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1 Department of Community Health Sciences, Brock University, St. Catharines, Canada
2 Department of Kinesiology, University of Waterloo, Waterloo, Canada
3 School of Kinesiology, University of Western Ontario, London, Canada
4 Sleep Consultants Inc., Fort Worth, Texas, United States
5 Department of Orthopaedic Surgery, University of California, San Diego, California, United States
* To whom correspondence should be addressed. E-mail: doleary{at}brocku.ca.
Early analysis into the role of genetics on cardiovascular regulation has been accomplished by comparing blood pressure and heart rate in homozygous twins during unstressed, resting physiological conditions. However, many variables, including cognitive and environmental factors, contribute to the regulation of cardiovascular hemodynamics. Therefore, the purpose of this study was to determine the hemodynamic response of identical twins to an orthostatic stress ranging from supine rest to presyncope. Heart rate, arterial blood pressure, middle cerebral artery blood velocity, an index of cerebrovascular resistance, cardiac output, total peripheral resistance and end-tidal carbon dioxide were measured in 16 healthy monozygotic twin pairs. Five minutes of supine resting baseline data were collected, followed by 5-min of 60° head-up tilt (HUT). After 5-min of HUT, lower body negative pressure (LBNP) was applied in increments of 10 mmHg every 3-min until the onset of presyncope, at which time the subject was returned to supine position for a 5-min recovery period. The data indicate that cardiovascular regulation under orthostatic stress demonstrates a significant degree of variance between identical twins, despite similar orthostatic tolerance. As the level of stress increases, so does the difference in the cardiovascular response within a twin pair. The elevated variance with increasing stress may be due to an increase in the role of environmental factors, as the influential role of genetics nears a functional limit. Therefore, although orthostatic tolerance times were very similar between identical twins, the mechanism involved in sustaining cardiovascular function during increasing stress was different.
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