VO2 max is associated with ACE genotype in postmenopausal women.

Relationships have frequently been found between angiotensin-converting enzyme (ACE) genotype and various pathological and physiological cardiovascular outcomes and functions. Thus we sought to determine whether ACE genotype affected maximal O2 consumption (VO2 max) and maximal exercise hemodynamics in postmenopausal women with different habitual physical activity levels. Age, body composition, and habitual physical activity levels did not differ among ACE genotype groups. However, ACE insertion/insertion (II) genotype carriers had a 6.3 ml . kg-1 . min-1 higher VO2 max (P < 0.05) than the ACE deletion/deletion (DD) genotype group after accounting for the effect of physical activity levels. The ACE II genotype group also had a 3.3 ml . kg-1 . min-1 higher VO2 max (P < 0.05) than the ACE insertion/deletion (ID) genotype group. The ACE ID group tended to have a higher VO2 max than the DD genotype group, but the difference was not significant. ACE genotype accounted for 12% of the variation in VO2 max among women after accounting for the effect of habitual physical activity levels. The entire difference in VO2 max among ACE genotype groups was the result of differences in maximal arteriovenous O2 difference (a-vDO2). ACE genotype accounted for 17% of the variation in maximal a-vDO2 in these women. Maximal cardiac output index did not differ whatsoever among ACE genotype groups. Thus it appears that ACE genotype accounts for a significant portion of the interindividual differences in VO2 max among these women. However, this difference is the result of genotype-dependent differences in maximal a-vDO2 and not of maximal stroke volume and maximal cardiac output.

[1]  G R Hagerman,et al.  Energy expenditure during simulated rowing. , 1978, Journal of applied physiology: respiratory, environmental and exercise physiology.

[2]  G W Heath,et al.  A physiological comparison of young and older endurance athletes. , 1981, Journal of applied physiology: respiratory, environmental and exercise physiology.

[3]  H. Schunkert.  Polymorphism of the angiotensin-converting enzyme gene and cardiovascular disease , 1997, Journal of Molecular Medicine.

[4]  B. Hurley,et al.  Endurance training in older men and women. I. Cardiovascular responses to exercise. , 1984, Journal of applied physiology: respiratory, environmental and exercise physiology.

[5]  N. C. Sharp,et al.  Guidelines for Exercise Testing and Prescription , 1993 .

[6]  L. Pérusse,et al.  Muscle-specific creatine kinase gene polymorphisms in elite endurance athletes and sedentary controls. , 1997, Medicine and science in sports and exercise.

[7]  M. Cerqueira,et al.  Cardiovascular responses to exercise. Effects of aging and exercise training in healthy men. , 1994, Circulation.

[8]  Bing Yu,et al.  Elite endurance athletes and the ACE I allele – the role of genes in athletic performance , 1998, Human Genetics.

[9]  P. A. Mauer,et al.  Physical activity and public health. , 1995, JAMA.

[10]  F C Hagerman,et al.  Applied Physiology of Rowing , 1984, Sports medicine.

[11]  J. Wilmore,et al.  Muscle-specific creatine kinase gene polymorphism and VO2max in the HERITAGE Family Study. , 1997, Medicine and science in sports and exercise.

[12]  N. Samani,et al.  A meta-analysis of the association of the deletion allele of the angiotensin-converting enzyme gene with myocardial infarction. , 1996, Circulation.

[13]  C. Bouchard,et al.  Genetics of aerobic and anaerobic performances. , 1992, Exercise and sport sciences reviews.

[14]  L. Tiret,et al.  Evidence, from combined segregation and linkage analysis, that a variant of the angiotensin I-converting enzyme (ACE) gene controls plasma ACE levels. , 1992, American journal of human genetics.

[15]  Shirley A. Miller,et al.  A simple salting out procedure for extracting DNA from human nucleated cells. , 1988, Nucleic acids research.

[16]  P. Williams,et al.  Physical activity and public health. , 1995, JAMA.

[17]  S. Humphries,et al.  Association of angiotensin-converting enzyme gene I/D polymorphism with change in left ventricular mass in response to physical training. , 1997, Circulation.

[18]  K. Patrick,et al.  Physical Activity and Public Health: A Recommendation From the Centers for Disease Control and Prevention and the American College of Sports Medicine , 1995 .

[19]  R S Paffenbarger,et al.  Physical fitness and all-cause mortality. A prospective study of healthy men and women. , 1989, JAMA.

[20]  C. Bouchard,et al.  Mitochondrial DNA sequence polymorphism, VO2max, and response to endurance training. , 1991, Medicine and science in sports and exercise.