Delay in post‐ovariectomy estrogen replacement negates post‐exercise estrogen augmentation of muscle satellite cell population in rats (1163.23)

Abstract

17β‐Estradiol (E2) enhances activation, proliferation and differentiation of muscle satellite cells (SCs) following exercise via activation of estrogen receptor‐α (ER) and phosphatidylinositol 3‐kinase (PI3K) signaling. Supplementation of E2 through hormone replacement has been shown to ameliorate muscle atrophic effects of menopause in women. Delay in post‐menopause E2 replacement in humans or following ovariectomy in rodents has resulted in negation of positive health or regenerative effects of E2 on various tissues. To determine if delay in E2 replacement influenced E2 effects on skeletal muscle, 64, nine‐week old, ovariectomized Sprague‐Dawley rats were divided into eight groups based on: E2 status (0.25 mg estrogen pellet or sham), exercise status (90 min run @ 17 m/min, ‐13.5° or unexercised) and E2 replacement (“proximal”; E2 replacement within one week or “delayed”; eleven‐weeks following ovariectomy). Significant increases in total SCs were found in soleus muscle (immunofluorescent co‐localization of nuclei with Pax7) 72 hr following eccentric exercise (p < 0.05). Only “proximal” estrogen‐replacement resulted in further enhancement in total muscle SCs in exercised rats (p < 0.05). Delayed estrogen‐supplementation did not produce a further augmentation in post‐exercise SCs. This suggests the existence of a short window of opportunity where E2 replacement must commence following loss of endogenous estrogen production in order for benefits to skeletal muscle regeneration to manifest. Grant Funding Source: Supported by NSERC