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Physical activity reduces genetic susceptibility to increased central systolic pressure augmentation: a study of female twins

Jerry R. Greenfield, MBBS, BSc (Med), FRACP^*,*, Katherine Samaras, MBBS, PhD, FRACP^*, Lesley V. Campbell, MBBS, FRCP, FRACP^*, Arthur B. Jenkins, BSc, PhD, Paul J. Kelly, MBBS, MD, FRACP^||, Tim D. Spector, MSc, MD, FRCP^¶ and Christopher S. Hayward, BMedSc, MBBS, MD, FRACP^#

^* Department of Endocrinology, St. Vincent’s Hospital, Sydney, Australia
Diabetes Centre, St. Vincent’s Hospital, Sydney, Australia
Department of Cardiology, St. Vincent’s Hospital, Sydney, Australia
Department of Biomedical Science, University of Wollongong, Wollongong, Australia
^|| Sequenom, San Diego, California, USA
^¶ Twin Research and Genetic Epidemiology Unit, St. Thomas’ Hospital, London, United Kingdom
^# Victor Chang Cardiac Research Institute, Sydney, Australia

View larger version (12K): [in a new window]   Figure 1 Graphical representation of central arterial pressure waveform. P1 = first systolic peak; P2 = second systolic peak (systolic pressure); D = diastolic pressure; Augmentation index = (P2 – D)/(P1 – D) x 100%.

View larger version (41K): [in a new window]   Figure 2 Gene-environment interaction analysis: the association between regular leisure-time physical activity and augmentation index in subjects at low and high genetic risk of increased augmentation index. Open bars = regular physical activity; hatched bars = no regular physical activity. Data are mean ± SEM. Interaction p = 0.01. *p = 0.008 compared to subjects at high genetic risk not participating in regular physical activity.