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Christabel Osei-Boateng

University of Guelph

Christabel Osei-Boateng, a graduate student at the University of Guelph, is investigating how contact sports impact cardiovascular and cerebrovascular health. Her research examines blood biomarkers linked to brain injury in junior football athletes and evaluates their physiological responses to lower-body negative pressure (LBNP) and hypercapnia throughout the season. Her findings suggest that repetitive trauma may alter autonomic cardiovascular regulation, even in the absence of a diagnosed concussion. This work could help refine athlete health monitoring and injury prevention strategies. Christabel will present her research at European College of Sport Science (ECSS Rimini) in July.

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Abstract

INTRODUCTION: The association between increased brain blood biomarker concentration and concussion in collegiate contact sport athletes [1] supports the notion that repetitive trauma causes blood brain barrier disruption [2]. Blunted heart rate (HR) and blood pressure (BP) in concussed athletes during sympathetic nervous system (SNS) activation reveals that alterations in cardiovascular function occur after mild brain injury [3]. Lower body negative pressure (LBNP) is a widely used approach to acutely increase SNS activity. Additionally, hypercapnia is used to assess vasomotor capacity of the brain. Thus, this study aimed to assess cardiovascular and cerebrovascular health in junior Canadian football athletes during a season, using blood biomarkers glial fibrillary acidic protein (GFAP) and neurofilament light polypeptide (Nf-L) as an index of injury and to evaluate cardiorespiratory and cerebrovascular function during LBNP and hypercapnia. We hypothesized that biomarkers would be elevated post-game compared to pre-game; and cardiorespiratory and cerebrovascular responses to LBNP and hypercapnia would be blunted post-season compared to pre-season, indicating a potential relationship between contact sport, cardiorespiratory and cerebrovascular function.

 

METHODS: 14 male junior football athletes had venous blood samples collected 24hrs pre- and 12hrs postgame to be analyzed for GFAP and Nf-L. Cardiorespiratory and cerebrovascular responses to LBNP (-20, -40, and -60 mmHg) and 3-minute stages of hypercapnia (+5 and +10 mmHg; end tidal forcing system) were evaluated by HR (electrocardiogram), BP (finger photoplethsmography) and blood velocity in the middle and posterior cerebral artery (MCA & PCA; transcranial doppler ultrasound).

 

RESULTS: GFAP concentration increased from 45.88+16.70pg/ml pre-game to 53.99+32.89pg/ml postgame (P=0.004). Nf-L trended towards a decrease (P=0.06). During LBNP, no changes in MCAv or PCAv were observed from baseline to -60 mmHg in both the pre- and post-season (both days; P>0.9). Mean arterial pressure remained (MAP) stable, while HR increased with intensity (P0.9; PCAv, P>0.3). Also, HR and MAP increased with hypercapnia, but there was no difference when comparing post-season to pre-season response. (HR, P>0.1; MAP, P>0.2).

 

CONCLUSIONS: This data demonstrates that GFAP acutely increases after a game of contact football, potentially indicating mild brain injury occurrence without a concussion diagnosis. Despite this rise in GFAP, only the HR response to LBNP was different post- compared to pre-season, as no differences in the cerebral blood flow response to LBNP and hypercapnia were observed. The clinical implications of these findings remain to be fully elucidated

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