Neuroplastic Mechanisms for Acquisition and Transfer of Injury-Resistant Movement Patterns Assessed in VR Simulated Sport

项目概要/摘要 前十字韧带 (ACL) 损伤是一种常见的活动相关膝关节损伤，具有显着的负面影响 关于个人和社会。每年直接成本超过130亿美元，长期间接成本远超 这个数字，因为 ACL 损伤也与数年内致残性骨关节炎的加速发展有关 受伤后数年。国家骨关节炎公共卫生议程建议扩大和加强 基于证据的 ACL 损伤预防可以减轻这种负担。我们已经确定了可修改的运动模式 会增加年轻女运动员 ACL 受伤的风险。虽然神经肌肉训练针对的是那些受伤风险 运动模式并显示出对高风险运动员的统计功效，这是低风险运动员的有意义的转移 比赛场地的机制受到限制。当前的方法无法确保抗损伤 运动模式向体育运动的转移是显而易见的，因为全国 ACL 损伤并未减少 尽管标准神经肌肉训练对改变生物力学的效果有效，但年轻女运动员的比率 实验室。确保有效地将伤害预防转移到运动中的关键知识差距是了解 神经系统从神经系统获取和转移抗损伤运动模式的机制 对运动场的干预或实验室。因此，本提案的总体目标是确定 支持将抗损伤运动模式转移到现实运动场景的神经机制。 我们最近发表的关于与损伤风险及后续相关的神经可塑性的初步数据 神经肌肉训练证明了特定的神经机制是抗损伤能力转移的基础 运动模式。这些初步数据支持该提案的中心假设，即大脑发生变化 活动是获得抗损伤运动模式并将其转移到现实运动场景的基础。 重要的是，这项工作表明神经可塑性可以通过增强生物反馈和其他临床 优化运动大脑激活模式的方法，促进抗损伤运动模式 收购和转让。针对减少伤害危险因素的神经机制的能力可以 彻底改变 ACL 损伤预防策略。一旦实现此应用程序的目标，我们将 能够通过确定的神经治疗目标来提高神经肌肉训练的效果。这个 对于提高 ACL 损伤预防训练的可转移性以减少损伤发生率具有重要意义 从而避免相关的长期负面健康后果。这对于年轻人尤其重要 女性运动员，因为她们是非接触性感觉运动错误相关 ACL 损伤风险最高的人群。 这是通过针对神经肌肉的神经机制来增强 ACL 损伤预防的独特机会 适应和转移凸显了该辅助项目为母公司 U01 提供的特殊机会 美国国立卫生研究院投资。

Project Summary/Abstract Anterior cruciate ligament (ACL) injury is a common activity-related knee injury with a substantial negative impact on individuals and society. Annual direct costs exceed $13 billion, and the long-term indirect costs far exceed that figure, as ACL injury is also linked to the accelerated development of disabling osteoarthritis within a few years after injury. The National Public Health Agenda for Osteoarthritis recommends expanding and enhancing evidence-based ACL injury prevention to reduce this burden. We have identified modifiable movement patterns that increase ACL injury risk in young female athletes. While neuromuscular training targets those injury risk movement patterns and shows statistical efficacy in high-risk athletes, a meaningful transfer of low-risk mechanics to the field of play has been limited. This inability of current approaches to ensure injury-resistant movement pattern transfer to sport is readily apparent as there has not been a decrease in national ACL injury rates in young female athlete despite efficacy of standard neuromuscular training to modify biomechanics in the lab. The key knowledge gap to ensure effective injury prevention transfer to sport is understanding the mechanisms the nervous system engages to acquire and transfer injury-resistant movement patterns from the intervention or laboratory to the athletic field. Thus, the overall objective of this proposal is to determine the neural mechanisms underpinning the transfer of injury-resistant movement patterns to realistic sport scenarios. Our published and recent preliminary data on the neuroplasticity related to injury risk and following neuromuscular training demonstrate a specific neural mechanism underlies the transfer of injury-resistant movement patterns. These preliminary data support this proposal's central hypothesis that changes in brain activity underlie the acquisition and transfer of injury-resistant movement patterns to realistic sport scenarios. Importantly this work indicates the neuroplasticity can be targeted by augmented biofeedback and other clinical methods to optimize brain activation patterns for movement that promote injury-resistant movement pattern acquisition and transfer. The ability to target the neural mechanisms of injury risk factor reduction could revolutionize ACL injury prevention strategies. Once the objectives of this application are achieved, we will be able to enhance the efficacy of neuromuscular training with the identified neuro-therapeutic targets. This contribution will be significant to improve ACL injury prevention training transferability to reduce injury incidence and thus avoid the associated long-term negative health consequences. This is especially relevant to young female athletes as they are the population at highest risk for non-contact sensorimotor error related ACL injury. This unique opportunity to enhance ACL injury prevention by targeting neural mechanisms of neuromuscular adaptation and transfer highlights the exceptional opportunity afforded by this ancillary project to the parent U01 NIH investment.