The Effects of Exercise on Depression Symptoms Using Levels of Neurotransmitters and EEG as Markers
The Effects of Exercise on Depression Symptoms Using Levels of Neurotransmitters and EEG as Markers
The purpose of this study is to examine the effects of exercise on the symptoms of depression using serum levels of serotonin, catecholamine's, Alpha EEG asymmetry, and self-report of symptoms as markers.
In an attempt to further understand the mechanisms of improved mood through exercise; this study will examine the known factors that contribute to depressed mood in a single study using serotonin and catecholamine levels via blood serum and EEG slow wave asymmetry. Such information can be useful in understanding the overall neurological components of depression and the effects of exercise on the brain in depressed individuals that would make the prescription of exercise a viable treatment option.
There is an increasing demand for clinical effective, safe, and cost conscious forms of treatment for depression. Research shows depression to account for the largest decrease in overall health compared to asthma, angina, arthritis, and diabetes (Maussavi, 2007). The cost of lost productivity at work due to depression is a new focus of research as no current and accurate numbers exist. Stewart, Ricci, Hahn, & Morganstein (2013) were among the first to examine this issue and found that lost productivity due to depression cost an estimated $44 billion dollars per year in spite of current medical treatments commonly prescribed. The lost productivity among those with depression and the low level of treatment suggest that there may be cost effective opportunities for improving depression outcomes within the general workforce and society at large.
The question of value regarding the use of exercise as a treatment for depression has remained a source of investigation in recent years. In cooperation with Centra Health and Liberty University, this study seeks to understand the mechanisms that make exercise a viable treatment in depression by examining self-report of symptoms, serum levels of serotonin and catecholamines (epinephrine, norepinephrin, and dopamine) and frontal slow wave EEG activity as markers. Although these markers have been examined individually in previous studies, this is the only known study that examines each of these components in a single study. Such information can be useful in understanding the overall neurological components of depression and the effects of exercise on the brain in depressed individuals that would make the prescription of exercise a viable treatment in depression.
Multiple trials, meta-analyses, and reviews have been conducted in the attempt to clarify the use of exercise in depressed patients. Research has shown that exercise as a treatment may result in fewer relapses than sertraline (Strohle, 2009). Similar results are indicated when exercise is prescribed as an adjunct treatment with psychotherapy (Balon, Sidhu, & Pankhuree, 2009; Blumenthal, Smith, & Hoffman, 2012; Gill, Womack, & Safranek, 2010). Preliminary characteristics of the ideal dosage of exercise as a treatment have been researched, although a definitive dose-response curve has yet to be produced (Callaghan, Khalil, Morres, & Carter, 2011; Perraton, Kumar, & Machotka, 2010).
Electroencephalographic (EEG) scans have been shown to demonstrate a left frontal bias in alpha (8-12 Hz) and theta (4-7 Hz) wave activity (Allen, Urry, Hitt, & Coan, 2004; Demos, 2005; Iosifescu et al., 2008; Nissen et al., 2006). The up-training or down-training of individual bandwidths in the treatment of depression, anxiety, ADHD, and traumatic brain injury have long been established (La Vaque, 2002). Although there are no established norms for neurotransmitter levels, we know through clinical medication trials that the inhibition of the reuptake of serotonin and or norepinephrine improve mood. Previous studies examining low levels of serotonin and decreased mood have found a correlation between exercise and increased serotonin availability without the use of pharmaceuticals (Chaouloff et al., 1985; Ernst, Olsen, Pinel, Lam, & Christie, 2006; Jacobs & Fornal, 1999). More routine type studies often use neurotransmitter levels as markers (Lande, Williams, Fileta, 2012; Lidberg, Tuck, Asberg, Scalia-Tomba, & Bertilsson, 1985; Mann & Stanley, 1984).
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