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Exercise, including resistance exercise, has been shown to significantly improve mental health outcomes by reducing symptoms of anxiety and depression. During exercise, a number of hormones are released in the brain which serve to modulate mood and emotion states, including anxiety and depression.

Several hormone-related hypotheses have been proposed. The monoamine hypothesis is the one with the most promise and suggests that exercise increase the ability of brain neurotransmitters—serotonin, dopamine, and norepinephrine—that are diminished with depression.

The monoamines norepinephrine and serotonin have known associations with anxiety and depression. Norepinephrine can induce both anxiogenic (anxiety-promoting) and anxiolytic (anxiety-reducing) effects depending on the nature of the stress. Serotonin plays a critical role in the central nervous system as a neurotransmitter that acts upon many different receptor subtypes in various regions of the brain and is involved in the neuroregulatory impacts on mood and emotion.

Exercise and Hormones

In response to acute physical or psychological stress, the hypothalamic-pituitary-adrenal (HPA) axis is stimulated. Hypothalamic neurons produce increased amounts of corticotropin releasing hormone (CRH), which subsequently stimulates release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. As a result, ACTH is released into circulation and stimulates release of cortisol from the adrenal gland. In people with major depression, there is a sustained hyperactivity of the HPA axis that perpetuates the depressive condition.  

Results showed that lifelong aerobic exercise was able to generate an adaptive response to a chronic stress state, thereby providing a strong positive impact on stress resilience.

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GABA is an inhibitory neurotransmitter within the brain and central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system. This activity produces effects such as relieving anxiety and reducing stress, and exercise has been shown to potentiate the effects of GABA.

Galanin is a neuropeptide that is widely expressed in the brain and spinal cord and possesses neuroprotective activity. It is closely involved in the modulation and inhibition in neural circuity involved in the regulation of mood, and is often co-localized with classical neurotransmitters such as acetylcholine, serotonin, and norepinephrine.

Neurophysiology, Exercise, Depression, and Anxiety

Low serotonin is one of the factors that may contribute to depression. A relationship between exercise and mood exists which suggests antidepressant and anxiety-reducing effects of exercise. Exercise has been shown to increase serotonin and 5-hydroxyindoleacetic acid (5-HIAA) levels in various areas of the brain. Two different mechanisms may be involved producing this effect: Motor activity increases the firing rates of serotonergic neurons resulting in the increased release and synthesis of serotonin and there is an increase in the brain of the serotonin precursor, tryptophan, that persists after exercise.

Another factor seems to be associated with the HPA axis and the role of CRH hyperactivity in depression. In response to acute physical or psychological stress, neurons within the hypothalamus produce increased amounts of CRH which trigger ACTH release from the anterior pituitary gland. In individuals with depression, however, there is sustained hyperactivity of the HPA system. This unrestrained CRH-related hyperdrive could result in a blunting of the impact of the HPA axis. It seems difficult to determine whether blunted ACTH response is caused by either elevated cortisol or by desensitized CRH receptors. Nevertheless, this scenario would likely explain many of the depressive symptoms.

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Effects of Exercise

Findings suggest that exercise improves a number of cognitive outcomes in patients with depression. For instance, 12 weeks of exercise improved various aspects of cognitive function (e.g., attention, working memory, etc.) among depressed patients with inadequate response to antidepressant medication.

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These pro-cognitive effects are suggested to represent behavioral consequences of exercise-induced neuroplasticity. Furthermore, this highlights a major premise for the overlapping mechanisms of exercise and standard treatments for depression. For instance, animal models of depression have demonstrated that the combination of antidepressant medication and exercise has been shown to increase brain neurotransmitter activity and decrease depressive-like behavior to a greater extent than antidepressant medication alone.

Based on available data, it is reasonable to suggest that exercise combined with standard treatments leads to significantly greater antidepressant effects over standard treatment alone.

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For resources regarding anxiety and depression, visit the website of the Anxiety and Depression Association of America:  

If you or someone you know is experiencing suicidal thoughts, please reach out for help. Call the National Suicide Prevention hotline at 1-800-273-8255 or visit their website at