DIETARY RESTRICTION, PHYSICAL ACTIVITY, AND THE PROPENSITY FOR WEIGHT LOSS

IntroductIon

In many countries, governments and health agencies are strongly promoting physi-cal activity (PA) as a means to prevent the accumulation of fatness that leads to weight gain and obesity. However, there is often a resistance to respond to health promotion initiatives. For example, in the UK, the chief medical officer has recently reported that 71 percent of women and 61 percent of men fail to carry out even the minimal amount of physical activity recommended in the government’s guidelines.

Similarly, the Food Safety Agency has promoted reductions in the intake of fat, sugar, and salt but with very little impact on the pattern of consumption. Why is it that recommendations to improve health are so difficult to implement and produce the desired outcome?

A major reason is that both physical activity and dietary intake are forms of behavior. These are not simple acts but can be regarded as integrated behavioral sequences that are held in place by various environmental contingencies together with attributions and cognitions (self-explanations) that maintain existing sequences (sedentariness, low amounts of leisure time physical activity, and high intakes of fat and sugar) as part of a daily repertoire. This repertoire is made up of habits (habitual sequences of integrated behavior) that are extremely resistant to change. No single statement or policy for change is likely to be applicable to all.

Further, there is considerable individual variability in the impact of physical activ-ity and diet on the body. People should not be expected to respond in the same way.

For example, not all people who are exposed to a high-fat diet gain weight; some remain lean,¹ and this leads to the concept of susceptible and resistant phenotypes.² Similarly not all individuals who undertake a compulsory program of physical activ-ity lose weight;³ some actually gain weight and appear to demonstrate a “resistance”

to weight loss.^3,4 These individual differences not only are a genuine biological fact (a fact of life) but also can be used to throw light on the mechanisms that link physi-cal activity and diet to fatness. The disclosure of such mechanisms, and the behav-ioral sequences with which they are associated, can be used to devise programs to motivate and empower people to change behavior. Recognition that individual dif-ferences exist and that no single model fits all human beings (not even the majority of those who are overweight, overconsuming, unfit, and living in Western societies) can help to promote an understanding of an extremely complex situation. First, it is important to be aware of some basic relationships among physical activity, diet, and fatness.

t^he r^oleof d^Ietand P^hysIcal a^ctIvItyIn W^eIght g^aIn

Using data from national surveys, Hill et al.⁵ estimated that the average increase in body weight for an adult American over the last decade was approximately 1 kg per year. It was suggested that this increase in weight could be explained by an “energy gap” of less than 50 kcal·day⁻¹, which is equivalent to that reported in middle-aged

Australian women.⁶ While it is accepted that a prolonged positive energy balance will result in weight gain, whether the current rates of obesity are primarily driven by imbalances created by increased energy intake (EI) or decreased energy expen-diture has been debated.^7–9 Recently, it has been suggested that an increased level of EI at the population level is the key driver of the current obesity epidemic, as levels of PA have remained unchanged since the 1980s.^10,11 For example, Westerterp and Speakman¹⁰ found no evidence that total energy expenditure or that expended on PA (measured using doubly labeled water) has declined in North Europe over the last two decades. However, it has been suggested that increases in EI could adequately account for the weight gain seen in the U.S, population.^11,12 Therefore, it is important to understand how PA and diet can lead to weight loss and the issues that can influ-ence the efficacy of both weight loss strategies.

dIetary restrIctIon, PhysIcal actIvIty, and WeIght loss

Dietary Restriction and Weight Loss

Dietary restriction is an obvious method for the promotion of weight loss, as EI can be readily reduced, at least in the short term, to create a negative energy bal-ance. While attention has been given to the macronutrient content of the diet, the energy deficit created by dietary restriction appears to have the greatest influence over weight loss.¹³ For example, when isoenergetic deficits are created by either high- or low-fat diets, similar changes in body composition are observed.¹⁴ However, under ad libitum feeding conditions where the total calorie intake is not fixed, the macro-nutrient composition of a diet may influence the hunger and satiety response, and therefore weight loss.¹⁵ Current recommendations suggest that any dietary restriction should be moderate in nature, and create an energy deficit of 500–1000 kcal·day⁻¹ below that required for body weight maintenance.¹⁶ For an individual consuming 2500 kcal·day⁻¹, this translates to a reduction of 20-40 percent of daily EI, and may result in a weekly loss in body weight of approximately 1 kg.¹⁷

