Following a 12 kg weight loss, adherence to either moderate volume (about 80 minutes/week) aerobic or resistance training resulted in reduced one-year weight regain (3.1 kg aerobic and 3.9 kg resistance versus 6.4 kg for the no exercise group). Perhaps more important, the aerobic and resistance training prevented visceral fat (IAAT) regain, despite modest weight regains, while the group that did not participate in exercise training increased visceral fat 25%. This was the case for both AA and EA women, suggesting that the exercise intervention was equally affective for both races. The adhering exercisers did regain body fat in other regions, however, such as an increase of about 18% in leg fat. These results not only are supportive of the concept that moderate volumes of exercise training are beneficial for decreasing weight regain following weight loss, but supportive of the concept that exercise training might direct energy storage during fat regain to depots other than the viscera.
It is important to point out that the smaller weight regain and prevention of visceral fat gain was achieved with a small volume of exercise training, only 80 minutes/week. Since other studies have reported that much longer training durations of more than 60 minutes/day are necessary to prevent weight regain (11
) it is not too surprising that weight regain was not totally prevented in this study. It is very encouraging, however, that this relatively small volume of exercise was sufficient to prevent visceral fat gain.
No consensus has been reached concerning the effects of exercise training on fat distribution. Both aerobic and resistance exercise training are associated with loss of body fat, particularly visceral fat suggesting either type of exercise training may result in proportionately small amounts of fat stored in the viscera (24
). Since diet induced weight loss is also associated with a disproportionately large visceral fat loss, it is possible that caloric deficit will create similar visceral fat losses whether the restriction is induced by diet or exercise. For example, a 10% weight loss is typically associated with a 30 to 35% visceral fat loss following diet induced weight loss (37
). In one of the few studies comparing exercise and diet induced weight loss, Ross et al (29
) showed similar visceral fat losses between diet and exercise interventions. However, others have found over two times more visceral fat loss for exercise induced weight loss when weight loss is matched between exercise and diet induction (28
). In addition, detrained athletes increase waist circumference despite decreasing body weight (38
) suggesting an increase in visceral fat as the athletes detrained. Although not conclusive, these studies, as well as the present study, suggest that exercise training may be beneficial in prevention of visceral obesity.
Although there was no increase in visceral adipose tissue in those who adhered to exercise, fat in other depots did increase. Prevention of visceral adipose tissue gain is important since visceral adipose tissue is more strongly related to cardiovascular disease and diabetes risk than fat in other depots (1
). In fact, multiple regression modeling shows that independent of visceral fat, leg fat is typically associated with improved blood lipid profile and insulin sensitivity (4
). Although this could be interpreted to mean that leg fat is protective, other interpretations are possible. For example, it is possible that the same factors that may cause an individual to preferentially partition fat in the legs may be responsible for improving risk. No definitive interpretation of these correlational findings are available at this time, however, it is clear that leg fat does little to increase cardiovascular and diabetes risk. Therefore, from a health risk standpoint repartitioning of fat away from the viscera by exercise training would be considered beneficial.
No significant differences were observed between those subjects who were assigned to exercise training but adhered poorly to the training and those subjects who were assigned to the no exercise group. This was not too surprising since adherence for the nonadhering exercisers was about 20 % of the twice weekly scheduled exercise sessions.
Little is known concerning potential mechanisms for exercise training success in preventing visceral fat regain, despite weight regains. One possibility would be that the exercise training prevented body fat regains despite modest weight regain. However, percent body fat increased even among the exercise adherers in our study (3.4 % and 4.4 % for the aerobic and resistance adherence groups). Despite this increase in percent body fat the two adherence exercise groups did not significantly increase visceral fat (mean of 1.6 % for the aerobic group and 0 % for the resistance group). Another plausible explanation, considering our results that suggest a repartitioning of fat gain, would be that the hormonal milieu changed so that it favored storage of fat in periphery rather than the viscera. Cortisol (39
), exogenous androgens (40
), and dopamine (41
) may increase storage of fat in the viscera while growth hormone (39
) may have a negative effect on storage of fat in the viscera in women. Exercise training has well established effects on a number of hormones including decreasing cortisol (42
) and increasing growth hormone (43
). More research is needed to confirm any potential positive effects exercise training may have on fat distribution and to explore potential mechanisms by which exercise might achieve in repartitioning fat distribution.
In conclusion, as little as 80 minutes/week aerobic or resistance training had modest positive effects on preventing weight regain following a diet induced weight loss. More importantly, though, both aerobic and resistance training prevented regain of potentially harmful visceral fat.