Dehydroepiandrosterone sulfate, resistive exercise training and cardiovascular disease risk factors in premenopausal females.
AuthorWilliams, Daniel Patrick.
Committee ChairLohman, Timothy G.
MetadataShow full item record
PublisherThe University of Arizona.
RightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
AbstractThe present study was designed to test the hypothesis that endogenous serum levels of dehydroepiandrosterone sulfate (DHEAS) would be inversely related to cardiovascular disease (CVD) risk factors and that circulating concentrations ofDHEAS would increase along with favorable alterations in CVD risk factors as a result of resistive exercise training. Serum concentrations ofDHEAS, lipids, lipoproteins, and fasting insulin were determined along with estimates of total and regional body composition from anthropometry and dual-energy x-ray absorptiometry (DEXA) in a crosssectional sample of premenopausal females aged 28-39 years (N=96) and in a 12 month longitudinal subsample randomly assigned to exercise (n=27) and control (n=27) groups. The date of subject entry into the intervention trial ranged from mid-autumn to late winter. The percentage of total fat located on the trunk from DEXA (r=0.32, P=0.002) was positively correlated with DHEAS, whereas the percentage of total fat located on the legs from DEXA (r=-0.25, P=0.015) was inversely correlated with DHEAS after adjusting for age, smoking and fasting status. Because obesity may be a prerequisite for the metabolic aberrations commonly associated with fat distribution, subjects were also classified by DEXA-determined %Fat (≥30 vs < 30) as obese or nonobese. In obese but not nonobese women, indexes of upper body and/or truncal fat distribution were positively correlated (r=0.31 to 0.51, P < 0.05) with fasting insulin, triglycerides, total and LDL cholesterol and negatively correlated (r=-0.45, P < 0.01) with HDL cholesterol. Correlations of similar magnitude yet opposite in direction were observed between indexes of lower body or leg fat distribution and metabolic CVD risk factors. DHEAS was inversely related to and accounted for 9.0% of the variation in LDL cholesterol after controlling for upper and lower body fat distribution and fasting insulin. DHEAS was also positively related to and accounted for 6.8% of the variation in HDL cholesterol after controlling for truncal fat percentage and distribution. Over the 12 month intervention, 42 subjects (18 controls and 24 exercisers) gained lean tissue mass (LTM) and 12 subjects (9 controls and 3 exercisers) lost LTM, whereas 26 subjects (15 controls and 11 exercisers) gained fat mass (FM) and 28 subjects (12 controls and 16 exercisers) lost FM. After adjusting for baseline HDL cholesterol, hematocrit change and subject study entry date, mean HDL cholesterol levels were significantly (P=0.026) maintained to a greater extent in LTM gainers (-1.3%) than in LTM losers (-15.0%). The HDL cholesterol-maintaining effect of gaining LTM was independent of control or exercise group status (P=0.042) and of the change in FM (P=0.015). The following was concluded from the study: 1.) increased amounts of total fat located on the trunk, and decreased amounts of total fat located on the legs, are associated with increased serum DHEAS concentrations in normally menstruating females; 2.) increased DHEAS levels are associated with decreased LDL and increased HDL cholesterol levels after controlling for the common associations of DHEAS and lipoproteins with fat distribution in obese premenopausal females; and 3.) the gain in soft tissue lean mass may prevent reductions in HDL cholesterol levels associated with lean tissue mass loss in healthy premenopausal females.
Degree ProgramPhysiological Sciences