Degree

Doctor of Philosophy (PhD)

Department

Kinesiology

Document Type

Dissertation

Abstract

Hypertension and cardiovascular disease remain leading causes of global morbidity and mortality, though many remain undiagnosed with normal resting blood pressure. Exercise testing can reveal abnormal cardiovascular regulation not evident at rest. A hypertensive response to exercise (HRE) has emerged as an early marker of cardiovascular dysfunction; however, its assessment has relied largely on maximal cardiopulmonary exercise testing (CPET), limiting clinical accessibility. This dissertation investigated HRE as an early cardiovascular risk indicator and evaluated accessible strategies for detecting abnormal exercise blood pressure responses in individuals without diagnosed hypertension.

The literature review summarized evidence on normal and abnormal exercise blood pressure responses, mechanisms underlying HRE, and its clinical relevance, highlighting associations with future hypertension, subclinical organ damage, and cardiovascular events, and noting inconsistent definitions and protocols as barriers to clinical translation.

The first study examined interactions between HRE and traditional cardiovascular risk factors, emphasizing vascular and autonomic dysfunction; findings suggested HRE reflects impaired blood pressure regulation during physiological stress rather than elevated resting blood pressure alone.

The second study examined HRE in sedentary adults with T2DM using HART-D trial data, finding HRE in 46.1% of participants, which was primarily predicted by the ΔSBP/ΔMET ratio and maximum heart rate; combined aerobic and resistance training produced the most clinically meaningful reduction in resting systolic blood pressure.         The third study compared the ΔSBP/ΔMET slope derived from the 6MTWT and the CPET in apparently healthy and at-risk adults without diagnosed hypertension. Both tests distinguished HRE from non-HRE participants, though they were not interchangeable at the individual level, positioning the 6MTWT as a complementary screening tool rather than a CPET substitute. However, raw SBP was statistically equivalent between tests at matched exercise intensity, indicating that this disagreement is specific to the ΔSBP/ΔMET slope construct rather than the 6MTWT's ability to approximate the CPET's underlying blood pressure response.

In conclusion, this dissertation supports HRE as a clinically meaningful marker of cardiovascular risk and underscores the limitations of resting blood pressure assessments. Submaximal exercise testing shows promise for early HRE detection, though protocol-specific thresholds and further validation are needed before it can replace maximal testing clinically.

Date

7-16-2026

Committee Chair

Johannsen, Neil

LSU Acknowledgement

1

LSU Accessibility Acknowledgment

1

Available for download on Sunday, July 15, 2029

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