Ducharme Jeremy B, Specht Jonathan W, Bailly Alyssa R, Deyhle Michael R
Department of Health, Exercise and Sports Sciences, University of New Mexico, Albuquerque, New Mexico, United States.
Department of Cell Biology and Physiology, School of Medicine, University of New Mexico, Albuquerque, New Mexico, United States.
Am J Physiol Regul Integr Comp Physiol. 2025 May 1;328(5):R581-R587. doi: 10.1152/ajpregu.00010.2025. Epub 2025 Mar 25.
Endurance training contributes to immune system changes that help manage exercise-induced stress and promote an anti-inflammatory effect. However, the specific mechanisms underlying these adaptations are still being explored. Cytokines play a key role in both acute and chronic exercise responses through interactions with their receptors, which are present in both membrane-bound and soluble forms. Yet, the impact of exercise on cytokines and soluble cytokine receptors in parallel remains understudied. Therefore, the purpose of this study was to assess how cytokines and their soluble receptors change in serum after vigorous exercise in endurance-trained and untrained men. Following 1-h of cycling at their respiratory compensation point, untrained men ( = 5) exhibited a significant increase in proinflammatory cytokines, including IL-6, TNF-α, IL-1β, CCL2, and VEGFA. In contrast, anti-inflammatory cytokines such as IL-10 and IL-1Ra were reduced. These effects were not observed in the trained group ( = 7). Instead, proinflammatory cytokine levels remained close to the baseline, whereas the anti-inflammatory cytokines IL-10 and IL-1Ra increased. In the trained group, these cytokine changes were accompanied by a marked increase in the expression of soluble cytokine receptors known to inhibit cytokine-mediated signaling, such as sIL-1RII, sGP130, sTNFRI, sTNFRII, sVEGFR1, and sVEGFR2, indicating reduced cytokine bioavailability. However, in the untrained group, the expression of these soluble cytokine receptors either remained unchanged or decreased, suggesting greater cytokine bioavailability. Together these findings highlight a novel potential anti-inflammatory adaptation such that trained men present a blunted inflammatory response by both reduced inflammatory cytokines and increased soluble cytokine receptors after exercise compared with untrained men. Our study identifies a novel potential anti-inflammatory adaptation to endurance training, where trained men present a blunted inflammatory response characterized by reduced inflammatory cytokines and increased soluble cytokine receptors, resulting in decreased cytokine bioavailability after exercise compared with untrained men.
耐力训练有助于免疫系统发生变化，从而有助于应对运动引起的压力并促进抗炎作用。然而，这些适应性变化背后的具体机制仍在探索之中。细胞因子通过与其受体相互作用在急性和慢性运动反应中发挥关键作用，这些受体以膜结合和可溶性两种形式存在。然而，运动对细胞因子和可溶性细胞因子受体的平行影响仍未得到充分研究。因此，本研究的目的是评估耐力训练和未训练男性在剧烈运动后血清中细胞因子及其可溶性受体如何变化。在呼吸补偿点进行1小时的骑行后，未训练男性（n = 5）的促炎细胞因子显著增加，包括白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、趋化因子配体2（CCL2）和血管内皮生长因子A（VEGFA）。相比之下，抗炎细胞因子如白细胞介素-10（IL-10）和白细胞介素-1受体拮抗剂（IL-1Ra）减少。在训练组（n = 7）中未观察到这些效应。相反，促炎细胞因子水平保持接近基线，而抗炎细胞因子IL-10和IL-1Ra增加。在训练组中，这些细胞因子变化伴随着已知可抑制细胞因子介导信号传导的可溶性细胞因子受体表达的显著增加，如可溶性白细胞介素-1受体II型（sIL-1RII）、可溶性糖蛋白130（sGP130）、可溶性肿瘤坏死因子受体I型（sTNFRI）、可溶性肿瘤坏死因子受体II型（sTNFRII）、可溶性血管内皮生长因子受体1型（sVEGFR1）和可溶性血管内皮生长因子受体2型（sVEGFR2），表明细胞因子生物利用度降低。然而，在未训练组中，这些可溶性细胞因子受体的表达要么保持不变，要么下降，表明细胞因子生物利用度更高。这些发现共同凸显了一种新的潜在抗炎适应性变化，即与未训练男性相比，训练有素的男性在运动后通过减少炎性细胞因子和增加可溶性细胞因子受体呈现出减弱的炎症反应。我们的研究确定了一种新的耐力训练潜在抗炎适应性变化，即训练有素的男性呈现出减弱的炎症反应，其特征是炎性细胞因子减少和可溶性细胞因子受体增加，与未训练男性相比，运动后细胞因子生物利用度降低。
