Association between circulating endogenous androgens and insulin sensitivity changes with exercise training in midlife women.
OBJECTIVE
Aging induces a shift in circulating hormones in women, accompanied by weight gain during the late reproductive, menopausal transition, and postmenopausal years. Exercise has been shown to counter weight gain; however, it might increase circulating androgens. A 6-month aerobic and resistance training exercise regimen was implemented to examine interrelationships between circulating sex hormones, body composition, aerobic capacity, insulin sensitivity, and insulin resistance.


METHODS
Twenty-eight women, aged 42 to 52 years, completed the 6-month intervention study. They were randomly assigned to either a control (CON; n = 10) group-and maintained their sedentary lifestyle-or an exercise intervention (EXE; n = 18) group. The exercise intervention consisted of combined aerobic and resistance workouts scheduled 6 days/week for 60 minutes/day. Body weight, composition, VO2 peak, plasma insulin, glucose, lipid profile, estradiol, testosterone, progesterone, dehydroepiandrosterone, and dehydroepiandrosterone sulfate (DHEAS) were measured at baseline and on month 6. Insulin sensitivity was estimated using the insulin sensitivity index and the quantitative insulin sensitivity check index, whereas insulin resistance was estimated using the homeostatic model for insulin resistance.


RESULTS
There was a trend toward increased DHEAS in both groups (P < 0.1), but not as a function of the intervention. Insulin sensitivity index increased in the EXE group compared with the CON group (P < 0.01). Multiple linear regression indicated that, at 6 months, DHEAS was a negative contributor to insulin sensitivity in the EXE group, but not in the CON group.


CONCLUSIONS
In midlife women, an increase in circulating DHEAS, such as that previously reported during the menopausal transition, is associated with higher insulin resistance, but exercise can mitigate this risk by improving insulin sensitivity, thereby countering the effects of DHEAS.
From the 1Department of Nutrition, University of California, Davis, CA; 2Physiology Support Laboratory, Western Human Nutrition Research Center, US Department of Agriculture Agricultural Research Services, Davis, CA; 3Department of Environmental Toxicology, University of California, Davis, CA; and 4Obesity and Metabolism Research Unit, Western Human Nutrition Research Center, US Department of Agriculture Agricultural Research Services, Davis, CA.
Sridevi
S
Krishnan
Mary B
MB
Gustafson
Caitlin
C
Campbell
Nilesh W
NW
Gaikwad
Nancy L
NL
Keim
D000328:Adult; D000728:Androgens / Q000097:blood; D001786:Blood Glucose; D001823:Body Composition; D002318:Cardiovascular Diseases / Q000517:prevention & control; D002784:Cholesterol / Q000097:blood; D003687:Dehydroepiandrosterone / Q000097:blood; D004967:Estrogens / Q000097:blood; D005081:Exercise Therapy; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D008593:Menopause / Q000097:blood*; D008875:Middle Aged; D011374:Progesterone / Q000097:blood; D013739:Testosterone / Q000097:blood
D000728:Androgens; D001786:Blood Glucose; D004967:Estrogens; D013739:Testosterone; D003687:Dehydroepiandrosterone; D011374:Progesterone; D002784:Cholesterol