Research has focused on the efficacy of a number of different types of dietary restriction strategies, including fat or -calorie diets, very-calorie diets, low-carbohydrate CHO diets, or diets with a low glycemic index.¹⁸ Traditional dietary approaches have emphasized low dietary fat intake (< 30 percent of daily energy intake), and there is good evidence that this can produce meaningful reductions in body weight under ad libitum feeding conditions.¹⁹ There has been a recent focus on the effectiveness of low-CHO diets, and there is some evidence to suggest that a low-CHO diet is more effective in the short term (six months) for inducing weight loss than a calorie-restricted low-fat diet.^20–24 However, it remains unclear whether differences in weight loss efficacy exist between specific diets in the long term.^25,26

Recent research has started to explore the influence of the energy density of a diet on weight loss. Energy density represents the energy content of a specific food relative to its weight (i.e., calories per gram of food).²⁷ Manipulation of the energy density of a diet through the addition of water-rich foods (i.e., lower-ing the energy density through the addition of fruit, vegetables, and soup) without calorie restriction has been shown to result in clinically meaningful reductions in

body weight under free-living conditions.^28,29 While acute and short-term studies have shown that energy density can mediate satiety³⁰ and satiation,³¹ further long-term studies are needed that address the mechanisms behind any long-long-term effects of energy density on body weight.²⁷

Although clinically meaningful weight loss can be achieved with a variety of dietary approaches, long-term maintenance of this new body weight remains a seri-ous issue.³² Based on findings from a systematic review, Curioni and Lourenco³³ reported weight regain at one year to be 50 percent of that initially lost through dietary restriction. Indeed, it has been suggested that only 20 percent of individuals on a dietary treatment will maintain a weight loss of greater than 10 percent of initial body weight after three years.¹⁸

Physical Activity and Weight Loss

Physical activity is also a commonly prescribed means of promoting body weight loss. This approach to weight management stems from the fact that PA is a mod-ifiable component of energy balance, accounting for approximately 30 percent of total daily energy expenditure in sedentary individuals.³⁴ As such, manipulating the amount of PA performed can create either an acute negative energy deficit (total daily energy expenditure > daily energy intake) or an acute positive energy balance (daily energy intake > total daily energy expenditure). Prolonged exposure to such imbalances will be reflected in changes in body weight, with a chronic negative bal-ance leading to a reduction in body weight and fat mass.³⁵

In 2001, the American College of Sports Medicine (ACSM) released a position statement recommending that overweight/obese individuals perform a minimum of 150 min/wk⁻¹ of moderate-intensity PA to improve health.³⁶ However, for weight loss it was suggested that 200–300 min/wk⁻¹ of moderate-intensity PA was needed to achieve long-term reductions in body weight. Importantly, these recommendations made the distinction between the level of PA needed to bring about improvements in general health and to induce weight loss. It is now becoming clear that differing levels of PA are needed to (1) prevent initial weight gain, (2) elicit weight loss, and (3) prevent subsequent weight regain. In a recent update,³⁵ the ACSM recommend that 150–250 min/wk⁻¹ (equivalent 1200 to 2000 kcal/wk⁻¹) of moderate-intensity PA is needed to prevent weight gain (greater than 3 percent of body weight) in adults.

This dose of exercise may also be associated with modest weight loss (1–3 kg). To achieve clinically significant weight loss (≥ 5 percent of body weight), it is suggested that moderate-intensity PA should be performed for at least 225 min·wk⁻¹, with a clear dose-dependent relationship existing whereby higher levels of PA facilitate greater weight loss. Following weight loss, the ACSM suggests that 60 minutes or more per day of moderate intensity PA is needed to prevent weight regain.³⁵ As such, it is apparent that the volume of exercise required to prevent weight regain follow-ing periods of intentional weight loss is much greater than that initially required to prevent weight gain.

Diet-Induced and Physical Activity-Induced Weight Loss

The combined efficacy of dietary restriction and increased PA has been recently examined.^26,37,38 These studies have concluded that a small but significantly greater

weight loss can be achieved through a combined approach rather than when dietary restriction or exercise is performed alone. For example, Wu, Chen, and Dam²⁶ exam-ined data from eighteen randomized control trials lasting six months or longer that compare the effects of diet alone versus diet and exercise in overweight individuals.

