Krüger Steffen, Khayat Dominik, Hoffmeister Meike, Hilberg Thomas
Department of Sports Medicine, University of Wuppertal, Pauluskirchstraße 7, 42285, Wuppertal, Germany.
Eur J Appl Physiol. 2016 Mar;116(3):535-40. doi: 10.1007/s00421-015-3307-5. Epub 2015 Dec 23.
Physical exercise causes alterations in pain sensitivity. Many studies verified so-called exercise-induced analgesia caused by submaximal aerobic intensity. This study aimed to determine the effect of an endurance exercise to exhaustion on pain sensitivity of healthy young men.
Pressure pain thresholds (PPTs) [in Newton, (N)] of 50 healthy males (mean age 26 ± 4 years) were applied to knee, ankle and elbow joints as well as to the sternum and forehead. This was followed by a bout of cycling ergometer exercise to exhaustion. The whole process was repeated after 20 and 60 min respectively.
Endurance exercise to exhaustion decreased PPTs at sternum and forehead significantly, while thresholds at the joints were not affected. Pain thresholds at forehead and sternum declined 20 min after exercise with the forehead's threshold being more reduced. PPTs remain decreased until 60 min after exercise (forehead: from 43.6 ± 15.2 N to 36.6 ± 19.8 N to 37.2 ± 13.4 N; sternum: from 46.8 ± 21.0 N to 42.5 ± 17.1 N to 44.8 ± 18.2 N). Modulation of pain sensitivity showed large effect sizes over time for both landmarks (forehead w = 0.65; sternum w = 0.50).
Exhaustive endurance exercise is followed by a hyperalgetic condition at forehead and sternum. This may be due to either a reduction in pain inhibiting or an activation in pain stimulating pathways.
体育锻炼会引起疼痛敏感性的改变。许多研究证实了由次最大有氧强度引起的所谓运动诱导镇痛。本研究旨在确定耐力运动至力竭对健康年轻男性疼痛敏感性的影响。
对50名健康男性(平均年龄26±4岁)的膝关节、踝关节、肘关节以及胸骨和前额施加压力痛阈(PPTs,单位为牛顿,N)。随后进行一轮自行车测力计运动直至力竭。整个过程分别在20分钟和60分钟后重复。
耐力运动至力竭显著降低了胸骨和前额的PPTs,而关节处的阈值未受影响。运动后20分钟,前额和胸骨的疼痛阈值下降,前额的阈值下降幅度更大。PPTs在运动后60分钟内一直降低(前额:从43.6±15.2 N降至36.6±19.8 N再降至37.2±13.4 N;胸骨:从46.8±21.0 N降至42.5±17.1 N再降至44.8±18.2 N)。随着时间的推移,两个部位的疼痛敏感性调节均显示出较大的效应量(前额w = 0.65;胸骨w = 0.50)。
力竭性耐力运动后,前额和胸骨会出现痛觉过敏状态。这可能是由于疼痛抑制作用减弱或疼痛刺激通路激活所致。