Effect of Estrogen on Musculoskeletal Performance

Effect of Estrogen on Musculoskeletal Performance and Injury Risk –  free full-text /PMC6341375/ – Jan 2019

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.

This can be important for those of us with EDS or HMS (or perhaps some other connective tissue problem) because it affects tendon & ligament function by decreasing stiffness.

High estrogen levels can decrease power and performance and make women more prone for catastrophic ligament injury.

Figure 1
Hormonal fluctuation during (A) a normal menstrual cycle, (B) while taking an oral contraceptive (OC) containing both estrogen and progesterone, and (C) in the years before and after menopause.

I’ve heard women state that at particular days in their cycle their joints would dislocate more easily, but I can’t remember with part of the cycle that was.

Both estrogen and progesterone are at their lowest during menstruation. Then estrogen rapidly climbs to its highest level right before ovulation at 2 weeks, and then it drops precipitously. Both estrogen and progesterone climb higher during the 3rd week and then go back to their lowest by the end of the 4th week.

I’d be interested in hearing from any of you if you’ve noticed the cycles in your joint laxity or pain levels.

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.

Conclusions and Future Research

recently the effect of estrogen on other musculoskeletal tissues such as muscle, tendon, and ligament has become the focus of more research.

These studies make it clear that estrogen improves muscle proteostasis [function] and increases sinew collagen content;

It seems that it would be better to have an increase in collagen content even if it’s defective. In general, estrogen seems like it could benefit functionality.

however, the benefits on bone and muscle come at the cost of decreased connective tissue stiffness.

Evolutionarily, this makes sense since laxer joints and better repair following injury would facilitate healthy childbirth and recovery.

However, as more women participate in sports it is clear that these physiological effects of estrogen contribute to decreases in power and performance and make women more prone for catastrophic ligament injury.

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In both tissues, the majority of the dry weight is collagen: 60–85% for tendon (Kjaer, 2004) and ~75% for ligament (Frank, 2004).

Of this collagen, the majority is type I: 60% in tendon and up to 85% in a ligament.

The mechanical properties of both the tendon and ligament are dependent on collagen fiber density, diameter, orientation, and cross-linking.

The fibers can be cross-linked in two ways: enzymatically and non-enzymatically. Enzymatic cross-links are mediated largely by lysyl oxidase (LOX; Siegel, 1976; Siegel and Fu, 1976). By contrast, cross-links can be formed without a specific enzyme through a Maillard reaction between a sugar and an amino acid. These cross-links are called advanced glycation end-products (AGE), and as would be expected are higher in diabetics (Dyer et al., 1993).

Both enzymatic cross-linking, through LOX, and non-enzymatic cross-linking through AGEs increase the stiffness of the tissues (Reddy et al., 2002; Svensson et al., 2013; Marturano et al., 2014). One of the main differences between enzymatic and non-enzymatic cross-links are their location and turnover rate, where AGEs decrease collagen turnover and over time this impairs sinew function (Hammes et al., 1991; Corman et al., 1998).


For excellent technical documentation of the menstrual cycle, I recommend the online “book” from the National Institute of Health:

Endotext (Endotext.org) is an online resource on endocrine disease written by physicians and directed toward physicians around the world caring for patients with endocrine disorders.

Other thoughts?

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