Impact of an Eight Week Exercise Intervention in Treating Major Depressive Disorder

2017-06-20 02:08:21 | BioPortfolio


To investigate the impact of a structured eight week exercise intervention as an add-on therapy in treating Major Depressive Disorder. Using behavioural techniques and neuroimaging to measure changes in brain function following an exercise intervention in people with clinical depression. By correlating changes in the hippocampus with changes in HPA axis hormones, inflammatory cytokines and growth factors it is possible to determine which of the biochemical markers is most predictive of improved neural function.


Memory impairment is the most frequently reported cognitive symptom in people with depression. However, research in this area has presented mixed findings in terms of the type, severity and specificity of memory deficits. One finding that has been well established is the impairment in episodic memory (memory for a specific past experience in one's life) with a sparing of semantic memory (present knowledge of universal truths such as "the sky is blue"), and short-term memory. Behavioural and neuroimaging studies investigating the stage of the memory deficit in people with depression have found that both the encoding and retrieval processes are impaired. Although the neural underpinnings of impaired memory in MDD are not completely understood, the majority of evidence implicates abnormal activity in the hippocampal region critical for normal memory formation.

Exercise for depression has been a common research theme for the past several years however its mechanism of action remains unknown. Many studies have reported higher levels of cardiorespiratory fitness and increased habitual physical activity being associated with lower depressive symptomatology and greater emotional well-being, while lower levels of cardiorespiratory fitness being associated with increased risk of developing depressive illness. Exercise alone or in combination with other treatment options, such as pharmacotherapy or cognitive behavioural therapy have all been effective in treating depression with response rates for exercise being comparable to these mainstream therapies. Exercise protects against the development of neurodegenerative diseases delays the negative effects of aging and improves sleep quality. Exercise also reduces inflammation, normalizes cortisol secretion, increases hippocampal neurogenesis, increases cerebrovascular perfusion, improves the structure and function of the hippocampus, facilitates neurocognitive recovery from traumatic brain injury reverses brain volume loss in elderly and schizophrenic individuals and improves learning and memory. These findings suggest that the relationship between fitness and cognition is partly mediated by processes that involve cerebral circulation. These positive effects of exercise on neuroanatomy and vascularization can be partly explained by the interactive cascade of growth factor signalling associated with exercise that increases the ability of cerebral blood vessels to respond to demand. Habitual exercise is an effective way to improve endothelial function by increasing arterial compliance and decreasing arterial stiffness, oxidative stress, and vascular inflammation.

The overall goal of this research study is to investigate the effects of a well-defined, structured, supervised exercise program on brain function in healthy and clinically depressed individuals. This research aims to fill the gaps in the literature by elucidating the anti-depressant mechanisms which exercise targets and if these effects parallel young healthy sedentary individuals.

To investigate the effects of a moderate-intensity structured, supervised 8 week exercise program in people with MDD when combined with a Mental Health Day Treatment (MHDT) program, as compared to the MHDT on its own. All outcome measures will be assessed at baseline and 8 weeks. A non-depressed exercise control group will be used to compare the effects of exercise in depressed and non-depressed individuals:

i. depressive symptoms ii. anxiety iii. sleep quality iv. plasma IL-1β, IL-1ra, IL-6, IFN-γ, TNF-α and IL-10, BDNF v. salivary cortisol vi. performance on an associative memory task and concomitant fMRI hippocampal activation.

Study Design


Major Depressive Disorder




University of Ontario Institute of Technology
L1H 7K4




University of Ontario Institute of Technology

Results (where available)

View Results


Published on BioPortfolio: 2017-06-20T02:08:21-0400

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Medical and Biotech [MESH] Definitions

A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence.

Marked depression appearing in the involution period and characterized by hallucinations, delusions, paranoia, and agitation.

A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309)

Inability to experience pleasure due to impairment or dysfunction of normal psychological and neurobiological mechanisms. It is a symptom of many PSYCHOTIC DISORDERS (e.g., DEPRESSIVE DISORDER, MAJOR; and SCHIZOPHRENIA).

An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent.

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