Active Voice: Does Estrogen Modulate Physical Activity in Women?
By Edward L. Melanson, Ph.D., FACSM, and Wendy M. Kohrt, Ph.D., FACSM
Edward L. Melanson, Ph.D., FACSM, is a professor of medicine at the University of Colorado Anschutz Medical Campus in Aurora, Colorado. His research is focused on how lifestyle factors impact energy and substrate metabolism, particularly related to obesity and aging.
Wendy M. Kohrt, Ph.D., FACSM, is a professor of medicine and director of research in the Division of Geriatric Medicine and the Center on Aging at the University of Colorado Anschutz Medical Campus in Aurora, Colorado. Dr. Kohrt presented the Joseph B. Wolfe Memorial Lecture at the 2012 ACSM Annual Meeting and received the ACSM Citation Award in 2010.
This commentary presents Dr. Melanson’s and Dr. Korht’s views on the topic of their research article that they co-authored with other colleagues. Their paper appeared in the August 2018 issue of Medicine & Science in Sports & Exercise® (MSSE).
The menopausal transition increases risk for weight gain and a redistribution of body fat. Prior to menopause, women tend to have more of a “pear shape.” After menopause, women tend to accumulate fat in the abdominal region, assuming the “apple shape” that is more common in overweight men. This apple-shaped pattern is associated with an increased risk of chronic diseases, including cardiovascular disease and diabetes.
Suppressing ovarian hormones or blocking estrogen signaling in rodents causes decreases in both resting energy expenditure (EE) and physical activity EE, leading to increases in weight and fat mass. These effects are prevented or reversed by estradiol (E2) treatment. In women, physical activity levels decrease across menopause. However, the specific effects of the loss of ovarian E2 on EE and physical activity in women have not been extensively studied. Using a pharmacological approach to control E2 status, we have demonstrated that the suppression of ovarian hormones causes a decrease in resting EE, and this is prevented by E2 treatment.
In the August 2018 issue of MSSE, we reported the results of our recent study in which we evaluated whether suppressing E2 reduces physical activity in women as it does in rodents. Sixty-one healthy premenopausal women (average age 35 years) received monthly intramuscular shots for five months to suppress ovarian hormones. In a double-blinded manner, 30 of these women received E2 treatment using a transdermal patch, and the remaining 31 received a placebo patch. Some women in each group were also randomized to perform supervised resistance exercise. Physical activity was measured for one week during each month of the intervention using a waist-worn accelerometer. We compared physical activity levels at month four, which is the time we expected the effects of ovarian hormone suppression to be maximal. Moderate-to-vigorous physical activity tended to be higher in the women who received E2 treatment, and these effects were more pronounced in women who were not participating in the exercise intervention. These findings suggest that E2 helped maintain spontaneous physical activity in women who were not otherwise exercising.
This exploratory study was conducted in a subset of women from a larger trial, the aim of which was to determine the effects of E2 on resting EE. In this context, the results must be considered as “proof of concept” rather than definitive evidence that E2 regulates spontaneous physical activity in women. It will be necessary to perform larger studies to confirm these results. We have only begun to understand how female sex hormones regulate energy balance and fat distribution. There remains much to learn about how menopausal changes in ovarian hormones impact health in women.