Effects of ACE I/D polymorphism and aerobic training on the immune-endocrine network and cardiovascular parameters of postmenopausal women.

Abstract

Estrogen deficiency, systemic low-grade inflammation, and reduction of adrenal gland function have central roles in noncommunicable chronic disease (NCD) development. With angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, the deletion variant (DD) is related to higher levels of circulating angiotensin II than I allele carriers (II/ID), which might interact with all of these molecular pathways to increase NCDs risk. On the other hand, physical exercise counteracts the occurrence of NCDs, potentially acting on the same pathways. The aim of the study was to investigate the effects of walking training on adrenal steroid and cytokine levels and on cardiovascular parameters in postmenopausal women with ACE I/D genotypes. Thirty-six (DD = 15, II/ID = 21) sedentary postmenopausal women (mean age, 56 ± 4 y) participated in a 13-week program of walking training at moderate intensity. Heart rate, blood pressure, double product, TNF-α, dehydroepiandrosterone sulfate (DHEA-S), and cortisol were evaluated before and after the intervention program. Before walking training, the ACE DD genotype showed significantly higher TNF-α (P = .007) and lower DHEA-S concentrations (P = .022) than the ACE II/ID individuals. After walking training, both subgroups significantly decreased TNF-α plasma levels and cortisol/DHEA-S ratio (P = .001 and P = .016, respectively) and significantly increased DHEA-S levels (P < .001). Moreover, all the cardiovascular parameters were significantly reduced in the ACE DD participants (P ≤ .05), whereas the ACE I-allele carriers showed a decrease in heart rate (P ≤ .05) and the double product (P ≤ .05). ACE I/D polymorphism is linked to different adrenal steroid and cytokine levels, and ACE I-allele carriers show a better adrenal activity and systemic inflammatory profile. The introduction of walking training positively influences the menopause immune-neuroendocrine changes, independent of ACE I/D genotype.