Our results indicate that moderately overweight AA and EA women benefitted in terms of CVD risk from a moderate weight loss. Both races significantly decreased overall fat and IAAT as well as improved all CVD risk factors measured. This was particularly surprising in the AA women who had IAAT well below the 110 cm2
set point previously proposed for identification of CVD risk (16
) and had a relatively benign blood lipid profile prior to weight loss. Consistent with cross-sectional studies in which IAAT is clearly related to CVD risk (3
), IAAT changes with weight loss explained reductions in TC, TG, and LDL. However, it is not clear which fat depot change mediated changes in other CVD risk factors.
EA women had higher absolute amounts IAAT, and lost more IAAT than AA women. However, proportional decreases in IAAT were similar between the races (AAs = −39.3%, EAs = −37.4%). In addition, the losses in IAAT in the two races fit recently developed models for predicting the well known preferential loss of IAAT that occurs during interventions, which induce weight loss (29
). It appears that the amount of IAAT lost was appropriate for the amount of IAAT that was present, prior to weight loss in both races.
It is well-established that IAAT is related to increased CVD risk, whereas LF is not (3
). In fact, LF has been associated with decreased CVD risk, at least in studies that have had individuals with relatively similar percent body fat or studies in which statistical adjustments have been made for either total fat or IAAT (5
). In the present study, IAAT changes were positively related to changes to all CVD risk variables with the exception of ΔHDL and ΔDBP. LF changes correlated negatively with changes in ΔTC and ΔTG. Multiple regression modeling shows that the respective positive and negative relationships for change in ΔIAAT and ΔLF with change in ΔTC and ΔTG are independent of each other. Consistent with the cross-sectional data the results of this study suggest that losses in IAAT may be beneficial to CVD risk. The findings that changes in LF are negatively associated with measured metabolic variables, and that changes in IAAT are positively associated with these variables may indicate that different fat depots have distinct biological activity. Thus, it could be envisioned that accumulation of subcutaneous fat is acting as a healthy way to accumulate energy surplus, whereas lipid partition to the IAAT depot promotes key metabolic perturbations such as high TG. These metabolic perturbations may originate from the biological activity of these fat depots. However, we do not find any significant relationships between blood lipids and BP with SAAT, suggesting that biological activity is different between subcutaneous fat in the abdomen and fat in the legs, which is also primarily subcutaneous. Other explanations are also possible, however. For example variables that may cause individuals to preferentially deposit fat in the viscera, such as parity (31
), cytokines (32
), catecholamines, cortisol (33
), estrogens, or some other hormones may be the mediating factor in reducing CVD risk rather than the LF per se
. This would mean of course that this variable or variables would have to be in the decreasing range during weight loss, mediating the preferential reduction in IAAT over LF while also mediating a larger decrease in CVD risk. Obviously, further research is needed in addressing this important conundrum.
Consistent with other studies (34
), exercise appeared to offer no enhanced benefit to CVD risk factors over diet weight loss; it seems plausible to conclude that loss of fat, especially IAAT, was the driving force for metabolic profile-improvements in this study. Confusion exists whether exercise training has an effect on causing a preferential loss of IAAT with some studies suggesting preferential loss of IAAT (17
) and others showing no preferential loss in IAAT (37
). The effects of weight loss from restricting calories may be masking the independent effects of exercise on fat distribution and CVD risk factors. It is possible that the exercise stimulus was insufficient to induce an additional improvement in blood lipid change over weight loss due to diet. We feel that it would be difficult to achieve a higher intensity of training with nonathletes as the aerobic exercisers trained for 40 min at 80% of maximum heart rate and the resistance exercisers did 2 sets of 10 repetitions for 10 exercises at 80% of 1-RM. Although both the aerobic and resistance exercisers were scheduled to train three times each week, adherence was only 78% for the resistance trainers and 80% for the aerobic trainers. This resulted in the two groups averaging just over 2.3 exercise sessions/week. It certainly can not be ruled out that more frequent exercise training may have resulted in greater improvements in the blood lipid profile.
It is interesting that a number of different reports on obese polycystic ovary syndrome patients have reported similar findings to those found in more normal subjects. They have shown that visceral fat is associated with cardiovascular risk (40
) and that exercise training is associated with improved fertility (41
), improved cardiopulmonary function, decreased C-reactive protein, and improved insulin sensitivity indexes (42
) but not TGs, TCs, or HDLs. However in a different study, the authors report significant improvements in blood lipids after 12 weeks of aerobic training that totally disappeared after 12 weeks of detraining (43
). Irrespective of whether a higher exercise frequency would have added to the improvement in blood lipids, these results should not be interpreted to mean that exercise has no benefit during diet-induced weight loss. Exercise has been previously shown to have positive effects on other factors, such as insulin sensitivity (38
), energy expenditure and maintenance of muscle (39
), and bone density (44
) during diet-induced weight loss. The average amount of time for exercise having taken place before metabolic testing was 60 h in the present study, and there may have been acute effects of exercise confounding the blood analyses, because some studies have reported temporary changes in blood lipids after 24–48 h (45
). The present study did not control for the acute effects of exercise, and it may have been a limitation in our results. It should also be mentioned that even though we did not find an independent effect of ΔIAAT or ΔLF on the BP, other studies (48
) have documented that decreases in waist circumference were related to changes in BP.
Both overweight and premenopausal AA and EA women benefitted from weight loss by decreasing IAAT and improving CVD risk. This finding occurred even in AA women who had little IAAT and relatively low CVD risk before weight loss. The changes in IAAT were significantly related to blood lipids. A loss of LF seems to be related to reduced improvement in TC and TG. Based on these results, interventions should focus on changes on IAAT.