Cardiac output-mediated regulation of cerebral blood flow during exercise: Clinical perspectives on the indirect impact of muscle metaboreflex

The muscle metaboreflex stimulates the elevation of arterial blood pressure, aiming to rectify the oxygen deficit by enhancing oxygen delivery to support muscle activity. Moreover, activating the muscle metaboreflex significantly increases cardiac output (CO) by increasing factors such as heart rate, ventricular contractility, preload, stroke volume and mobilization of central blood volume. Previous studies indicate that ageing and cardiovascular diseases modify the muscle metaboreflex during exercise, limiting the ability to increase CO during physical activity. Alongside reduced exercise capacity, the attenuated rise in CO due to abnormal muscle metaboreflex in these patients impedes the increase in cerebral blood flow during exercise. Considering that CO plays a pivotal role in regulating cerebral blood flow adequately during exercise, this occurrence might contribute to an elevated risk of cerebral diseases, and it could also, at least, reduce the effective role of exercise in preventing cerebral disease and dementia among elderly individuals and patients with cardiovascular conditions. Therefore, it is important to consider this phenomenon when optimizing the effectiveness of exercise rehabilitation in patients with cardiovascular disease to prevent cerebral diseases and dementia. What is the topic of this review? This review focuses on the role of muscle metaboreflex-induced augmentation of cardiac output during exercise in patients with cardiovascular disease. What advances does it highlight? Sufficient regulation of cardiac output is crucial for maintaining cerebral perfusion. Cerebral hypoperfusion might play a pivotal role in the development of brain disease in patients with heart failure. This review highlights the impact of the metaboreflex on the exercise-induced rise in cardiac output and explores its related pathophysiology.