Résumé
Recurrent contact and concussion in rugby union remains a significant public health concern given the potential increased risk of neurodegeneration in later-life. This study determined to what extent prior-recurrent contact impacts molecular-haemodynamic biomarkers underpinning cognition in current professional rugby union players with a history of concussion. Measurements were performed in 20 professional rugby union players with an average of 16 [interquartile range (IQR), 13-19] years playing history, reporting 3 (IQR, 1-4) concussions. They were compared to 17 sex-, age-, physical activity- and education-matched non-contact controls with no prior history of self-reported concussion. Venous blood was assayed directly for the ascorbate free radical (A•- , electron paramagnetic resonance spectroscopy), nitric oxide metabolites (NO, reductive ozone-based chemiluminescence) and select biomarkers of neurovascular unit integrity (NVU, chemiluminescence/ELISA). Middle cerebral artery blood flow velocity (MCAv, doppler ultrasound) was employed to determine basal perfusion and cerebrovascular reactivity (CVR) to hyper/hypocapnia (CVRCO2HYPER/HYPO ). Cognition was assessed by neuropsychometric testing. Elevated systemic oxidative-nitrosative stress was confirmed in the players through increased A•- (P < 0.001) and suppression of NO bioavailability (P < 0.001). This was accompanied by a lower CVR range (CVRCO2RANGE , P = 0.045), elevation in neurofilament light-chain (P = 0.010) and frontotemporal impairments in immediate-memory (P = 0.001), delayed-recall (P = 0.048) and fine-motor coordination (P < 0.001). Accelerated cognitive decline subsequent to prior recurrent contact and concussion history is associated with a free radical-mediated suppression of CVR and neuronal injury providing important mechanistic insight that may help better inform clinical management.