Genetic factors associating the effects of habitual exercise on arterial stiffness

Regular exercise improves the risk of arterial stiffness by improving arterial endothelial function and regulating smooth muscle tone and proliferation. However, individual responses to exercise training can vary. Gene polymorphism, namely individual differences in the DNA sequence, is a main causal factor of phenotypic variation in adaptations of physiological function and morphology to regular exercise. In the abdominal aorta of aerobically trained rats, more than 300 genes were detected with differential expression. Additionally, many candidate gene polymorphisms, associated with the risk of arterial stiffening, have been identified. Therefore, various vasodilation and vasoconstriction-related gene polymorphisms may be associated with individual variation in the effects of physical exercise and cardiorespiratory fitness on arterial stiffness risks. Recently, several studies reported that gene polymorphisms, such as atrial natriuretic peptide, endothelial nitric oxide synthase, estrogen receptor-α, endothelin receptor-A, endothelin receptor-B, angiotensinogen, angiotensin-converting enzyme, methylenetetrahydrofolate reductase and fatty acid binding protein 2, were associated with individual variation in the effects of physical exercise or cardiorespiratory fitness on arterial stiffness risks. This article reviews the recent findings on genetic factors influencing the effects of exercise on the risk of cardiovascular diseases, i.e., arterial stiffness.