Int J Sports Med 2006; 27(1): 31-36
DOI: 10.1055/s-2005-837628
Physiology & Biochemistry

© Georg Thieme Verlag KG Stuttgart · New York

Genome-Wide Scan to Identify Quantitative Trait Loci for Baseline Resting Heart Rate and Its Response to Endurance Exercise Training: The HERITAGE Family Study

P. An1 , T. Rice1 , T. Rankinen2 , A. S. Leon3 , J. S. Skinner4 , J. H. Wilmore5 , C. Bouchard2 , D. C. Rao1 , 6
  • 1Division of Biostatistics, Washington University School of Medicine, St. Louis, Missouri, USA
  • 2Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, USA
  • 3Division of Kinesiology, University of Minnesota, Minneapolis, Minnesota, USA
  • 4Department of Kinesiology, Indiana University, Bloomington, Indiana, USA
  • 5Department of Health and Kinesiology, Texas A&M University, College Station, Texas, USA
  • 6Departments of Genetics and Psychiatry, Washington University School of Medicine, St. Louis, Missouri, USA
Further Information

Publication History

Accepted after revision: January 25, 2005

Publication Date:
02 June 2005 (online)

Abstract

Evidence of a genetic component for resting heart rate (RHR) has been found. Quantitative trait loci (QTLs) for baseline RHR have been reported, but not for RHR training response. It is of interest to identify QTLs that may harbor genes influencing RHR variation at baseline and in response to regular exercise training. Here, a multipoint variance components linkage scan using 654 markers was performed to search for QTLs that influence RHR adjusted for several covariates at baseline and in response to 20 weeks of endurance training (post-training minus baseline) in 99 White and 127 Black families in the HERITAGE Family Study. Potentially interesting linkages were revealed on 4 q and 11 p for baseline RHR, and on 1 q and 21 q for RHR training response in Whites. The QTLs on 2 q, 6 q, 7 q, 12 q, 14 q, and 15 q for baseline RHR, and on 3 p, 20 p and 21 q for RHR training response were found in Blacks. Promising linkages (lod scores ≥ 1.75, p ≤ 0.0023) involved 11 p for baseline RHR in Whites and 3 p for RHR training response in Blacks, which did not replicate across races. Interestingly in this study, the linkage evidence on 11 p at the SUR locus was somewhat enhanced (lod score went up from 1.7 to 2.0) in a prehypertensive (BP ≥ 135/80 mm Hg) subset of 40 White families suggesting a pleiotropic gene for BP and RHR with interactions. In conclusion, among QTLs on 1 q, 2 p, 3 p, 4 q, and 11 p that replicated across subsamples and studies, 11 p is most promising for dense mapping and association studies in HERITAGE and other cohorts.

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P. An

Division of Biostatistics (Campus Box 8067), Washington University School of Medicine

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Email: anping@wustl.edu