Jones Matthew D, Taylor Janet L, Booth John, Barry Benjamin K
School of Medical Sciences, University of New South WalesSydney, NSW, Australia; Neuroscience Research AustraliaSydney, NSW, Australia.
School of Medical Sciences, University of New South Wales Sydney, NSW, Australia.
Front Physiol. 2016 Nov 29;7:581. doi: 10.3389/fphys.2016.00581. eCollection 2016.
Exercise-induced hypoalgesia is well described, but the underlying mechanisms are unclear. The aim of this study was to examine the effect of exercise on somatosensory evoked potentials, laser evoked potentials, pressure pain thresholds and heat pain thresholds. These were recorded before and after 3-min of isometric elbow flexion exercise at 40% of the participant's maximal voluntary force, or an equivalent period of rest. Exercise-induced hypoalgesia was confirmed in two experiments (Experiment 1-SEPs; Experiment 2-LEPs) by increased pressure pain thresholds at biceps brachii (24.3 and 20.6% increase in Experiment 1 and 2, respectively; both > 0.84 and < 0.001) and first dorsal interosseous (18.8 and 21.5% increase in Experiment 1 and 2, respectively; both > 0.57 and < 0.001). In contrast, heat pain thresholds were not significantly different after exercise (forearm: 10.8% increase, = 0.35, = 0.10; hand: 3.6% increase, = 0.06, = 0.74). Contrasting effects of exercise on the amplitude of laser evoked potentials (14.6% decrease, = -0.42, = 0.004) and somatosensory evoked potentials (10.9% increase, = -0.02, = 1) were also observed, while an equivalent period of rest showed similar habituation (laser evoked potential: 7.3% decrease, = -0.25, = 0.14; somatosensory evoked potential: 20.7% decrease, = -0.32, = 0.006). The differential response of pressure pain thresholds and heat pain thresholds to exercise is consistent with relative insensitivity of thermal nociception to the acute hypoalgesic effects of exercise. Conflicting effects of exercise on somatosensory evoked potentials and laser evoked potentials were observed. This may reflect non-nociceptive contributions to the somatosensory evoked potential, but could also indicate that peripheral nociceptors contribute to exercise-induced hypoalgesia.
运动诱发的痛觉减退已有充分描述，但其潜在机制尚不清楚。本研究的目的是研究运动对体感诱发电位、激光诱发电位、压力痛阈和热痛阈的影响。在参与者最大自主力量的40%进行3分钟的等长屈肘运动前后，或在同等时长的休息前后，对这些指标进行记录。在两项实验（实验1 - 体感诱发电位；实验2 - 激光诱发电位）中证实了运动诱发的痛觉减退，肱二头肌处的压力痛阈升高（实验1升高24.3%，实验2升高20.6%；均>0.84且<0.001），第一背侧骨间肌处的压力痛阈也升高（实验1升高18.8%，实验2升高21.5%；均>0.57且<0.001）。相比之下，运动后热痛阈无显著差异（前臂：升高10.8%，P = 0.35，NS = 0.10；手部：升高3.6%，P = 0.06，NS = 0.74）。还观察到运动对激光诱发电位幅度（降低14.6%，P = -0.42，P = 0.004）和体感诱发电位幅度（升高10.9%，P = -0.02，P = 1）的不同影响，而同等时长的休息也显示出类似的适应性变化（激光诱发电位：降低7.3%，P = -0.25，NS = 0.14；体感诱发电位：降低20.7%，P = -0.32，P = 0.006）。压力痛阈和热痛阈对运动的不同反应与热伤害感受对运动急性痛觉减退效应的相对不敏感一致。观察到运动对体感诱发电位和激光诱发电位的相互矛盾的影响。这可能反映了体感诱发电位的非伤害性成分，但也可能表明外周伤害感受器对运动诱发的痛觉减退有贡献。
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