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Estrogens Are for More Than Just Reproductive Endocrinology

Bowen, Robert S.

Exercise and Sport Sciences Reviews: January 2019 - Volume 47 - Issue 1 - p 2
doi: 10.1249/JES.0000000000000175
Commentary to Accompany

Pilgram Marpeck School of STEM Truett McConnell University Cleveland, GA

Authors for this section are recruited by Commentary Editor: Russell R. Pate, Ph.D., FACSM, Department of Exercise Science, University of South Carolina, Columbia, SC 29208 (E-mail: rpate@mailbox.sc.edu).

Editor’s note: This commentary addresses the article Modulation of Energy Expenditure by Estrogens and Exercise in Women that was published in the October 2018 issue of the journal. The article can be found at https://journals.lww.com/acsm-essr/Fulltext/2018/10000/Modulation_of_Energy_Expenditure_by_Estrogens_and.6.aspx

Estrogen deficiency seems to be a fact of life for the aging female. At the onset of menopause, the biology of the 11 organ systems changes in response to the reduction of this physiologically potent sex steroid. Despite the well-known anecdotes surrounding menopause, surprisingly little is known regarding the scientific complexities of this natural biological process. In a recent issue of Exercise and Sport Sciences Reviews, Gavin et al. (1) add to the scientific understanding of estrogen deficiency proposing that a loss of estrogen at the onset of menopause leads to an increased risk for metabolic disease development and progression. The authors suggest that as estrogen levels decrease, concomitant reductions in physical activity and brown adipose tissue activity and increased synthesis of bone marrow–derived adipocytes begin to adversely affect energy expenditure and induce an accumulation of fat mass in visceral depots. Fortunately, however grim the scenario of menopause-induced estrogen deficiency and associated metabolic alterations might appear on the surface, strategies to counter the adversities of this unavoidable age-related process may be on the horizon. There is hope in the recognition that estrogens are more than just for the regulation of reproductive endocrinology.

Reduced physical activity associated with estrogen deficiency has long been postulated in rodent (2) and human (3) subjects and is certainly a prime causative candidate for the reduced energy expenditure observed after menopause. The beneficial impact of physical activity on a wide range of health outcomes has been extensively documented. For example, Mokdad et al. (4) estimate that physical inactivity and poor dietary choices result in nearly 400,000 deaths annually; a global burden of 16.6% of all deaths in the United States, second only to smoking, and fully 315,000 more deaths per year than the third leading actual cause of death. Any factor that systematically reduces physical activity in a large segment of the population should be seen as a threat to public health. This concern certainly applies to estrogen deficiency during menopause. On the other side of this hypothesis, the contribution of brown adipose tissue activity and bone marrow-derived adipocytes to the reduction of energy expenditure and proliferation of visceral fat are less well-characterized in general and specifically in relation to the observed physiological changes associated with the menopause transition and estrogen deficiency. Mounting evidence from both animal and human studies are compelling, and these other factors in the postulated model seem to have important effects as estrogen levels decrease and postmenopause disease risks increase. Ending the story here paints a picture of despair and hopelessness; fortunately, the story continues.

Strategies to counterbalance estrogen level changes during the menopause transition are readily available. Pharmacological treatments and hormone replacement options are clinically available to ease the physiological burdens associated with menopause that appear, in part, to alter several of the factors postulated in the present model of estrogen depletion. Furthermore, physical activity and exercise are virtually free with just a good pair of walking shoes. Sidewalks, hiking trails, bike paths, and a host of other entities within the built environment are scattered all across the nation and are ready to be tarried, tracked, and trudged. One of the remaining conundrums is to figure out why, given our global recognition of the benefits of physical activity, most people fail to meet the minimum recommended quantities of weekly physical activity participation — a phenomenon that occurs during most stages of the human life cycle including during menopause (hint: The answer to the physical activity participation conundrum is likely related to a biological mechanism that influences the ability and motivation to participate in physical activity).

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References

1. Gavin KM, Klemm DJ, Kohrt WM, Melanson EL. Modulation of energy expenditure by estrogens and exercise in women. Exerc. Sport Sci. Rev. 2018; 46(4):232–9.
2. Lightfoot JT. Sex hormones' regulation of rodent physical activity: a review. Int. J. Biol. Sci. 2008; 4(3):126–32.
3. Bowen RS, Turner MJ, Lightfoot JT. Sex hormone effects on physical activity levels: why doesn't Jane run as much as Dick? Sports Med. 2011; 41(1):73–86.
4. Mokdad AH, Marks JS, Stroup DF, et al. Actual causes of death in the United States, 2000. JAMA. 2004; 291(10):1238–45.
© 2019 American College of Sports Medicine