MicrobiotaMi Comment 19_21  by Stefania Blasa

Related Journal Article:  Antihypertensive effects of exercise involve reshaping of gut microbiota and improvement of gut-brain axis in spontaneously hypertensive rat

This article was published in the: Gut Microbes. 2021 Jan-Dec;13(1):1-24. doi: 10.1080/19490976.2020.1854642.

Exercise produces beneficial effects on hypertension via gut-brain axis improvement

Hypertension (HTN) is a serious condition in which blood pressure in the arteries is constantly elevated due to several causes, such as smoking, elevate body weight, alcohol or genetic factors and if not treated it could lead to stroke, heart failure, vision loss, chronic kidney disease and dementia. Several evidences support the presence of a dysfunctional gut-brain axis in HTN, including changes in neural trafficking regulation and in microglia activation. For example, fecal microbiota transplantation from hypertensive to normotensive rats could results in elevated blood pressure and sympathetic activity, demonstrating the direct influence of the microbiota on blood pressure regulation.

Moderate-intensity aerobic activity is an established treatment to control HTN. Exercise could reshape gut microbiota by increasing its diversity and abundance, ameliorate cardiac hypertrophy and diastolic function, reduce pro-inflammatory cytokines, attenuate oxidative stress and these effects could persist in a long-term period.

In order to test if the hypothesis that exercise could rebalance impaired gut-brain axis and to test if changes in gut microbiota were involved in the antihypertensive effects induced by exercise, Xia and colleagues performed a study in spontaneously hypertensive rats randomized in sedentary (SED), trained (EX) and detrained (DET, which underwent 8 weeks of exercise followed by 4 weeks at rest) groups.

Results reveal that after twelve weeks of exercise, blood pressure (BP) was significantly decreased in EX- and DET-rats and they showed an attenuation of the cross-sectional area of cardiomyocytes and perivascular fibrosis compared to the control. Moreover, continuous exercise training changed the composition of the gut microbial communities, increasing acetate and butyrate-producing bacteria and a decreasing lactate-producing bacteria. EX- and DET-rats showed a decrease in the fibrotic area and in thickness of the muscle layer and an increase in the globe cells/villi and villi length in the ileum and in the proximal colon; exercise training attenuated pro-inflammatory cytokines m-RNA levels and increased tight junction proteins m-RNA levels in the ileum of Ex-rats. Continuous exercise decreased the total number of microglia and the percentage of activated microglia, in fact, it deceased the microglial size and increased the length of microglial cell processes, which are signs of non-activated microglial cells. A decrease of paraventricular nucleus neuronal activity was also observed in EX-rats, demonstrated that exercise could regulate excessive sympathetic activity, which contributes to the pathogenesis of HTN.

Evidences suggest that gut microbiota and gut-brain axis are crucial in the development and establishment of HTN. Exercise training could increase diversity and abundance of several microbial organisms involved in energy extraction and in carbohydrates fermentation to produce butyrate, and these effects persisted in a long-time period, as seen in DET-rats. Further studies are needed to investigate the mechanisms of exercise-induced changes in gut microbiota and gut-brain axis, but these data indicate that a well-balanced gut microbiota may be a novel effect of the exercise-induced HTN treatment.

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<a href="https://microbiotami.com/author/stefania/" target="_self">Stefania Blasa</a>

Stefania Blasa

Stefania Blasa is a Postdoc in “Converging Technologies for Biomolecular Systems” at University of Milan-Bicocca; she is interested in neurophysiology and works on in-vitro neuronal differentiation induced by innovative technologies. During her master thesis, she worked on the simultaneous detection of mutations responsible of peripheral nerve system genetic diseases.