Farina Dario, Arendt-Nielsen Lars, Roatta Silvestro, Graven-Nielsen Thomas
Center for Sensory-Motor Interaction, Department of Health Science and Technology, Aalborg University, Fredrik Bajers Vej 7 D-3, DK-9220 Aalborg, Denmark.
Clin Neurophysiol. 2008 Jan;119(1):43-51. doi: 10.1016/j.clinph.2007.10.003. Epub 2007 Nov 26.
Activation of nociceptive afferents decreases motor unit discharge rates in static contractions. There is also evidence that during experimental muscle pain the motor unit twitch force increases, which has been hypothesized to compensate for the decrease in discharge rate to maintain constant force. This study examined whether there is an association between the magnitude of change in motor unit discharge rate and the amount of increase in the spike-triggered average torque during experimental muscle pain.
Sixteen subjects performed three constant-torque isometric ankle dorsi-flexions at 10% of the maximal force (MVC) alternated with two contractions at constant discharge rate of a target motor unit, before and following injection of 0.5 ml of hypertonic (painful) or isotonic (control) saline into the tibialis anterior muscle.
The discharge rate of the target unit at 10% MVC decreased following injection of hypertonic saline (P<0.05; mean+/-SD, before: 9.9+/-1.3 pulses per second, pps; after injection: 8.9+/-1.0 pps). The peak of the spike-triggered average torque increased with pain (P<0.05; before: 0.56+/-0.55 mNm; during pain: 0.95+/-1.02 mNm) but the increase was not correlated with the decrease in discharge rate (R=0.08). Propagation velocity and action potential peak-to-peak amplitude did not change with pain.
The pain-induced modifications in the estimated motor unit twitch torque (1) were not caused by changes in muscle fiber action potential, and (2) were not associated with the decrease in discharge rate.
Maintenance of constant force during static painful contractions is not explained by a matching between changes in contractile and control motor unit properties.
伤害性传入神经的激活会降低静态收缩时运动单位的放电率。也有证据表明，在实验性肌肉疼痛期间，运动单位的抽搐力会增加，据推测这是为了补偿放电率的降低以维持恒定的力量。本研究探讨了在实验性肌肉疼痛期间，运动单位放电率的变化幅度与触发脉冲平均扭矩的增加量之间是否存在关联。
16名受试者在向胫骨前肌注射0.5毫升高渗（疼痛）或等渗（对照）盐水之前和之后，以最大力量（MVC）的10%进行三次恒定扭矩的等长踝关节背屈，与以目标运动单位的恒定放电率进行的两次收缩交替进行。
注射高渗盐水后，10%MVC时目标单位的放电率降低（P<0.05；平均值±标准差，注射前：每秒9.9±1.3个脉冲，pps；注射后：8.9±1.0 pps）。触发脉冲平均扭矩的峰值随疼痛增加（P<0.05；注射前：0.56±0.55 mNm；疼痛期间：0.95±1.02 mNm），但增加与放电率的降低无关（R = 0.08）。传播速度和动作电位峰峰值幅度未随疼痛而改变。
疼痛引起的估计运动单位抽搐扭矩的改变（1）不是由肌纤维动作电位的变化引起的，（2）与放电率的降低无关。
静态疼痛收缩期间恒定力量的维持不能用收缩和控制运动单位特性变化之间的匹配来解释。
