The available studies on cerebrovascular reactivity and cerebral oxygenation in obstructive sleep apnoea (OSA) patients brought conflicting results, yet the overall evidence suggests that resting state cerebral perfusion is diminished in these patients. Interestingly, in a group of healthy professional breath-hold divers who are exercising very long apnoeas - episodes corresponding to the ones observed in patients with OSA - demonstrated that cerebral oxygenation may remain stable at the expense of extreme sympathetic nervous system (SNS) activation. In the present review we address several mechanisms that could potentially explain these discrepancies. We focus in depth on mechanisms of central SNS reinforcement in OSA including dysfunctional baroreflex response, and inflammatory processes within the brain centres controlling the cardiovascular system. Additionally, novel insights into physiology of cerebral blood flow regulation are proposed, including the role of short-term blood pressure changes, heart rate fluctuations and baroreflex alterations. Finally, a potential role of increased blood flow pulsatility in cerebrospinal fluid circulation changes and its influence on SNS drive is highlighted. The presented review provides insights into how sympathetic nervous system reinforcement in OSA promotes maladaptive mechanisms that could alter cerebral perfusion regulation, and result in functional and structural cerebral changes.

2nd Department of Radiology Medical University of Gdansk Gdansk Poland

Department of Cardiovascular Diseases International Clinical Research Center St Anne's University Hospital in Brno Brno Czech Republic

Department of Hypertension and Diabetology Medical University of Gdansk Gdansk Poland

Institute of Health Sciences Pomeranian University of Slupsk Slupsk Poland

Institute of Human Physiology Medical University of Gdansk Gdansk Poland

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