The pooled weight loss for the combined treatments was 1.14 kg greater than that seen with diet alone, which is consistent with the additional weight loss of 1.1 kg reported by Shaw et al.³⁷ It has been proposed that diet restriction plays the dominant role in weight loss following a combined treatment, with diet contributing to approx-imately 80 percent of the weight.³⁹ However, the exact contribution is unknown and may be moderated by the degree of calorie restriction imposed, with exercise only providing additional weight loss when combined with moderate dietary restriction.³⁵

It is also important to note that the addition of exercise to dietary restriction will bring about improvements in cardiovascular fitness⁴⁰ and metabolic factors such as glucose tolerance⁴¹ and lipoprotein profiles⁴² not seen with diet restriction alone. For example, Larson-Meyer et al.⁴³ examined the cardiometabolic responses in thirty-six overweight participants during thirty-six months of isoenergetic calorie restriction (a 25 percent reduction in EI; n = 12), calorie restriction and exercise (a 12.5 percent reduction in EI and a 12.5 percent increase in ExEE; n = 12), or a weight mainte-nance diet (n = 12). While there was no difference in weight loss between the calo-rie restriction and combined groups, maximal aerobic capacity (VO_2max) improved only in the combined treatment group (22 ± 5 percent; P < 0.001). Furthermore, the combined treatment group experienced greater improvements in insulin sensitivity (P < 0.05), LDL cholesterol (P < 0.05), and diastolic blood pressure (P < 0.05) than the diet-only group.

the ImPactof dIetary restrIctIonand PhysIcal actIvItyon energy Balance: ImPlIcatIonsforthe e^ffIcacyof W^eIght l^oss

Given that dietary restriction and increased PA are promoted for weight loss due to their theoretical ability to create energy deficits, it is important to understand how the homeostatic regulatory system responds to perturbations in energy balance. The classic depiction of weight loss occurring by simply increasing energy expenditure (via PA) or decreasing EI (via dietary restriction) to produce a negative energy bal-ance is simplistic in nature.⁴⁴ Such a view assumes that the remaining components of energy balance remain static following the manipulation of EI or PA. However, the regulation of energy balance is a dynamic process in which perturbations to one component can produce responses in other areas.⁴⁵ These responses may be com-pensatory in nature and act to minimize disruptions to homeostasis.⁴⁶ For example, dietary restriction (alone) is often associated with concurrent reductions in resting metabolic rate,⁴⁷ which may attenuate the energy deficit created and subsequent weight loss.⁴⁶ Similarly, it is assumed that increased levels of PA or exercise are met with an increased level of EI, again acting to undermine any exercise-induced energy deficit.⁴⁸ This notion of a dynamic energy balance system that adjusts to perturba-tions is not new, with Jean Mayer suggesting fifty years ago⁴⁹ that exercise induces compensatory increases in EI to restore energy balance.

The efficacy of dietary restriction and PA must therefore be viewed in the context of this dynamic model, where perturbation to energy balance may elicit behavioral or biological compensatory responses that minimize the energy deficit created.^45,46 While acute periods of exercise-induced energy surfeits are met with a weak regu-latory response to restore energy balance, energy deficit appears to trigger a num-ber of potent signals designed to attenuate any imbalance and resist weight loss.^45,46 This asymmetry is noted by Westerterp,⁴⁸ who reports based on studies employing doubly labeled water that while overfeeding does not impact PA levels, underfeed-ing is met with a reduction in energy expenditure (via decreases in restunderfeed-ing metabolic rate [RMR], diet-induced, or activity-induced energy expenditure). Therefore, the appetite regulation responses appear to be more sensitive to dietary manipulations compared with exercise interventions.

This “resistance” to weight loss is apparent in studies examining the efficacy of dietary restriction or PA as a means of reducing body weight. The effectiveness of exercise to reduce body weight in overweight and obese individuals has been exten-sively reviewed.37–39,50–54 These studies consistently conclude that the degree of weight loss associated with PA or exercise interventions is typically 1.5–3.0 kg. Importantly, the observed weight loss seen is often below that theoretically expected based on objective measures of exercise-induced energy expenditure (ExEE). Indeed, Borer⁵³ suggests that when performed without dietary restriction, a daily exercise-induced energy expenditure of 400 kcal produces losses in body fat equivalent to approxi-mately one-third of that predicted. Differences between the measured and predicted weight loss have also been reported following dietary restriction. Goele et al.⁵⁵ reported that the mean weight loss in forty-eight overweight and obese females (31.5 ± 6.1 years; BMI 35.4 ± 4.4 kg·m²) following fourteen weeks of dietary restric-tion (1,000 kcal·day⁻¹) was only 44 percent of the predicted value.

Until recently, there has been little attempt to understand this disparity between predicted and actual weight loss. Differences in the adherence to a prescribed dietary or exercise intervention will undoubtedly introduce variability in any biological out-come measured. This will be particularly evident under free-living conditions, even if adherence to the prescribe intervention is monitored.^56–59 For example, Colley et al.⁵⁹ monitored adherence to a 16-week free-living exercise intervention in twenty-nine obese women, by comparing the prescribed exercise dose (1500 kcal·wk⁻¹) to that objectively measured using heart rate monitors. When the prescribed physical activity was unsupervised, participants on average only achieved approximately half of the prescribed weekly exercise dose (768 ± 516 kcal·wk⁻¹).

