Estrogen status and skeletal muscle recovery from disuse atrophy

Abstract

Although estrogen loss can alter skeletal muscle recovery from disuse, the specific components of muscle regrowth that are estrogen sensitive have not been described. The primary purpose of this study was to determine the components of skeletal muscle mass recovery that are biological targets of estrogen. Intact, ovariectomized (OVX), and ovariectomized with 17beta-estradiol replacement (OVX+E2) female rats were subjected to hindlimb suspension for 10 days and then returned to normal cage ambulation for the duration of recovery. Soleus muscle mass returned to control levels by day 7 of recovery in the intact animals, whereas OVX soleus mass did not recover until day 14. Intact rats recovered soleus mean myofiber cross-sectional area (CSA) by day 14 of recovery, whereas the OVX soleus remained decreased (42%) at day 14. OVX mean fiber CSA did return to control levels by day 28 of recovery. The OVX+E2 treatment group recovered mean CSA at day 14, as in the intact animals. Myofibers demonstrating central nuclei were increased at day 14 in the OVX group, but not in intact or OVX+E2 animals. The percent noncontractile tissue was also increased 29% in OVX muscle at day 14, but not in either intact or OVX+E2 groups. In addition, collagen 1a mRNA was increased 45% in OVX muscle at day 14 of recovery. These results suggest that myofiber growth, myofiber regeneration, and extracellular matrix remodeling are estrogen-sensitive components of soleus muscle mass recovery from disuse atrophy.

Naringenin modulates skeletal muscle differentiation via estrogen receptor α and β signal pathway regulation

“…In addition, previous data from our laboratory show the ability of E2 to increase the levels of well-known skeletal muscle differentiation (i.e., Myo and fetal MHC) and metabolic (i.e., GLUT-4 translocation) markers in growing L6 rat myoblasts (i.e., 10 % serum) (Galluzzo et al 2009). In good agreement with the literature (McClung et al 2006;Brown et al 2005;Thomas et al 2010;Barros and Gustafsson 2011), this E2 effect is dependent on the receptor subtype a signaling initiating at the plasma membrane (Galluzzo et al 2009), although the involvement of ERb in the expression of satellite cell and muscle regeneration markers (i.e., MHC embryonic, MyoD, Pax7) after injury with a myotoxin (notexin) has been also reported (Velders et al 2012). Here, we also confirm this E2 effect in differentiating conditions.…”

“…Several studies indicate that E2 deficiency inhibits the muscle regeneration, and E2 supplementation enhances muscle mass and strength (Wust et al 2008) accelerating skeletal muscles regeneration (McClung et al 2006;Brown et al 2005). In addition, previous data from our laboratory show the ability of E2 to increase the levels of well-known skeletal muscle differentiation (i.e., Myo and fetal MHC) and metabolic (i.e., GLUT-4 translocation) markers in growing L6 rat myoblasts (i.e., 10 % serum) (Galluzzo et al 2009).…”

“…In particular, many studies have demonstrated sex differences in skeletal muscle response to injury and in the indices of skeletal muscle damage, inflammation, and repair that are largely attributable to E2 (Bar et al 1988;McClung et al 2006). Skeletal muscle expresses both ERs, and in rodents, ERb is the predominant subtype (Barros and Gustafsson 2011;Galluzzo et al 2009).…”

Effects of resistive exercise and stretching on the soleus muscle of ovariectomized rats

“…The muscle loss is primarily due to an imbalance between muscle protein synthesis and muscle protein breakdown and the increase of connective tissue and fat, reduction in the muscle fiber cross sectional area and a decrease in the estrogen muscle receptor 18 . In addition, McClung et al 19 observed that while ovarietomized rats took 28 days to recover the myofiber cross-sectional area when kept free in the cages, those ovariectomized with 17-estradiol replacement took only 14 days. The authors concluded that myofiber growth, myofiber regeneration, and extracellular matrix remodeling are estrogen-sensitive components of soleus muscle mass recovery from disuse atrophy.…”

“…McClung et al 19 observed that the MFCSA of ovariectomized rats was able to recover compared to rats subjected to suspension of the lower limbs. Therefore, these authors observed that the soleus muscle mass of intact animals recovered by around the 7th day, whereas the ovariectomized rats' muscle masses did not recuperate until the 14th day.…”