Gajsar Hannah, Nahrwold Katharina, Titze Christina, Hasenbring Monika I, Vaegter Henrik B
Mind and Pain in Motion Group, Department of Medical Psychology and Medical Sociology, Ruhr-University of Bochum, Bochum, Germany.
Pain Research Group, Pain Center South, Odense University Hospital, Odense, Denmark.
Scand J Pain. 2018 Apr 25;18(2):311-320. doi: 10.1515/sjpain-2018-0024.
Exercise-induced hypoalgesia (EIH) and conditioned pain modulation (CPM) are assumed to reflect descending pain inhibition. Potential interactions between EIH and CPM may be important in the therapy of chronic pain, as reduced CPM and increased pain after exercise are frequently observed. This study compared the EIH response after CPM was activated using a cold pressor task with the EIH response after a control condition.
Thirty-one participants (age: 27.7±9.8; 15 female) completed two sessions: a cold pressor task (CPT) session, i.e. testing EIH with preceding CPM activation induced using a 2 min CPT at approximately 2°C, and a control session, i.e. testing EIH after a control condition (2 min of quiet rest). EIH was induced using a 15 min bicycling exercise at a target heart rate corresponding to 75% VO2 max. Repeated measures ANOVAs on pressure pain thresholds (PPTs) at the hand, back and leg were used to determine the effects of exercise after the cold pressor test and control condition. Furthermore, correlations between CPM and EIH, in the CPT session as well as control session, were calculated at each assessment site.
A significant time x condition interaction (F(1, 30)=43.61, p<0.001, partial η2=0.59), with Bonferroni-corrected post-hoc t-tests showed that PPTs increased after exercise in the control session (p<0.001), but not in the CPT session (p=0.125). Furthermore, there was a small positive correlation of EIH in the control session and CPM at the hand (r=0.37, p=0.043). There was a moderate negative correlation of EIH in the CPT session and CPM at the hand (r=-0.50, p=0.004), and smaller negative correlations at the back (r=-0.37, p=0.036) and at the leg (r=-0.35, p=0.054).
Attenuated EIH after the CPM activation in comparison to a control condition suggests that EIH and CPM may share underlying pain inhibitory mechanisms on a systemic level. This assumption is further supported by the finding of small to moderate significant correlations between EIH and CPM at the hand. The attenuated EIH response furthermore suggests that these mechanisms are exhaustible, i.e. that its effects decline after a certain amount of inhibition.
In patients with chronic pain, assessing the current capacity of the descending pain inhibitory system - as indicated by the CPM response - may aid to make better predictions about how patients will respond to exercise with respect to acute pain reduction.
运动诱发的痛觉减退（EIH）和条件性疼痛调制（CPM）被认为反映了下行性疼痛抑制。EIH与CPM之间的潜在相互作用在慢性疼痛治疗中可能很重要，因为经常观察到运动后CPM降低和疼痛增加。本研究比较了使用冷加压任务激活CPM后与对照条件下的EIH反应。
31名参与者（年龄：27.7±9.8；15名女性）完成了两个阶段：一个冷加压任务（CPT）阶段，即使用约2°C的2分钟CPT诱导CPM激活后测试EIH，以及一个对照阶段，即在对照条件（安静休息2分钟）后测试EIH。使用15分钟的自行车运动在对应于75%最大摄氧量的目标心率下诱发EIH。对手部、背部和腿部的压力疼痛阈值（PPTs）进行重复测量方差分析，以确定冷加压测试和对照条件后运动的影响。此外，在每个评估部位计算CPT阶段和对照阶段CPM与EIH之间的相关性。
存在显著的时间×条件交互作用（F(1, 30)=43.61，p<0.001，偏η²=0.59），经Bonferroni校正的事后t检验表明，对照阶段运动后PPTs增加（p<0.001），但CPT阶段未增加（p=0.125）。此外，对照阶段手部的EIH与CPM存在小的正相关（r=0.37，p=0.043）。CPT阶段手部的EIH与CPM存在中度负相关（r=-0.50，p=0.004），背部（r=-0.37，p=0.036）和腿部（r=-0.35，p=0.054）存在较小的负相关。
与对照条件相比，CPM激活后EIH减弱表明EIH和CPM可能在全身水平上共享潜在的疼痛抑制机制。手部EIH与CPM之间存在小到中度的显著相关性这一发现进一步支持了这一假设。EIH反应减弱还表明这些机制是可耗尽的，即其作用在一定量的抑制后会下降。
在慢性疼痛患者中，评估下行性疼痛抑制系统的当前能力——如CPM反应所示——可能有助于更好地预测患者在急性疼痛减轻方面对运动的反应。
