Neurovascular implications of life-long exposure to contact in rugby union; the link to cognition

    Student thesis: Doctoral Thesis


    Introduction: Recurrent contact and concussion in sport represents a significant and growing public health concern which may contribute to long-term neurologic sequela in later-life. To what extent this relates to an accelerated decline in cerebral perfusion, a major risk factor for cognitive impairment and neurodegeneration remains to be explored.

    Aims: This thesis sought to: 1) determine the molecular, cerebrovascular and cognitive signatures of professional rugby union players over a single season, stratified by frequency of contact events, playing position and concussion risk, and 2) determine the chronic molecular, cerebrovascular and cognitive signatures of formerly concussed retired rugby players exposed to recurrent contact.

    Hypothesis: It was hypothesised that compared to controls, formerly concussed rugby union players would present with elevated oxidative-nitrosative (OXNOS) stress, suppressed cerebrovascular function and a decline in cognition.

    Methodology: Study 1 – A longitudinal study was conducted across one rugby union season. Participants were divided into two separate groups. Twenty-one professional rugby union players aged 25 ± 4 years with 3± 2 previous concussions incurred over 16 ± 4years were compared with 17 sex, age-, physical activity-and education-matched controls, with no participation in contact sports or concussion history. Data were collected at three timepoints: 1) pre-season, 2) in-season, and 3) post-season. During pre-and post-season, venous concentrations of the ascorbate radical (A•-) and total bioactive nitric oxide (NO–nitrite[NO] and S-nitrosothiols [RSNO]) were obtained. Transcranial Doppler (TCD) ultrasonography was used to determine cerebral perfusion via middle cerebral artery velocity (MCAv). The range of cerebrovascular reactivity to changes in end tidal carbon dioxide (CVRCO2RANGE) was assessed using hypercapnia (CVRCO2HYPER) and hypocapnia (CVRCO2HYPO). Cognition was assessed via neuropsychometric tests and screened for mild cognitive impairment (MCI) using the Montreal Cognitive Assessment (MoCA). In-season notational analysis observed all match events throughout each game of the season with all incurred injuries noted. Study 2 –Twenty retired rugby players aged 64 ± 5 years with 3 ± 3 concussions incurred over 22 ± 7 years were compared to 21 sex, age-, cardiorespiratory fitness (CRF)-and education-matched controls with no participation in contact sports or concussion history. Venous concentrations of A•-, and total bioactive NO were obtained. Cerebral perfusion was determined via MCAv. Cerebrovascular reactivity was assessed in response to hypercapnia/hypocapnia. Cognition was assessed via neuropsychometric tests and screened for MCI using the MoCA.

    Results: Study 1–Elevated OXNOS was apparent in players during pre-season. Players had lower CVRCO2RANGE, memory, fine-motor coordination and executive function compared to controls. The concussion incidence rate corresponded to 10 concussions per 1000 match hours throughout the season. When players were divided into forwards (n = 13) and backs (n = 8), forwards were subject to more contact events per game, most notably for collisions, jackals and tackles. During post-season, elevated nitrosative stress remained apparent in players compared to controls, despite no differences in oxidative stress. Similarly, CVRCO2RANGE decreased by 18% across the season in players. Players confirmed reductions in memory, fine-motor coordination and executive function compared to controls. Study 2 –Retired players had lower total NO bioactivity, despite an absence of elevated oxidative stress compared to controls. Cerebral perfusion was lower in players at rest and throughout hyper/hypocapnia, however no differences in CVRCO2 were detected between-groups. Prolonged concussion symptomology was apparent in players during completion of a Sports Concussion Assessment. Mild cognitive impairment was identified in players, including a reduction in executive function and fine-motor coordination of the non-dominant hand.

    Discussion: Recurrent contact and concussion history accelerates the age-related decline in cognition among young and aged rugby union players. The findings of this thesis indicate that molecular, cerebral haemodynamic and cognitive decline are apparent among current professional rugby union players. While subtle impairments can be identified over the course of a playing season among current players, greater physiological decline can be observed following retirement from sport.

    Conclusion: Methods to lower recurrent contact and concussion incidence should remain a priority of the sports-medicine community with more dedicated focus towards prevention, molecular-diagnostic capabilities and longitudinal observations of contact sport athletes across the globe.
    Date of AwardFeb 2022
    Original languageEnglish
    SupervisorDamian Bailey (Supervisor) & Christopher Marley (Supervisor)

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