International Collaboration on Repair Discoveries (ICORD), Vancouver, British Columbia, Canada.
Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
J Neurophysiol. 2024 May 1;131(5):789-796. doi: 10.1152/jn.00472.2023. Epub 2024 Feb 14.
Movement-evoked pain is an understudied manifestation of musculoskeletal conditions that contributes to disability, yet little is known about how the neuromuscular system responds to movement-evoked pain. The present study examined whether movement-evoked pain impacts force production, electromyographic (EMG) muscle activity, and the rate of force development (RFD) during submaximal muscle contractions. Fifteen healthy adults (9 males; age = 30.3 ± 10.2 yr, range = 22-59 yr) performed submaximal isometric first finger abduction contractions without pain (baseline) and with movement-evoked pain induced by laser stimulation to the dorsum of the hand. Normalized force (% maximal voluntary contraction) and RFD decreased by 11% ( < 0.001) and 15% ( = 0.003), respectively, with movement-evoked pain, without any change in normalized peak EMG ( = 0.77). Early contractile RFD, force impulse, and corresponding EMG amplitude computed within time segments of 50, 100, 150, and 200 ms relative to the onset of movement were also unaffected by movement-evoked pain ( > 0.05). Our results demonstrate that movement-evoked pain impairs peak characteristics and not early measures of submaximal force production and RFD, without affecting EMG activity (peak and early). Possible explanations for the stability in EMG with reduced force include antagonist coactivation and a reorganization of motoneuronal activation strategy, which is discussed here. We provide neurophysiological evidence to indicate that peak force and rate of force development are reduced by movement-evoked pain despite a lack of change in EMG and early rapid force development in the first dorsal interosseous muscle. Additional evidence suggests that these findings may coexist with a reorganization in motoneuronal activation strategy.
运动诱发疼痛是肌肉骨骼疾病中研究较少的一种表现形式，它会导致残疾，但人们对神经肌肉系统如何对运动诱发疼痛做出反应知之甚少。本研究旨在探讨运动诱发疼痛是否会影响亚最大肌肉收缩过程中的力量产生、肌电图（EMG）肌肉活动和力量发展速率（RFD）。15 名健康成年人（9 名男性；年龄=30.3±10.2 岁，范围 22-59 岁）在手背激光刺激下产生运动诱发疼痛时，进行无疼痛（基线）和亚最大等长第一指外展收缩。与无疼痛时相比，运动诱发疼痛使力量的归一化值（%最大自主收缩）和 RFD 分别降低了 11%（<0.001）和 15%（=0.003），但归一化峰值 EMG 没有变化（=0.77）。在运动开始后 50、100、150 和 200ms 的时间段内计算的早期收缩 RFD、力冲量和相应的 EMG 幅度也不受运动诱发疼痛的影响（>0.05）。我们的结果表明，运动诱发疼痛会损害亚最大力量产生和 RFD 的峰值特征，而不会影响 EMG 活动（峰值和早期）。在力量降低的情况下，EMG 保持稳定的可能解释包括拮抗肌的共同激活和运动神经元激活策略的重新组织，本文对此进行了讨论。我们提供了神经生理学证据，表明尽管第一背侧骨间肌的 EMG 没有变化且早期快速力发展，但运动诱发疼痛会降低峰值力和力发展速率。进一步的证据表明，这些发现可能与运动神经元激活策略的重新组织并存。
