ORCID

https://orcid.org/0009-0000-3006-5663

Year

2024

Season

Spring

Paper Type

Master's Thesis

College

Brooks College of Health

Degree Name

Master of Science in Health: Kinesiology (MSH)

Department

Clinical & Applied Movement Sciences

NACO controlled Corporate Body

University of North Florida. Department of Clinical & Applied Movement Sciences

First Advisor

Dr. James Churilla

Second Advisor

Dr. Yann Klimentidis

Third Advisor

Dr. Youngdeok Kim

Department Chair

Dr. Joel Beam

College Dean

Dr. Mei Zhao

Abstract

Purpose: The objective of this study was to assess the causal relationship between both subjectively and objectively measured sedentary time (ST) and physical activity (PA) with heart failure (HF) risk, utilizing Mendelian Randomization (MR) approach.

Methods: The present MR used genetic instruments identified for self-reported ST and PA extracted from 51 genome wide association studies (GWAS), encompassing data from 703,901 individuals. The GWAS identified 89 independent single nucleotide polymorphisms (SNPs) associated with leisure screen time. Eleven loci were reported to be associated with moderate to vigorous physical activity (MVPA). From another GWAS examining accelerometer-based activities, three loci were found to be associated with PA and four with ST. Outcome HF data were extracted from a GWAS HF including cases and controls. Univariable MR estimates were obtained using various methods including MR-Egger, inverse variance weighted (IVW), weighted median, simple mode, and weighted mode.

Results: The results from univariable MR analysis showed a significant association of genetically-predicted ST with an increased risk of HF. However, this association was not supported across all sensitivity analyses (P >0.05 for all). Results also showed a significant association of genetically-predicted PA with increased risk of HF. This association was not supported when utilizing different sensitivity analyses (P >0.05 for all). Results demonstrate a potential positive association between objectively measured ST and HF risk across all methods. A potential negative association between objectively measured PA and HF risk was also discovered. Conclusions: The findings suggest a significant causal relationship between self-reported ST and increased HF risk, supported by univariate MR analysis using the IVW method. However, the association was attenuated under different sensitivity analyses, and when utilizing objectively measured ST. Similarly, while there is indication of a potential protective effect of physical activity against HF, inconsistencies among sensitivity analyses warrant cautious interpretation.

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