I have been involved in research since the fall of 2016. I joined my personal advisor’s research laboratory as

an undergraduate student with the anticipation of gaining experience to “boost” my resume for medical school

applications. However, I fell in love with science and decided to peruse my Ph.D. instead. The research I have

pursued over the last 4 years has been focused on autonomic control of blood pressure and blood flow during

exercise in health and disease.

The ability to perform exercise and activities of daily living is critically dependent on appropriate adjustments

to the autonomic, cardiorespiratory, and cardiovascular systems. A reflex arising from within contracting skeletal

muscles termed the exercise pressor reflex contributes importantly to the increases in sympathetic nervous

system activity, ventilation, heart rate, myocardial contractility, and blood pressure during exercise. The sensory

arm of this reflex is comprised of thinly myelinated group III and unmyelinated group IV muscle afferents whose

endings are stimulated primarily by mechanical and metabolic signals, respectively. In healthy individuals,

activation of this reflex during exercise facilitates exercise performance by appropriately increasing ventilation

and cardiac output. Conversely, the exercise pressor reflex is exaggerated in patient populations such as heart

failure, peripheral artery disease (PAD), and diabetes mellitus which contributes to exercise intolerance in all

these populations.

During my graduate training, I have gained technical surgical skills on rodent models of cardiovascular

disease which facilitate our ability to pharmacologically target specific enzymes and receptors located on sensory

endings with the goal of identifying potential receptor(s) that may be playing a role in the exaggerated blood

pressure response during exercise pressor reflex activation in patients with PAD and heart failure. I have also

published data using the radiolabeled microsphere technique to measure blood flow distribution at rest and

during exercise in rats with heart failure and rats with type 2 diabetes mellitus. In addition to in vivo experimental

data, I have learned various molecular techniques including protein and gene expression analysis by Western

blot, enzyme-linked assays, and qRT-PCR. Together, in vivo and molecular data allow us to uncover the

mechanistic underpinnings of the exaggerated blood pressure response during exercise in cardiovascular

disease conditions. My specific interests have developed into studying the consequences of and mechanisms

behind the exaggerated exercise pressor reflex in a rat model of heart failure. My experience as a graduate

student has led to 5 first author publications, 5 co-author publications, and 3 conference presentations.