Document Type


Degree Name

Master of Science (MSc)


Kinesiology and Physical Education


Faculty of Science

First Advisor

Peter Tiidus

Advisor Role

Thesis Supervisor


This study investigated the role of estrogen receptor activation on total and proliferating satellite cells following running exercise in rats, by using an estrogen receptor-alpha (ER-α) specific agonist, 4,4,4 (4-Propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT). PPT is the first ER-α specific agonist (Stauffer et al 2000) which binds the ER-a subtype with a 410-greater affinity than ER-β (Stauffer et al 2000). Previous studies have demonstrated that estrogen can augment muscle satellite cell numbers following exercise (Enns and Tiidus, 2008) and that this augmentation may be due to mechanisms activated via estrogen receptors that can influence total, proliferating, and differentiating satellite cell numbers (Enns et al 2008). Ovariectomised female rats (n = 64) were divided into four groups: sham, estrogen (0.25 mg estrogen), agonist (PPT), and estrogen plus PPT. Each group was further divided into exercisers and controls (non-exercisers). PPT administration commenced 2 days after estrogen implantation and continued for 6 days. After 7 days of estrogen exposure, exercisers ran intermittently for 90 minutes (17m/min, -13.5 degree grade). Soleus and white vastus muscles were removed 72 hours post-exercise and immunohistochemically stained for total (pax7) and activated (MyoD) satellite cells. Severity of muscle damage was assessed indirectly by measuring betaglucuronidase activity. The results revealed that there were significant increases (p < 0.05) in fibers staining positive for total (pax7) and activated (MyoD) satellite cells when compared to shams in both the soleus and white vastus muscles. However, there was no significant difference (p > 0.05) observed between the treatment conditions supplemented with estrogen, PPT, and estrogen plus PPT. Augmented increases observed in muscle satellite cells post-exercise in the PPT supplemented group suggests that their activation is an estrogen receptormediated process. Due to no significant difference (p > 0.05) observed between PPT- and estrogen-mediated activation of ER-α receptors, ER-α is implicated as the receptor responsible for most, if not all, of the activation of satellite cell activity when induced by estrogen.

Convocation Year