Key result
Exercise training may lower basal blood pressure by altering neuroactive ligand-receptor interactions, such as the serotoninergic system, within the nucleus of the solitary tract.
This review highlights that the anti-hypertensive effects of exercise training may be mediated by functional plasticity and altered gene expression in the brainstem's nucleus of the solitary tract, improving baroreceptor reflex function and reducing sympathetic outflow.
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May inform exercise prescriptions for hypertension; leaves open human validation of solitary tract mechanisms.
Neurogenic hypertension, the primary form of essential hypertension, is one of the most common diseases worldwide. Hypertension is a risk factor for many cardiovascular diseases such as heart attacks and stroke; therefore, it is crucial to maintain arterial blood pressure (BP) within the normal range. Regular aerobic exercise at moderate intensities can lower basal BP, and is a recommended therapy to prevent or improve primary hypertension. However, the mechanisms underlying the anti-hypertensive effects of exercise remain unknown. In this review, we discuss the mechanisms for the anti-hypertensive effects of exercise training/therapy that are hypothesised from recent findings, including our own. In particular, we discuss the nucleus of the solitary tract (NTS) of the brainstem, which is involved in mechanisms underlying the manifestation of neurogenic hypertension. Moreover, the NTS may also be involved in the anti-hypertensive effects of exercise training. However, exercise training does not seem to improve causative genetic factors for neurogenic hypertension in the NTS. Nevertheless, exercise training may affect other mechanisms responsible for neuroactive ligand-receptor interactions within the NTS, which also regulate BP homeostasis. We hope this review will further enhance research in this and promote exercise habits that help delay or even prevent the progression of essential hypertension.
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Waki et al. (2014) conducted a review in Hypertension. Exercise training was evaluated. Exercise training may lower basal blood pressure by altering neuroactive ligand-receptor interactions, such as the serotoninergic system, within the nucleus of the solitary tract.
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