Date of Award

8-22-2025

Date Published

September 2025

Degree Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Exercise Science

Advisor(s)

Joon Young Kim

Keywords

Aerobic Exercise;Arterial Stiffness;Autonomic Dysfunction;Cardiometabolic Disease Risk;Inflammation

Abstract

Autonomic dysfunction (AD) is a precursor for cardiometabolic disease development; however, identifying AD and its associated risks presents significant challenges due to multi-system dysregulation and diverse symptom presentation. We examined subclinical cardiometabolic disease risk in AD and the utility of simple autonomic symptom assessments to identify subclinical disease risk. Study 1 thematically explored potential associations linking Postural Orthostatic Tachycardia Syndrome (POTS) to cardiometabolic disease risk. Neuropathic and hyperadrenergic POTS phenotypes may be related to metabolic dysregulation through autonomic neuropathy, sympathetic activity, inflammation, insulin resistance, and elevated vasoactive gut hormones. Study 2 investigated subclinical cardiovascular disease risk in POTS and whether acute aerobic exercise can improve central hemodynamic load. POTS patients had similar central hemodynamic load compared to controls and a bout of aerobic exercise did not alter hemodynamic responses in POTS or controls. Study 3 examined whether changes in cerebral blood flow (CBF) contribute to orthostatic intolerance (OI) symptomology in response to acute aerobic exercise in POTS. OI symptomology was higher in POTS compared to controls, but higher OI symptomology was not related to decreased CBF in POTS patients. Study 4 examined the relationship between AD symptom severity with inflammation and arterial stiffness in adults of the general population. AD symptom severity was not an independent predictor for inflammation and arterial stiffness. These studies suggest that 1) POTS patients may not be at increased subclinical cardiovascular disease risk compared to their healthy counterparts and 2) simple assessments of AD symptomology may not be a practical stand-alone screening tool for cardiometabolic disease risk in generally healthy adults. Our findings highlight the complexity of cardiometabolic risk in AD and utility of symptom-based assessment tools.

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Open Access

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