Black Christopher D, Tynes Brandon K, Gonglach Alexander R, Waddell Dwight E
*Department of Health and Exercise Science, University of Oklahoma, Norman, Oklahoma
Department of Health, Exercise Science and Recreation Management, University of Mississippi, Oxford, Mississippi.
Pain Med. 2016 Dec;17(12):2422-2433. doi: 10.1093/pm/pnw077. Epub 2016 Jun 27.
Isometric exercise has been shown to activate endogenous pain inhibitory pathways in healthy adults, but not in some clinical pain populations.
Exercise-induced muscle damage (EIMD) and the associated delayed-onset muscle soreness (DOMS) are a model for studying clinical pain; thus, our purpose was to examine the effects of isometric exercise on pressure pain threshold (PPT) in the presence and absence of DOMS.
Data were collected on 23 males (22.8 ± 2.5 yrs). PPT was assessed in the right (exercising) and left (resting) quadriceps prior to, every 30 seconds during, and 2 and 15 minutes following an isometric contraction of the right quadriceps at 25% of maximal voluntary contraction (MVC) held until fatigue. Unilateral eccentric exercise was performed to induce DOMS in the exercising leg and testing was repeated 48 hours later.
DOMS increased (P < 0.001) and resting PPT decreased (P = 0.03) following EIMD. PPTs were elevated during exercise in the exercising (P ≤ 0.002) and resting (P ≤ 0.002) quadriceps but did not differ between the control and EIMD conditions in either leg (P ≤ 0.61). PPT remained elevated 2 and 15 minutes postexercise (P < 0.05) in the exercised quadriceps in both conditions, but values returned to baseline at 2 (P = 0.91) and 15 minutes (P = 0.28) postisometric exercise in the resting quadriceps.
Unlike clinical pain, DOMS had no effect on the PPT response during exercise in either the exercising or resting quadriceps. The fact that exercise altered PPT in both quadriceps during exercise suggests a generalized pain inhibitory mechanism was activated. However, the restriction of postexercise effects to the exercised limb suggests localized inhibitory mechanism(s) were activated after exercise.
等长运动已被证明可激活健康成年人内源性疼痛抑制通路，但在一些临床疼痛人群中并非如此。
运动诱导的肌肉损伤（EIMD）及相关的延迟性肌肉酸痛（DOMS）是研究临床疼痛的一个模型；因此，我们的目的是在有和没有DOMS的情况下，研究等长运动对压力疼痛阈值（PPT）的影响。
收集了23名男性（22.8±2.5岁）的数据。在右侧股四头肌以最大自主收缩（MVC）的25%进行等长收缩直至疲劳之前、期间每30秒以及之后2分钟和15分钟，对右侧（运动侧）和左侧（休息侧）股四头肌的PPT进行评估。进行单侧离心运动以在运动腿诱导DOMS，并在48小时后重复测试。
EIMD后DOMS增加（P<0.001），休息时PPT降低（P = 0.03）。运动时运动侧（P≤0.002）和休息侧（P≤0.002）股四头肌的PPT均升高，但在任一腿部，对照组和EIMD组之间无差异（P≤0.61）。在两种情况下，运动后2分钟和15分钟，运动侧股四头肌的PPT仍升高（P<0.05），但休息侧股四头肌等长运动后2分钟（P = 0.91）和15分钟（P = 0.28）时，PPT值恢复到基线。
与临床疼痛不同，DOMS对运动时运动侧或休息侧股四头肌的PPT反应均无影响。运动时两侧股四头肌的PPT均发生改变，这一事实表明激活了一种全身性疼痛抑制机制。然而，运动后效应仅限于运动肢体，这表明运动后激活了局部抑制机制。
