercise on appetite—causing an increase in hunger while paradoxically increasing postprandial satiety (25)—and has since been confirmed by others (e.g., Martins et al. ). One factor that could explain the improvements in SQ observed in the present study is an increase in appetite hormone sensitivity. There is evidence to suggest that changes in the concentrations of gut peptides associated with the satiety response to food, such as polypeptide YY (PYY) and glucagon-like peptide 1 (GLP-1), are increased after long-term exercise (24). Therefore, the increase in fasting hunger in the present study may have been balanced by an increase in the satiating potency of ingested food during the postprandial period (as supported by the effects on SQ). Indeed, the whole day’s AUCs for hunger were not influenced by exercise. Although exercise did lead to adjustments in certain appetite variables, these changes were of a similar strength and direction in males and females.
In passing, it can be observed that the effects of exercise on sensations of appetite seem to differ in their action compared to those of dietary restriction. Whereas both exercise and dietary restriction lead to an increase in fasting hunger (1,12,13,18,24,27), only exercise seems to result in an increase in the strength of postprandial satiety (Fig. 2) (25,29).
The findings reported here showing no sex difference in response to the 12-wk supervised exercise stand in contrast to other studies that argue for a sex-based difference in weight loss and compensatory responses. For example, it has been reported by Hagobian et al. (21) that mechanisms to maintain body fat are more effective in females than in males. Nine overweight males and nine overweight females completed four bouts of exercise where the energy expended from the exercise was replenished and four bouts without energy replenishment. After the exercise, appetite-related hormones (acylated ghrelin, leptin, and insulin) were measured in response to a test meal. In females, exercise resulted in an increase in acylated ghrelin and lower insulin, which, the authors suggested, might have stimulated EI. However, the study showed no difference in the subjective appetite response, and there was also no measurement of ad libitum EI in response to the exercise intervention. Although the results were suggestive of a basis for sex-based differences, they demonstrated differences in hormonal responses, which have yet to be shown to have functional consequences. Another important difference between the studies is the period over which exercise was carried out: 8 d versus 12 wk. The differences in methodological approaches adopted by separate groups of researchers indicate that no single approach is likely to fully resolve whether males and females show similar or different compensatory responses to exercise. However, our results indicate that, during a substantial period with a closely monitored and measured dose of exercise, males and females respond similarly despite what is observed in acute or short-term studies (22,30,35,36).
We feel that the outcomes reported in the present research may help to correct an unnecessarily negative view of exercise as method of weight control for females. For example, it has been reported that “exercise is not an effective modality in women” (20) and “women tend to preserve their energy balance more than men” (37). We have demonstrated that a supervised period of exercise can lead to a reduction in FM in both males and premenopausal females to an equal degree. Moreover, the compensatory appetite responses arising from the increased EE was equivalent in males and females. We conclude that, when exercise is closely monitored so that the EE for males and females is similar, there are no sex-based differences in the compensatory response to exercise. Exercise should be promoted for weight control in females (as for males) provided that compliance is maintained.
This study was supported by BBSRC grant number BB/G005524/1 and European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement number 266408.
There are no conflicts of interest to declare.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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