Exercise for depression

Abstract

Rationale
Depression is a common cause of morbidity and mortality worldwide. Depression is commonly treated with antidepressants and/or psychological therapy, but some people may prefer alternative approaches such as exercise. There are a number of theoretical reasons why exercise may improve depression. This is an update of an earlier review first published in 2009.

Objectives
To determine the effectiveness of exercise in the treatment of depression in adults compared with no treatment or an active intervention (e.g., psychological, pharmacological, alternative treatments).

Search methods
We searched the Cochrane Depression, Anxiety and Neurosis Review Group’s Controlled Trials Register (CCDANCTR) to February 2016. As CCDANCTR was not updated after this search, we searched MEDLINE, EMBASE, PsycINFO and the Cochrane Central Register of Controlled Trials (CENTRAL) from 2016 to November 2023. No date or language restrictions were applied.

Eligibility criteria
Randomised controlled trials (RCTs) in which exercise was compared to standard treatment, no treatment or a placebo treatment, pharmacological treatment, psychological treatment or other active treatment in adults (aged 18 and over) with depression, as defined by trial authors. We included individual participant and cluster randomised trials. We excluded trials of postnatal depression. Two authors independently undertook study selection and data extraction.

Outcomes
The primary outcome assessed was a measure of depression or mood at treatment end and at any longer term follow-up. Other outcomes reported were acceptability of treatment, quality of life, cost and adverse events.

Risk of bias
Risk of bias was assessed using the Cochrane Collaboration 'Risk of bias' tool (version 1). Two authors independently performed the assessment.

Synthesis methods
Two authors extracted data on primary and secondary outcomes at the end of the trial and end of follow-up (if available). We calculated effect sizes for each trial using Hedges' g method and a means difference (MD) or standardised mean difference (SMD) for the overall pooled effect for continuous data, or a risk ratio for dichotomous data. Where trials used a number of different tools to assess depression, we included the main outcome measure only in the meta-analysis. Where trials provided several 'doses' of exercise, we used data from the biggest 'dose' of exercise, and performed sensitivity analyses using the lower 'dose'. We performed subgroup analyses to explore the influence on effect sizes of method of diagnosis of depression, intensity of exercise, number of sessions of exercise, type of exercise and type of control focusing on 'control' and the 'no treatment, waiting list, usual care and self monitoring'. Our sensitivity analyses explored the influence of study quality on outcome. Included studies Seventy-three RCTs (4985 participants) fulfilled our inclusion criteria, with 69 provided data for meta-analyses.

Synthesis of results
For the 57 trials (2189 participants) comparing exercise with no treatment or a control intervention, the pooled SMD for the primary outcome of depression at the end of treatment was -0.67 (95% confidence interval (CI) -0.82 to -0.52; GRADE: low), showing that exercise may result in a reduction in depressive symptoms. When we included only the seven trials (447 participants) with adequate allocation concealment, intention-to-treat analysis and blinded outcome assessment, the pooled SMD for this outcome was smaller (SMD -0.46, 95% CI -0.88 to -0.04). Pooled data from the 9 trials (405 participants) providing long-term follow-up was very uncertain about the effect of exercise on depressive symptoms (SMD -0.53, 95% CI -1.11 to 0.06; GRADE: very low). Ten trials compared exercise with psychological therapy (414 participants) finding little to no difference in the effect on depression symptom severity (SMD 0.03, 95% CI -0.16 to 0.23; GRADE: moderate). Five trials (n = 330) compared exercise with pharmacological treatment and found little to no difference in their effect on depression symptom severity (SMD -0.11, -0.33, 0.10; GRADE: low). Of five studies reporting measures of quality of life for exercise compared to no treatment or a control intervention, it was found that exercise may result in an increase environment (2 studies, 80 participants) (SMD 0.51 (95% CI: 0.05 to 0.96); I² = 0%, p = 0.82, GRADE: low) and physical domains (5 studies, 178 participants) (SMD 0.57 (95% CI: 0.15 to 0.98); I² = 44%, p = 0.13, GRADE: very low). Fifty-one trials
reported acceptability of treatment, the risk ratio was 1.00 (95% CI 0.98 to 1.02; GRADE: moderate). Adverse events were limited, with musculoskeletal injuries and depression affecting those undertaking exercise and diarrhoea, sexual dysfunction and fatigue reported by those receiving sertraline. When assessed using the Cochrane Collaboration 'Risk of bias' tool it was evident that many trials were affected by multiple sources of bias; randomisation was adequately concealed in 22 studies, 31 used intention-to-treat analyses and 23 used blinded outcome assessors. Blinding of those receiving and those delivering the interventions was inherently difficult, with trials judged at high risk of bias. Many trials used participant self-report rating scales, which also has the potential to bias findings.

Authors' conclusions
Exercise is moderately more effective than a control intervention for reducing symptoms of depression. When compared to psychological or pharmacological therapies, exercise appears to be no more effective, though this conclusion is based on a few small trials. Long-term follow-up was rare. The addition of 35 RCTs (2526 participants) in this update has had limited effect on the estimate of the benefit of exercise on symptoms of depression. If further research was to take place, it should focus on improving the quality of RCTs, on assessing which characteristics of exercise are effective for different people and explore issues around health equity.