Physical activity reduces genetic susceptibility to increased central systolic pressure augmentation: a study of female twins.
OBJECTIVE
We sought to examine associations between the augmentation index (AI) and metabolic, adiposity, and lifestyle factors, independent of genetic influences, and to determine whether gene-environment interactions modulate these relationships.


BACKGROUND
Reported associations between AI, an index of systemic arterial stiffness, and metabolic, adiposity, and lifestyle factors remain contradictory. The modulating effect of genetic risk is unknown.


METHODS
We studied 684 female twins (age 18 to 71 years); AI was derived from the pressure waveform measured at the radial artery by applanation tonometry. Percentage of total body fat (TBF) and percentage of central abdominal fat (CAF) were assessed by dual-energy X-ray absorptiometry.


RESULTS
In univariate analysis, age-adjusted AI was significantly associated with fasting triglyceride levels (r = 0.1, P = 0.03), apolipoprotein-B/A1 (r = 0.1, P = 0.04), percentage of TBF (r = 0.11, P = 0.006), and percentage of CAF (r = 0.11, P = 0.004). In co-twin case-control (monozygotic twin) analysis, a 3.1% absolute within-pair difference in percentage of CAF accounted for a 6% within-pair difference in AI, independent of genetic effects. Smokers and subjects with alcohol intakes >15 U/week had higher AI than nonsmokers (p = 0.01) and nondrinkers (p = 0.02), respectively. Forty percent of the variance in AI was explained by age, central mean arterial pressure, heart rate, height, percentage of CAF, and smoking. In gene-environment interaction analysis, subjects at high genetic risk of increased AI participating in regular leisure-time physical activity had AI values similar to low genetic risk subjects.


CONCLUSIONS
Central abdominal adiposity is a significant determinant of AI in female twins, independent of hemodynamic, lifestyle, and, importantly, genetic effects. Smoking is associated with increased AI, even after controlling for abdominal obesity and other AI determinants. Physical activity reduces genetic predisposition to increased AI.
Greenfield
Jerry R
JR
Department of Endocrinology, St. Vincent's Hospital, Sydney, Australia. j.greenfield@garvan.org.au
Samaras
Katherine
K
Campbell
Lesley V
LV
Jenkins
Arthur B
AB
Kelly
Paul J
PJ
Spector
Tim D
TD
Hayward
Christopher S
CS
D000293:Adolescent; D000328:Adult; D000368:Aged; D000428:Alcohol Drinking / Q000009:adverse effects; D000704:Analysis of Variance; D000886:Anthropometry; D001823:Body Composition; D015992:Body Mass Index; D016022:Case-Control Studies; D002496:Central Venous Pressure / Q000235:genetics*; D015444:Exercise; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics / Q000517:prevention & control*; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism / Q000517:prevention & control*; D008019:Life Style; D008875:Middle Aged; D009765:Obesity / Q000150:complications* / Q000175:diagnosis / Q000517:prevention & control*; D011237:Predictive Value of Tests; D012044:Regression Analysis; D012307:Risk Factors; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects; D013599:Systole / Q000235:genetics; D014429:Twins, Dizygotic; D014430:Twins, Monozygotic / Q000235:genetics