Different degree of intervention in 6-month weight-loss support and arterial stiffness: Secondary analysis of a randomized controlled trial.

BACKGROUND AND AIMS: Weight reduction by lifestyle modification (i.e., low-calorie diet and/or exercise) decreases arterial stiffness in overweight or obese individuals. We previously demonstrated that weight loss differs depending on the degree of intervention in weight-loss support in a randomized controlled trial (UMIN000001259). However, the effect of different degrees of intervention on arterial stiffness remains unclear. METHODS AND RESULTS: A total of 188 middle-aged men and women with overweight or obesity (51 ± 7 years, BMI: 29.0 ± 3.2 kg/m2) participated in the 6-month trial wherein they were assigned to a low (LI, n = 63), moderate (MI, n = 62), or high intensive intervention (HI, n = 63) group. Initially, one motivational lecture on weight loss was provided to all three groups, whereas educational materials (textbooks, notebooks, and a pedometer) were provided to groups MI and HI. Additionally, the HI group participated in a series of group-based sessions. Body weight and arterial stiffness assessed by brachial-ankle pulse wave velocity (baPWV) were measured at 0, 3, and 6 months. Six-month weight loss was greater in the order of HI, MI, and LI groups. The interventions reduced baPWV in all groups, and the reduction was not significantly different among the groups (114.3 ± 16.3, 82.6 ± 15.2, and 98.8 ± 90.4 cm/s, respectively). CONCLUSION: In overweight or obese individuals, different degrees of intervention in weight-loss support affect body weight; however, the extent to which arterial stiffness improves does not differ among support programs.

Effects of endothelin-related gene polymorphisms and aerobic exercise habit on age-related arterial stiffening: a 10-yr longitudinal study.

Increased arterial stiffness has emerged as a strong predictor of future cardiovascular events and all-cause mortality. The aim of this study was to elucidate influences of endothelin (ET)-related genetic polymorphisms and regular physical activity on age-related arterial stiffening through a 10-yr longitudinal study. A decadal change in brachial-ankle pulse wave velocity (baPWV), an index of arterial stiffness, was evaluated retrospectively among 92 volunteers (63 ± 14 yr, 51 men). The targeted single-nucleotide polymorphisms were ET-A receptor SNP rs5333 (ET-A) and ET-B receptor SNP rs5351 (ET-B). Subjects with either ET-A TC or CC genotypes exhibited significantly greater increases in baPWV (+15.3 ± 11.7 and +16.6 ± 15.7%/dec, respectively) than ET-A TT genotype holders (+9.2 ± 9.0%/dec), whereas subjects with the ET-B GG genotype showed a significantly greater increase in baPWV (+17.7 ± 14.1%/dec) than other ET-B genotype holders (AA: +9.5 ± 10.0%/dec; AG: +11.2 ± 9.6%/dec). The combination of these ET-related genetic risks was associated with a 2.4 times greater decadal increase in baPWV compared with no genetic risk (+8.1 ± 8.4 vs. 19.5 ± 16.0%/dec). In contrast, individuals engaging in >15 METs·h/wk of aerobic exercise showed substantially smaller increases in baPWV (+5.0 ± 9.7%/dec) compared with their physically inactive peers (approximately +13%/dec). These differences remained significant after adjusting for confounding factors, including baseline baPWV and ET-related genotype risk. Our current longitudinal study found that ET-related gene polymorphisms contribute to diverse age-related changes in arterial stiffness, and that regular sufficient aerobic exercise attenuates the age-related arterial stiffening independently of ET-related gene polymorphisms. NEW & NOTEWORTHY This 10-yr longitudinal study suggests that endothelin-related gene polymorphisms contribute to divergent increases in arterial stiffness with advancing age, whereas regular sufficient aerobic exercise attenuates age-related arterial stiffening independently of ET-related gene polymorphisms. This notion partly supports prevailing evidence that regular aerobic exercise contributes to a lower incidence of cardiovascular disease.