Impaired cerebral haemodynamic function associated with chronic traumatic brain injury in professional boxers.
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 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 cortical oxyhaemoglobin 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 (P<0.05 compared with controls). Likewise, CVRCO₂ was also reduced resulting in a lower CVRCO₂ range (P<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, P<0.05). These impairments 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 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.
Neurovascular Research Laboratory, Faculty of Health, Science and Sport, University of Glamorgan, Pontypridd, Wales, UK. dbailey1@glam.ac.uk
Damian M
DM
Bailey
Daniel W
DW
Jones
Andrew
A
Sinnott
Julien V
JV
Brugniaux
Karl J
KJ
New
Danielle
D
Hodson
Christopher J
CJ
Marley
Jonathan D
JD
Smirl
Shigehiko
S
Ogoh
Philip N
PN
Ainslie
D000328:Adult; D062186:Arterial Pressure / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology; D001914:Boxing / Q000293:injuries*; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000378:metabolism; D002540:Cerebral Cortex / Q000098:blood supply / Q000503:physiopathology*; D002908:Chronic Disease; D003071:Cognition / Q000502:physiology; D003072:Cognition Disorders / Q000209:etiology / Q000503:physiopathology; D006439:Hemodynamics; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007024:Hypotension, Orthostatic / Q000209:etiology / Q000503:physiopathology; D008297:Male; D020768:Middle Cerebral Artery / Q000503:physiopathology; D010108:Oxyhemoglobins / Q000378:metabolism; D017156:Photoplethysmography; D055815:Young Adult
D010108:Oxyhemoglobins; D002245:Carbon Dioxide