疼痛是全球范围内的主要公共卫生问题。治疗失败率高。在有前途的非药物疗法中,体育锻炼是一种吸引人的,便宜,可获得和无害的方法;超越其他健康益处。然而,其高度可变的治疗效果和不完全理解的潜在机制(可能涉及GABA能神经传递)需要进一步研究.这项病例对照研究旨在研究长期高强度耐力运动练习(实验时最后6个月≥7小时/周)对实验性寒冷引起的疼痛(作为合适的慢性疼痛模型)的反应的影响。假设训练有素的人更好地抵抗疼痛,开发有利的疼痛复制策略并增强其GABA能信号传导。为此,临床疼痛相关数据,记录了对冷加压测试和高密度EEG高(Hβ)和低β(Lβ)振荡的反应。在27名运动员和27名年龄调整后的非训练对照组(右撇子男性)中,一类高度耐痛的参与者(主要是运动员,48.1%)被确定,表现出对疼痛的较低恐惧,与非抵抗的非运动员相比。此外,他们耐受更长时间的冷水浸泡和感觉较低的最大感觉疼痛。然而,在基线时具有相似的Hβ和Lβ功率,他们在寒冷和疼痛感知之间以及疼痛阈值和耐受性之间表现出降低(分别为-60%和-6.6%;-179.5%和-5.9%;标准化差异),与非抗性非运动员的增加相反(分别为21%和14%;23.3%和13.6%)。我们的结果表明,长期体育锻炼对疼痛和疼痛相关行为的抵抗力有有益的影响,和大脑GABA能信号的修饰。根据目前的知识,我们建议GABA能神经传递可以显示出多方面的变化,以进行不同的解释,取决于训练配置文件和稳态设置(例如,在无痛和慢性疼痛的情况下)。尽管限制了样本量和缺乏急性体育锻炼下的直接观察,这项前兆研究揭示了耐药个体的独特特征(可能受到训练的青睐),从而可以对体育锻炼诱导的镇痛进行高度翔实的观察,并为将来的临床转化铺平了道路.进一步表征抗痛个体将为有针对性和生理知情的疼痛管理开辟道路。
Pain is a major public health problem worldwide, with a high rate of treatment failure. Among promising non-pharmacological therapies, physical exercise is an attractive, cheap, accessible and innocuous method; beyond other health benefits. However, its highly variable therapeutic effect and incompletely understood underlying mechanisms (plausibly involving the GABAergic neurotransmission) require further research. This
case-control study aimed to investigate the impact of long-lasting intensive endurance sport practice (≥7 h/week for the last 6 months at the time of the experiment) on the response to experimental cold-induced pain (as a suitable chronic pain model), assuming that highly trained individual would better resist to pain, develop advantageous pain-copying strategies and enhance their GABAergic signaling. For this purpose, clinical pain-related data, response to a cold-pressor test and high-density EEG high (Hβ) and low beta (Lβ) oscillations were documented. Among 27 athletes and 27 age-adjusted non-trained controls (right-handed males), a category of highly pain-resistant participants (mostly athletes, 48.1%) was identified, displaying lower fear of pain, compared to non-resistant non-athletes. Furthermore, they tolerated longer cold-water immersion and perceived lower maximal sensory pain. However, while having similar Hβ and Lβ powers at baseline, they exhibited a reduction between cold and pain perceptions and between pain threshold and tolerance (respectively -60% and - 6.6%; -179.5% and - 5.9%; normalized differences), in contrast to the increase noticed in non-resistant non-athletes (+21% and + 14%; +23.3% and + 13.6% respectively). Our results suggest a beneficial effect of long-lasting physical exercise on resistance to pain and pain-related behaviors, and a modification in brain GABAergic signaling. In light of the current knowledge, we propose that the GABAergic neurotransmission could display multifaceted changes to be differently interpreted, depending on the training profile and on the homeostatic setting (e.g., in pain-free versus chronic pain conditions). Despite limitations related to the sample size and to absence of direct observations under acute physical exercise, this precursory study brings into light the unique profile of resistant individuals (probably favored by training) allowing highly informative observation on physical exercise-induced analgesia and paving the way for future clinical translation. Further characterizing pain-resistant individuals would open avenues for a targeted and physiologically informed pain management.