The present study examined to what extent professional boxing compromises cerebral haemodynamic function and its association with CTBI (chronic traumatic brain injury). A total of 12 male professional boxers were compared with 12 age-, gender- and physical fitness-matched non-boxing controls. We assessed dCA (dynamic cerebral autoregulation; thigh-cuff technique and transfer function analysis), CVRCO2 (cerebrovascular reactivity to changes in CO2: 5% CO2 and controlled hyperventilation), orthostatic tolerance (supine to standing) and neurocognitivefunction (psychometric tests). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound),mean arterial blood pressure (finger photoplethysmography), end-tidal CO2 (capnography) and corticaloxyhaemoglobin concentration (near-IR spectroscopy) were continuously measured. Boxers were characterized byfronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation andautoregulatory index (P<0.05 compared with controls). Likewise, CVRCO2 was also reduced resulting in a lowerCVRCO2 range (P<0.05 compared with controls). The latter was most marked in boxers with the highest CTBIscores and correlated against the volume and intensity of sparring during training (r= -0.84, P<0.05). Theseimpairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (P<0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxersdue to the mechanical trauma incurred by repetitive, sub-concussive head impact incurred during sparring training. This may help explain why CTBI is a progressive disease that manifests beyond the active boxing career. © The Authors Journal compilation. © 2013 Biochemical Society.