Figure 4.

Schematic of how estrogens may benefit muscle strength. Ovariectomized mice display a reduction in muscle strength and this is attributed to a decrement in the fraction of strong-binding myosin during contraction. Conversely, treatment with estrogens increases strong-binding myosin and ultimately strength. Estrogen receptor (ER) content in muscle is responsive to circulating estrogens, and we hypothesize that ERs may initiate signaling cascades and/or regulate genes that result in an overall reduction in oxidative stress in fibers. Alternatively, estrogens may have some direct antioxidant affect. We speculate that reducing oxidative stress would preserve myosin structure-function, conferring a beneficial effect on strength. Solid arrows represent experimental evidence from our lab and others. Dashed arrows represent hypothesized mechanisms of estrogens’ actions in skeletal muscle. Abbreviations: adenosine triphosphate (ATP), inorganic phosphate (P_i), G protein-coupled receptor (Gper).