The aim of the current study was to compare the effects of 6 months of caloric restriction by dietary restriction only or dietary restriction in combination with exercise, on body composition and abdominal fat distribution in overweight men and women. Our data suggest that when the level of caloric restriction imposed is precisely matched and carefully controlled, the changes in body composition and abdominal fat distribution are not further enhanced by the addition of exercise, rejecting our hypothesis. A novel finding was that fat depots, regardless of their location, were reduced by approximately 30% in men and 25% in women in such a way that fat distribution throughout the whole body (DXA) and specifically within the abdominal compartment (CT) was not altered by caloric restriction.
A major strength of the study is that the prescribed energy deficits were carefully determined from two 14-d assessments of energy requirements by doubly labeled water and from a 14-d weight maintenance feeding period. Furthermore, the energy expended during exercise was clearly defined and quantified throughout the study for energy cost. Estimates of energy balance calculated from changes in energy stores vs. the energy intake provided for weight maintenance at baseline indicates that both CR and CR+EX had a similar degree of energy restriction throughout the study.
The losses in fat mass (-27% for men and -22% for women) and VAT mass (-31% for men and -24% for women) were similar in both treatment groups. However, due to the small sample size, it is conceivable that this result represents a type II statistical error. In other words, we could not reject the null hypothesis when a true difference exists between CR and CR+EX. One might then ask whether these treatments were different, what size difference could we detect with our methods and these sample sizes. For VAT mass, for example, the smallest difference we could detect between CR and CR+EX with 12 participants per group, alpha less than 0.05 and power 0.80 or greater is 210 g, an amount probably not clinically relevant.
The inability of caloric restriction to alter the distribution of fat suggests that individuals are genetically or epigenetically programmed for fat storage in a particular pattern and that this programing cannot be easily overcome by weight loss. In support of this contention, twin studies have shown that FM and regional fat distribution are largely determined by genetic factors (17
) and that genetic heritage can explain changes in body composition and fat distribution during positive and negative energy balance (19
). In contrast to our results, many studies of caloric restriction or weight loss in obese and morbidly obese individuals report more profound reductions in visceral fat, compared with sc fat (2
). These findings have been explained by the larger VAT depots to begin with (20
) and also because lipolysis is higher in the VAT vs
. non-VAT depots (21
). However, when results are appropriately adjusted for differences in VAT mass before treatment, the enhanced reduction in VAT was no longer apparent (22
There is some debate whether the inclusion of exercise in weight loss interventions is protective against the loss of FFM (23
). In our study, FFM was reduced with the 6-month intervention and was not different between the intervention groups. Our data suggest that FFM is reduced in parallel with the degree of caloric restriction and that regular aerobic exercise (5 d/wk), at least in nonobese individuals, does not preserve lean mass.
To assess fully the independent role of exercise on changes in body composition and fat distribution this study would need to be repeated with an exercise-only group in the study design. To produce a 25% energy deficit by exercise only, it would require approximately 120 min of exercise per day for women and approximately 90 min for men, a daunting task. Few randomized, controlled trials of this nature have therefore been attempted. A 12-wk weight loss intervention, induced by either diet or exercise in obese men (2
) showed that despite equivalent weight loss (~7.5%) and changes in ab- dominal fat distribution, exercise produced a greater reduction in fat mass. When the same trial was repeated in obese women (3
), a similar reduction in weight (~6.5%) was achieved by both groups, but the exercise group lost approximately 6% more fat mass and approximately 10% more fat from VAT. A possible explanation of these findings could be that exercise independently reduces fat loss in men and women and selectively targets VAT. Indeed, a recent randomized, controlled trial of exercise only (24
) supports this argument, showing that exercise reduces weight, FM, and VAT in a dose-dependent manner. However, retrospective analyses from both studies (2
) indicated that the energy deficit achieved by the exercise groups exceeded those of the diet groups. Therefore, it is difficult to conclude that exercise can independently lead to greater improvements in fat distribution when the energy deficit achieved is a confounding factor in the interpretation.
Despite its role in energy balance, exercise can produce health benefits independent of changes in body weight such as improvements in glucose tolerance (9
) and aerobic fitness (26
). A low level of aerobic fitness has been identified as a stronger predictor of cardiovascular disease mortality than other risk factors including body fatness (28
). Improved mitochondrial function and muscle oxidative capacity are believed to be important adaptations of exercise that link aerobic fitness to cardiovascular and metabolic disease (31
). Participants in the CR+EX group significantly improved their peak aerobic capacity, whereas the CR and control groups did not (change in peak oxygen uptake; CR: 2.01 ± 1.76; CR+EX: 5.88 ± 1.27; control: -1.87 ± 1.05 ml·kg-1
) and as detailed in a previous report (14
), insulin sensitivity as measured by frequently sampled iv glucose tolerance test was increased at month 6 in both CR and CR+EX but only reached significance in the combined CR+EX intervention. We can speculate therefore that the combined CR+EX intervention may induce greater cardioprotective benefits through an improvement in aerobic fitness.
Participants in the CR+EX group self-selected their level of exercise intensity throughout the study because we believed compliance to the intervention would be enhanced with this strategy. Exercise intensity has been shown to influence body composition and cardiovascular and other metabolic outcomes in a dose-response manner (25
). Studies of exercise-induced weight loss suggest that high intensity exercise (65–80% maximal oxygen uptake) leads to greater improvements in visceral fat loss, insulin sensitivity, and lipoprotein profiles than moderate (40–55% maximal oxygen uptake) or low intensities. It might be argued that our approach may underestimate the role of exercise in the CR+EX intervention. Alternatively it could be argued that differences in body composition changes between these kinds of treatments are dependent on the resultant energy expenditure and energy deficit created by higher intensity exercise, rather than the exercise intensity itself (33
Previous randomized, controlled trials determining the role of dietary restriction in conjunction with exercise on body composition and metabolic risk factors have been confounded by the degree of energy restriction and therefore have produced conflicting results. Contrary to our hypothesis, our data indicate that when the degree of energy restriction is carefully matched, improvements in metabolic risk factors (body composition and fat distribution) in overweight men and women are dependent on the net energy deficit and that the inclusion of exercise does not contribute any added benefit in terms of changes body composition. Exercise therefore plays an equivalent role to caloric restriction in terms of energy balance; however, it can also improve aerobic fitness, which has other important cardiovascular and metabolic implications.