Graduation Year

2026

Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts

Department

Biology

Reader 1

Jenna Monroy

Reader 2

Ashley Heers

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Terms of Use for work posted in Scholarship@Claremont.

Abstract

Skeletal muscles are essential for vertebrate locomotion and structural integrity. During contraction, calcium release into the muscle cell allows the thin (actin) and thick (myosin) filaments to bind and slide past one another. Titin, a filamentous protein spanning the half-sarcomere, contributes to passive stiffness, active force regulation, and structural stability in cardiac and skeletal muscle. Estradiol (E2) deficiency, common after menopause and modeled in rodents with ovariectomy (OVX), is known to alter titin isoforms, calcium handling, and, potentially, phosphorylation, in cardiac muscles, but its effect in skeletal muscle cells remains less researched. This systematic review examines how ovariectomy in rodents influence titin-related contractile properties in skeletal muscle, including fiber type composition, fiber type cross sectional area (CSA), passive and active stiffness, and isometric tetanic force (Po). Following database searches and precise exclusion criteria, five studies measuring soleus, extensor digitorum longus (EDL), or tibialis anterior (TA) muscle contractile properties fit the criteria. Across studies, OVX generally shifted CSA within type II fibers towards more oxidative fast-twitch fibers. Three studies found that OVX mice expressed lower isometric tetanic force, lower active stiffness, and higher passive stiffness, with effects typically reversed by estrogen supplementation. However, one study reported opposite trends, likely due to methodological inconsistencies and a decreased focus on the interaction between OVX and control groups. Collectively, the evidence suggests that estrogen influences skeletal muscle contractility through titin dependent mechanisms, but variability in methods and outcomes limit definitive conclusions. Future studies using titin-mutant models are needed to confirm that estrogen deficiency does alter muscle contractile properties due to a change in titin.

This thesis is restricted to the Claremont Colleges current faculty, students, and staff.

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