Owens Thomas S, Calverley Thomas A, Stacey Benjamin S, Iannatelli Angelo, Venables Lucy, Rose George, Fall Lewis, Tsukamoto Hayato, Berg Ronan M G, Jones Gareth L, Marley Christopher J, Bailey Damian M
Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University of South Wales, Pontypridd, UK.
Faculty of Computing, Engineering and Science, University of South Wales, Pontypridd, UK.
Exp Physiol. 2021 Sep;106(9):1971-1980. doi: 10.1113/EP089330. Epub 2021 Aug 5.
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.
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 ] 7.49; 95% CI, 2.58-12.40; P = 0.005), tackles (M 3.49; 95% CI, 0.42-6.56; P = 0.028) and jackals (M 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 = 10.589, P = 0.004) and corresponding suppression of NO bioavailability (F = 11.492, P = 0.003) was apparent in forwards and backs across the season. This was accompanied by a reduction in cerebral oxygen delivery ( , F = 9.440, P = 0.006) and cognition (F = 4.813, P = 0.041). Forwards exhibited a greater decline in the cerebrovascular reactivity range to changes in PET ( compared to backs (M 1.378; 95% CI, 0.74-2.02; P < 0.001).
本研究的核心问题是什么？在一个职业橄榄球联盟赛季中反复发生的身体接触如何影响分子、脑血管和认知功能？主要发现及其重要性是什么？一个职业橄榄球联盟赛季会增加全身氧化亚硝化应激（OXNOS），这通过自由基介导的一氧化氮生物利用度抑制得到证实。与后卫相比，前锋遭遇身体接触事件的频率更高，表现出更高的氧化亚硝化应激水平以及更低的脑血管功能和认知能力。总体而言，这些发现为职业橄榄球联盟中脑血管功能氧化还原调节受损后认知能力下降的可能原因提供了机制性见解。
橄榄球联盟中的身体接触事件仍然是一个公共卫生问题。我们确定了职业橄榄球赛季中身体接触事件对分子、脑血管和认知方面的影响。从一支由前锋（n = 13）和后卫（n = 8）组成的职业橄榄球队中招募了21名平均年龄为25（均值）±4（标准差）岁的男性球员。在整个赛季收集数据。在赛季前和赛季后，采集静脉血检测抗坏血酸自由基（A ，电子顺磁共振波谱法）和一氧化氮（NO，基于还原臭氧的化学发光法），以量化氧化亚硝化应激（OXNOS）。通过多普勒超声测量大脑中动脉血流速度（MCAv）以评估脑血管反应性（CVR），并使用蒙特利尔认知评估量表（MoCA）评估认知能力。通过记录分析确定整个赛季的身体接触事件。前锋遭遇更多的碰撞（平均差值[M ] 7.49；95%置信区间，2.58 - 12.40；P = 0.005）、擒抱（M = 3.49；95%置信区间，0.42 - 6.56；P = 0.028）和扑搂球（M = 2.21；95%置信区间，0.18 - 4.24；P = 0.034）。前锋有5次脑震荡，而后卫有1次脑震荡。整个赛季中，前锋和后卫的全身氧化亚硝化应激均明显增加，表现为A 升高（F = 10.589，P = 0.004）以及相应的一氧化氮生物利用度受到抑制（F = 11.492，P = 0.003）。这伴随着脑氧输送减少（ ，F = 9.440，P = 0.006）和认知能力下降（F = 4.813，P = 0.041）。与后卫相比，前锋在对PET变化的脑血管反应性范围内下降幅度更大（ ）（M = 1.378；95%置信区间，0.74 - 2.02；P < 0.001）。
