Key result
Exercise training reduces plasma angiotensin-II, aldosterone, and norepinephrine and lowers SBP by ~6 mmHg.
Why the study?
Blood pressure management reduces cardiovascular disease risk, and the renin-angiotensin-aldosterone system regulates blood volume and pressure, but the effect of exercise training across RAAS components required systematic investigation.
Does exercise training reduce RAAS activity, sympathetic nervous system activity, and blood pressure in human participants?
Meta-Analysis (n=803)
Does exercise training reduce RAAS activity, sympathetic nervous system activity, and blood pressure in human participants?
Exercise training significantly reduces plasma angiotensin-II, aldosterone, norepinephrine, and blood pressure, providing a mechanistic explanation for its anti-hypertensive effects.
Supports exercise training to lower RAAS activity and BP in hypertension; strengthens mechanistic evidence across trials.
Blood pressure (BP) management reduces the risk of cardiovascular disease (CVD). The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating and maintaining blood volume and pressure. This analysis aimed to investigate the effect of exercise training on plasma renin, angiotensin-II and aldosterone, epinephrine, norepinephrine, urinary sodium and potassium, BP and heart rate (HR). We systematically searched PubMed, Web of Science, and the Cochrane Library of Controlled Trials until 30 November 2022. The search strategy included RAAS key words in combination with exercise training terms and medical subject headings. Manual searching of reference lists from systematic reviews and eligible studies completed the search. A random effects meta-analysis model was used. Eighteen trials with a total of 803 participants were included. After exercise training, plasma angiotensin-II (SMD -0.71; 95% CI -1.24, -0.19; p = 0.008; n = 9 trials), aldosterone (SMD -0.37; 95% CI -0.65, -0.09; p = 0.009; n = 8 trials) and norepinephrine (SMD -0.82; 95% CI -1.18, -0.46; p < 0.001; n = 8 trials) were reduced. However, plasma renin activity, epinephrine, and 24-h urinary sodium and potassium excretion remained unchanged with exercise training. Systolic BP was reduced (MD -6.2 mmHg; 95% CI -9.9, -2.6; p = 0.001) as was diastolic BP (MD -4.5 mmHg; 95% CI -6.9, -2.1; p < 0.001) but not HR (MD -3.0 bpm; 95% CI -6.0, 0.4; p = 0.053). Exercise training may reduce some aspects of RAAS and sympathetic nervous system activity, and this explains some of the anti-hypertensive response.
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Baffour-Awuah et al. (2023) reported a meta-analysis. Exercise training vs. Control was evaluated on Plasma angiotensin-II (SMD -0.71, 95% CI -1.24, -0.19, p=0.008). Exercise training significantly reduced plasma angiotensin-II (SMD -0.71; 95% CI -1.24, -0.19; p=0.008), aldosterone, norepinephrine, and systolic blood pressure (MD -6.2 mmHg).
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