(Hypertension. 2000;36:885.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
NOS3 Glu298Asp Genotype and Blood Pressure Response to Endurance Training
The HERITAGE Family Study
From the Pennington Biomedical Research Center (T. Rankinen, C.B.), Human Genomics Laboratory, Baton Rouge, La; Division of Biostatistics (T. Rice, D.C.R.), Washington University Medical School, St Louis, Mo; Physical Activity Sciences Laboratory (L.P., Y.C.C., J.G.) and Laboratory of Molecular Endocrinology (J.G.), Laval University, Ste-Foy, Québec, Canada; School of Kinesiology and Leisure Studies (A.S.L.), University of Minnesota (Minneapolis); Department of Kinesiology (J.S.S.), Indiana University, Bloomington, Ind; Department of Health and Kinesiology (J.H.W.), Texas A&M University, College Station, Tex; and Departments of Genetics and Psychiatry (D.C.R.), Washington University Medical School, St Louis, Mo.
Correspondence to Tuomo Rankinen, PhD, Pennington Biomedical Research Center, Human Genomics Laboratory, 6400 Perkins Rd, Baton Rouge, LA 70808-4124. E-mail rankint{at}pbrc.edu
Abstract—Endothelium-dependent vasodilation is a mechanism that may affect blood pressure response to endurance training. Because NO plays a central role in this process, the endothelial NO synthase gene is a good candidate for the regulation of exercise blood pressure. We investigated the associations between an endothelial NO synthase gene polymorphism (Glu298Asp) and endurance training–induced changes in resting and submaximal exercise blood pressure in 471 white subjects of the HERITAGE Family Study. Two submaximal exercise tests at 50 W were conducted both before and after a 20-week endurance training program. Steady-state exercise blood pressure was measured twice in each test with an automated unit. The Glu298Asp polymorphism was typed with a PCR-based method and digestion with BanII. Both systolic and diastolic blood pressure at 50 W decreased in response to the training program, whereas resting blood pressure remained unchanged. The decrease in diastolic blood pressure at 50 W was greater (P=0.0005, adjusted for age, gender, baseline body mass index, and baseline diastolic blood pressure at 50 W) in the Glu/Glu homozygotes (4.4 [SEM 0.4] mm Hg, n=187) than in the heterozygotes (3.1 [0.4] mm Hg, n=213) and the Asp/Asp homozygotes (1.3 [0.7] mm Hg, n=71). The genotype accounted for 2.3% of the variance in diastolic blood pressure at 50 W training response. Both the Glu298 homozygotes and the heterozygotes had a greater (P=0.013) training-induced reduction in rate-pressure product at 50 W than the Asp298 homozygotes. These data suggest that DNA sequence variation in the endothelial NO synthase gene locus is associated with the endurance training–induced decreases in submaximal exercise diastolic blood pressure and rate-pressure product in sedentary normotensive white subjects.
Key Words: exercise • genetics • blood pressure • endothelial-derived factor • nitric oxide
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