Thomas A. Calverley became interested in physiology while studying for a Bachelor's degree in Sport and Exercise Science at the University of South Wales. Upon graduation, he enrolled as a PhD student investigating the neuroprotective benefits of high-intensity interval training in older adults under the auspices of Professor Bailey. Currently in the final year of his studentship, he enjoys playing cricket/rugby and is a keen guitarist making the most of his spare time. Damian M. Bailey trained at the

Contact events in rugby union remain a public health concern. We determined the molecular, cerebrovascular and cognitive consequences of contact events during a season of professional rugby. Twenty-one male players aged 25 (mean) ± 4 (SD) years were recruited from a professional rugby team comprising forwards (n = 13) and backs (n = 8). Data were collected across the season. Pre-and post-season, venous blood was assayed for the ascorbate free radical (A •-, electron paramagnetic resonance spectroscopy) and nitric oxide (NO, reductive ozone-based chemiluminescence) to quantify oxidative-nitrosative stress (OXNOS). Middle cerebral artery velocity (MCAv, Doppler ultrasound) was measured to assess cerebrovascular reactivity (CVR), and cognition was assessed using the Montreal Cognitive Assessment (MoCA). Notational analysis determined contact events over the season. Forwards incurred more collisions (Mean difference [M D ] 7.49; 95% CI, 2.58-12.40; P = 0.005), tackles (M D 3.49; 95% CI, 0.42-6.56; P = 0.028) and jackals (M D 2.21; 95% CI, 0.18-4.24; P = 0.034). Forwards suffered five concussions while backs suffered one concussion. An increase in systemic OXNOS, confirmed by elevated A •-(F 2,19 = 10.589, P = 0.004) and corresponding suppression of NO bioavailability (F 2,19 = 11.492, P = 0.003) was apparent in forwards and backs across the season. This was accompanied by a reduction in cerebral oxygen delivery (cD O 2 , F 2,19 = 9.440, P = 0.006) and cognition (F 2,19 = 4.813, P = 0.041).Forwards exhibited a greater decline in the cerebrovascular reactivity range to changes in PET CO2 (CVR CO 2 RANG compared to backs (M D 1.378; 95% CI, 0.74-2.02; P < 0.001).

How to cite this article: Owens TS, Calverley TA, Stacey BS, et al. Concussion history in rugby union players is associated with depressed cerebrovascular reactivity and cognition.

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The aim of the present study was to determine the extent to which hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral blood flow (CBF) and oxygen delivery (CDO 2 ), with corresponding implications for the pathophysiology of the neurological syndrome, acute mountain sickness (AMS). Eight healthy men were randomly assigned single blind to 7 h of passive exposure to both normoxia (21% O 2 ) and hypoxia (12% O 2 ). The peripheral and central respiratory chemoreflex, internal carotid artery, external carotid artery (ECA) and vertebral artery blood flow (duplex ultrasound) and AMS scores (questionnaires) were measured throughout. A reduction in internal carotid artery CDO 2 was observed during hypoxia despite a compensatory elevation in perfusion.In contrast, vertebral artery and ECA CDO 2 were preserved, and the former was attributable to a more marked increase in perfusion. Hypoxia was associated with progressive activation of the peripheral respiratory chemoreflex (P < 0.001), whereas the central respiratory chemoreflex remained unchanged (P > 0.05). Symptom severity in participants who developed clinical AMS was positively related to ECA blood flow (Lake Louise score, r = 0.546-0.709, P = 0.004-0.043; Environmental Symptoms Questionnaires-Cerebral symptoms score, r = 0.587-0.771, P = 0.001-0.027, n = 4).Collectively, these findings highlight the site-specific regulation of CBF in hypoxia that maintains CDO 2 selectively in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. Furthermore, ECA vasodilatation might represent a hitherto unexplored haemodynamic risk factor implicated in the pathophysiology of AMS.