Date Thesis Awarded


Access Type

Honors Thesis -- Access Restricted On-Campus Only

Degree Name

Bachelors of Science (BS)


Kinesiology & Health Sciences


Michael Brennan Harris

Committee Members

Randolph A. Coleman

Scott B. Ickes


Cardiovascular disease (CVD) is the leading cause of death in United States and worldwide. Exercise has been shown to improve endothelial function and provide protection against cardiovascular diseases. Endothelial nitric oxide synthase, or eNOS, is an enzyme that produces the potent vasodilator nitric oxide (NO). Interruptions in NO bioavailability and oxidative stress are commonly linked to CVD. SIRT1, a NAD-dependent deacetylase, is a regulator of eNOS and endothelial function. The mechanism by which SIRT1 is involved in endothelium dependent vasodilation is poorly understood. SIRT3, another NAD-dependent deacetylase of the same family as SIRT1, is implicated in oxidative stress response. Exercise has been shown to enhance both SIRT1 and SIRT3 expression, however, changes in expression across an exercise-training program has yet to be determined. The first study examines endothelial function with or without SIRT1 inhibition and SIRT1 and eNOS protein expression with or without Vitamin E supplementation (a known reducer of oxidative stress) after different durations of training in rat aortas. The purpose of the second study is to determine SIRT1 and SIRT3 protein expression in skeletal muscles (soleus, plantaris, and extensor digitorum longus (EDL)) and heart muscles. These results demonstrate that mechanisms regulating vascular reactivity during the course of an exercise-training program involve dynamic changes in SIRT1 and eNOS and exercise also induces changes in skeletal muscle expression of SIRT1 and SIRT3.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-No Derivative Works 3.0 License.


Thesis is part of Honors ETD pilot project, 2008-2013. Migrated from Dspace in 2016.

On-Campus Access Only