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Review
. 2020;16(4):292-305.
doi: 10.2174/1573403X15666190729153026.

Estrogen Deprivation and Myocardial Infarction: Role of Aerobic Exercise Training, Inflammation and Metabolomics

Olívia M Ruberti  1 , Bruno Rodrigues  1
Affiliations
Review

Estrogen Deprivation and Myocardial Infarction: Role of Aerobic Exercise Training, Inflammation and Metabolomics

Olívia M Ruberti et al. Curr Cardiol Rev. 2020.

Abstract

In general, postmenopausal women present higher mortality, and worse prognosis after myocardial infarction (MI) compared to men, due to estrogen deficiency. After MI, cardiovascular alterations occur such as the autonomic imbalance and the pro-inflammatory cytokines increase. In this sense, therapies that aim to minimize deleterious effects caused by myocardial ischemia are important. Aerobic training has been proposed as a promising intervention in the prevention of cardiovascular diseases. On the other hand, some studies have attempted to identify potential biomarkers for cardiovascular diseases or specifically for MI. For this purpose, metabolomics has been used as a tool in the discovery of cardiovascular biomarkers. Therefore, the objective of this work is to discuss the changes involved in ovariectomy, myocardial infarction, and aerobic training, with emphasis on inflammation and metabolism.

Keywords: Ovariectomy; aerobic training; estrogen; inflammation; metabolomics; myocardial infarction.

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Figures

Fig. (1)
Fig. (1)
Alterations triggered by the loss of ovarian function and myocardial infarction. Loss of ovarian function may lead to changes in the central nervous system. Increased sympathetic control triggers debilitating physical symptoms such as heatwaves and sleep disturbances, decreases heart rate variability and baroreflex sensibility. Menopause is also related to changes in adipose tissue metabolism, culminating in abdominal fat accumulation. Estrogen promotes vascular remodeling, elasticity, and regulates vasodilation and local inflammatory activity. Thus, postmenopausal estrogen deficiency culminates in vascular changes, activation of the renin-angiotensin system, supra-regulation of endothelin, and impairment of nitric oxide-mediated vasodilation that may increase blood pressure. In addition, oxidative stress, increased by endothelin and angiotensin II, also results in increased blood pressure and may contribute even more to an atherosclerotic process. (A higher resolution / colour version of this figure is available in the electronic copy of the article).
Fig. (2)
Fig. (2)
Effects of aerobic training previously myocardial infarction. Physical exercise has a cardioprotective effect in increasing vagal activity. This change in the central nervous system culminates in increased heart rate variability and baroreflex sensitivity and decreased the release of pro-inflammatory cytokines through the cholinergic anti-inflammatory reflex. In addition, aerobic training culminates in angiogenesis, increased concentration of endothelial nitric oxide synthase (eNOs) and antioxidant protection. These factors decrease endothelial dysfunction and vascular resistance, culminating in lower blood pressure. These benefits are related to lower risk of coronary artery disease and consequently lower incidence of myocardial infarction. (A higher resolution / colour version of this figure is available in the electronic copy of the article).
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