Aerobic Exercise and Stretching as Add-On to Inpatient Treatment for Depression Have No Differential Effects on Stress-Axis Activity, Serum-BDNF, TNF-Alpha and Objective Sleep Measures

Christian Imboden,Johannes Beck,Uwe Pühse,Markus Gerber,Anne Eckert,Imane Lejri,Edith Holsboer-Trachsler,Martin Hatzinger

doi:10.3390/brainsci11040411

Abstract

(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 (N = 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 (VO2max) 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.

Highlights

This article is an open access articleDepression is one of the most important causes of disability worldwide with still growing numbers within the last 20 years [1]
While the results of the primary outcome are already published elsewhere [11], the present paper focuses on the analysis of secondary outcomes (CAR, serum Brain Derived Neurotrophic Factor (sBDNF), TNF-alpha and sleep data)
Our study showed that aerobic exercise (AE) had no additional effects on Cortisol Awakening Response (CAR), sBDNF, TNF-alpha and sleep parameters

Summary

Introduction

Depression is one of the most important causes of disability worldwide with still growing numbers within the last 20 years [1]. Due to increased all-cause morbidity and mortality, depression leads to a significant reduction of life expectancy [2] and has a large impact on public health. Depression is associated with a variety of neurobiological features that might serve as biological markers. These include (a) a dysregulation of the hypothalamic-pituitary-adrenal axis (HPA-axis) with over secretion of stress hormones and reduced negative feedback [3];. (b) impaired sleep with reduced sleep continuity and increased rapid eye movement (REM) pressure [4]; (c) reduced expression of serum Brain Derived Neurotrophic Factor (sBDNF) [5] and (d) changes in inflammatory cytokines such as Tumor Necrosis Factor alpha (TNF- alpha) [6].

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