Imboden Christian, Gerber Markus, Beck Johannes, Eckert Anne, Lejri Imane, Pühse Uwe, Holsboer-Trachsler Edith, Hatzinger Martin
Psychiatric Services Solothurn, 4503 Solothurn, Switzerland and University of Basel, 4031 Basel, Switzerland.
Private Clinic Wyss, 3053 Muenchenbuchsee, Switzerland.
Brain Sci. 2021 Mar 24;11(4):411. doi: 10.3390/brainsci11040411.
(1) Background: While the antidepressant effects of aerobic exercise (AE) are well documented, fewer studies have examined impact of AE as an add-on treatment. Moreover, various effects on neurobiological variables have been suggested. This study examines effects of AE on Cortisol Awakening Reaction (CAR), serum Brain Derived Neurotrophic Factor (sBDNF), Tumor Necrosis Factor alpha (TNF-alpha) and sleep. (2) Methods: Inpatients with moderate-to-severe depression ( = 43) were randomly assigned to the AE or stretching condition (active control) taking place 3x/week for 6 weeks. CAR, sBDNF and TNF-alpha were assessed at baseline, after 2 weeks and post-intervention. The 17-item Hamilton Depression Rating Scale (HDRS17), subjective sleep quality measured by the Pittsburgh Sleep Quality Index (PSQI) and polysomnography (PSG) were obtained at baseline and post-intervention. (3) Results: Stress axis activity decreased in both groups from baseline to post-intervention. sBDNF showed a significant increase over time, whereas the number of awakenings significantly decreased. No significant time by group interactions were detected for any of the study variables. Correlational analyses showed that higher improvements in maximum oxygen capacity (VOmax) from baseline to post-intervention were associated with reduced scores on the HDRS17, PSQI and REM-latency post-intervention. (4) Conclusions: While some neurobiological variables improved during inpatient treatment (CAR, sBDNF), no evidence was found for differential effects between AE and an active control condition (stretching). However, patients in which cardiorespiratory fitness increased showed higher improvements in depression severity and depression-related sleep-parameters.
(1) 背景:虽然有氧运动(AE)的抗抑郁作用已有充分记录,但较少有研究考察其作为辅助治疗的效果。此外,已有研究表明其对神经生物学变量有多种影响。本研究考察有氧运动对皮质醇觉醒反应(CAR)、血清脑源性神经营养因子(sBDNF)、肿瘤坏死因子α(TNF-α)和睡眠的影响。(2) 方法:将43例中重度抑郁症住院患者随机分为有氧运动组或伸展运动组(积极对照组),每周进行3次干预,共6周。在基线、2周后和干预后评估CAR、sBDNF和TNF-α。在基线和干预后获取17项汉密尔顿抑郁量表(HDRS17)、匹兹堡睡眠质量指数(PSQI)测量的主观睡眠质量以及多导睡眠图(PSG)。(3) 结果:两组从基线到干预后的应激轴活动均降低。sBDNF随时间显著增加,而觉醒次数显著减少。对于任何研究变量,均未检测到显著的组间时间交互作用。相关性分析表明,从基线到干预后最大摄氧量(VOmax)改善程度越高,干预后HDRS17、PSQI得分及快速眼动睡眠潜伏期缩短越明显。(4) 结论:虽然住院治疗期间一些神经生物学变量有所改善(CAR、sBDNF),但未发现有氧运动与积极对照条件(伸展运动)之间存在差异效应的证据。然而,心肺功能增强的患者在抑郁严重程度和与抑郁相关的睡眠参数方面改善更为明显。