TY - JOUR
T1 - Contact events in rugby union and the link to reduced cognition
T2 - evidence for impaired redox-regulation of cerebrovascular function
AU - Owens, Thomas S.
AU - Calverley, Thomas A.
AU - Stacey, Benjamin S.
AU - Iannatelli, Angelo
AU - Venables, Lucy
AU - Rose, George
AU - Fall, Lewis
AU - Tsukamoto, Hayato
AU - Berg, Ronan M.G.
AU - Jones, Gareth L.
AU - Marley, Christopher J.
AU - Bailey, Damian M.
N1 - Funding Information:
The authors would like to thank all participants for their cheerful co‐operation in the study, including all staff at the rugby team for their support. We would like to thank Daniel Jones for assistance with organization of study dates and player availability. We would like to thank Rhodri Manning for assistance with notational analysis. We would like to thank Trevor Harris, Alister Du Rose, Teresa Filipponi and Pip Laugharne for their assistance on study visits. Finally, the authors would like to thank Professor M. Steggall for assistance with the ethics review. D.M.B. is supported by a JPR Williams Research Fellowship (for T.S.O.’s PhD) and Royal Society Wolfson Research Fellowship (no. WM170007), Royal Society International Exchanges Award (no. IES∖R2∖192137) and Japan Society for the Promotion of Science Research Fellowship (no. JSPS/OF317).
Publisher Copyright:
© 2021 The Authors. Experimental Physiology © 2021 The Physiological Society
PY - 2021/9/1
Y1 - 2021/9/1
N2 - New Findings: What is the central question of this study? How does recurrent contact incurred across a season of professional rugby union impact molecular, cerebrovascular and cognitive function? What is the main findings and its importance? A single season of professional rugby union increases systemic oxidative–nitrosative stress (OXNOS) confirmed by a free radical-mediated suppression in nitric oxide bioavailability. Forwards encountered a higher frequency of contact events compared to backs, exhibiting elevated OXNOS and lower cerebrovascular function and cognition. Collectively, these findings provide mechanistic insight into the possible cause of reduced cognition in rugby union subsequent to impairment in the redox regulation of cerebrovascular function. Abstract: 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 [MD] 7.49; 95% CI, 2.58–12.40; P = 0.005), tackles (MD 3.49; 95% CI, 0.42–6.56; P = 0.028) and jackals (MD 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•– (F2,19 = 10.589, P = 0.004) and corresponding suppression of NO bioavailability (F2,19 = 11.492, P = 0.003) was apparent in forwards and backs across the season. This was accompanied by a reduction in cerebral oxygen delivery ((Formula presented.), F2,19 = 9.440, P = 0.006) and cognition (F2,19 = 4.813, P = 0.041). Forwards exhibited a greater decline in the cerebrovascular reactivity range to changes in PETCO2 ((Formula presented.) compared to backs (MD 1.378; 95% CI, 0.74–2.02; P < 0.001).
AB - New Findings: What is the central question of this study? How does recurrent contact incurred across a season of professional rugby union impact molecular, cerebrovascular and cognitive function? What is the main findings and its importance? A single season of professional rugby union increases systemic oxidative–nitrosative stress (OXNOS) confirmed by a free radical-mediated suppression in nitric oxide bioavailability. Forwards encountered a higher frequency of contact events compared to backs, exhibiting elevated OXNOS and lower cerebrovascular function and cognition. Collectively, these findings provide mechanistic insight into the possible cause of reduced cognition in rugby union subsequent to impairment in the redox regulation of cerebrovascular function. Abstract: 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 [MD] 7.49; 95% CI, 2.58–12.40; P = 0.005), tackles (MD 3.49; 95% CI, 0.42–6.56; P = 0.028) and jackals (MD 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•– (F2,19 = 10.589, P = 0.004) and corresponding suppression of NO bioavailability (F2,19 = 11.492, P = 0.003) was apparent in forwards and backs across the season. This was accompanied by a reduction in cerebral oxygen delivery ((Formula presented.), F2,19 = 9.440, P = 0.006) and cognition (F2,19 = 4.813, P = 0.041). Forwards exhibited a greater decline in the cerebrovascular reactivity range to changes in PETCO2 ((Formula presented.) compared to backs (MD 1.378; 95% CI, 0.74–2.02; P < 0.001).
KW - cerebral blood flow
KW - cognition
KW - contact
KW - rugby union
U2 - 10.1113/EP089330
DO - 10.1113/EP089330
M3 - Article
C2 - 34355451
AN - SCOPUS:85111824136
SN - 0958-0670
VL - 106
SP - 1971
EP - 1980
JO - Experimental Physiology
JF - Experimental Physiology
IS - 9
ER -
