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 utoregulation; 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 neurocognitive function (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 by fronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation and autoregulatory index (Pandlt;0.05 compared with controls). Likewise, CVRCO2 was also reduced resulting in a lowerCVRCO2 range (Pandlt;0.05 compared with controls). The latter was most marked in boxers with the highest CTBI scores and correlated against the volume and intensity of sparring during training (r= −0.84, Pandlt;0.05). These impairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (Pandlt;0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxers due 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.
|Tudalennau (o-i)||177 - 189|
|Nifer y tudalennau||12|
|Dynodwyr Gwrthrych Digidol (DOIs)|
|Statws||Cyhoeddwyd - 22 Awst 2012|