While poor adherence can clearly undermine the outcome of an intervention, it cannot fully explain the discrepancies in predicted and actual weight loss. While the mean weight loss was only 44 percent of that predicted based on the prescribed energy deficit in the study by Goele et al.,⁵⁵ poor compliance explained only 50 per-cent of the difference between measured and predicted weight loss. Indeed, reper-cent longer term exercise interventions, which have imposed a tighter control (i.e., moni-tored) of the ExEE, still report large variability in weight loss.^3,4,60–63 As such, bio-logical or behavioral responses should be expected to interact during periods of energy deficit to modify the outcomes of an intervention. However, despite being a common means of weight control, a sound understanding of how dietary restriction

or increased PA effects total energy expenditure within a dynamic and flexible regu-latory system is lacking.

InterIndIvIdual v^arIaBIlItyIn B^IologIcaland B^ehavIoral r^esPonses

Large interindividual variability in the biological and behavioral responses to PA has been reported, independent of the ExEE.^64,65 These included changes in VO_2max,^66,67 insulin sensitivity,⁶⁸ resting substrate metabolism,⁶¹ and body composition.^3,4,60–63 Bouchard⁶⁷ reported a mean increase of 50 percent in aerobic capacity following twenty weeks of endurance training. However, improvements ranged from 16 per-cent to 97 perper-cent, despite the volume of exercise being consistent between indi-viduals. However, few studies have attempted to characterize this variability and have focused on the group response to an exercise stimulus. Hence, the phenomenon of individual variability has not been exploited. Overlooking the variability makes the incorrect assumption that all individuals will respond similarly and that any subsequent recommendations concerning the use of PA will be appropriate for all individuals. This is not the case.

Clear evidence exists that the body weight response to long-term exercise will vary between individuals, independently of ExEE (see Figure  5.1). King et al.³ reported highly divergent changes in body weight and fat mass following twelve weeks of supervised aerobic exercise in thirty-five overweight and obese individu-als. Mean weight loss over the intervention was 3.7 ± 3.6 kg, which was concordant with the predicted weight loss based on the total ExEE. However, inspection of the individual responses revealed that changes in body weight and fat mass ranged from

−14.7 kg to +1.7 kg and −9.5 kg to +2.6 kg, respectively. Indeed, a clear dichotomy in response could be seen when participants were retrospectively classified as either

6.0 4.0 2.0 0.0 –2.0 –4.0 –6.0 –8.0 –10.0 –12.0 –14.0 –16.0

Change in Body and Fat Mass (kg)

Body mass Fat mass Mean change in body mass = 3.3 ± 3.3 kg Mean change in fat mass = –3.8 ± 3.5 kg

FIGURE 5.1 Individual changes in body mass and fat mass following twelve weeks of supervised aerobic exercise (2500 kcal·wk⁻¹) in fifty-eight overweight and obese individuals.

Data are modified from King et al.^3,4

noncompensators (NCs; n = 17) or compensators (Cs; n = 18), based on the relation-ship between actual and predicted weight loss. Compensators lost only −1.5 ± 2.5 kg (approximately half the predicted weight loss), while NCs lost −6.3 ± 3.2 kg. This was independent of total net exercise-induced energy expenditure, which did not dif-fer between groups (C = 2393 ± 547 kcal·wk⁻¹; NC = 2272 ± 542 kcal·wk⁻¹; P > 0.05).

Similarly, Barwell et al.⁶¹ reported that following seven weeks of aerobic exercise, large variability in the change in fat mass was evident in fifty-five sedentary women.

While the mean loss of fat mass was only −0.97 ± 1.5 kg, examination of the indi-vidual responses indicated a range of −5.3 to +2.1 kg. In this instance, the total net ExEE accounted for 36 percent of the variance in fat mass. However, when differ-ences in ExEE were accounted for, wide variation in the residual change in fat mass was still evident (+2.5 to −2.9 kg). These two studies demonstrate the importance of examining the individual responses to exercise, as group or mean data can mask important information regarding the efficacy of an exercise intervention. While the mean weight loss in these studies was consistent with that previously reported (i.e., 1.5–3.0 kg),37–39,50–54 it is clear that individuals will not respond the same to the same exercise stimuli even under conditions of high compliance.

B^IologIcaland B^ehavIoral comPensatIonto d^Ietary r^estrIctIon

and P^hysIcal a^ctIvIty

The phenomenon of individual variability also points to marked differences in the susceptibility (and indeed resistance) to weight loss following periods of dietary- or

The phenomenon of individual variability also points to marked differences in the susceptibility (and indeed resistance) to weight loss following periods of dietary- or