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Front. Physiol. | doi: 10.3389/fphys.2018.01834

Effect of Estrogen on Musculoskeletal Performance and Injury Risk

  • 1College of Engineering, University of California, Davis, United States
  • 2Department of Neurobiology, Physiology, and Behavior, University of California, Davis, United States
  • 3Department of Physiology and Membrane Biology, School of Medicine, University of California, Davis, United States

Estrogen has a dramatic effect on musculoskeletal function. Beyond the known relationship between estrogen and bone, it directly affects the structure and function of other musculoskeletal tissues such as muscle, tendon, and ligament. In these other musculoskeletal tissues, estrogen improves muscle mass and strength and increases the collagen content of connective tissues. However, unlike bone and muscle where estrogen improves function, in tendons and ligaments estrogen decreases stiffness and this directly affects performance and injury rates. High estrogen levels can decrease power and performance and make women more prone for catastrophic ligament injury. The goal of the current work is to review the research that forms the basis of our understanding how estrogen affects muscle, tendon and ligament and how hormonal manipulation can be used to optimize performance and promote female participation in an active lifestyle at any age.

Keywords: Estrogen (17β-estradiol), Exercise, Tendon, Ligament, ACL (anterior cruciate ligament), Muscle, injury risk

Received: 07 Sep 2018; Accepted: 06 Dec 2018.

Edited by:

Mette Hansen, Department of Public Health, Faculty of Health, Aarhus University, Denmark

Reviewed by:

Victoria Wyckelsma, Karolinska Institute (KI), Sweden
Aaron Petersen, Victoria University, Australia, Australia  

Copyright: © 2018 Chidi-Ogbolu and Baar. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Keith Baar, Department of Neurobiology, Physiology, and Behavior, University of California, Davis, Davis, United States,