Physical activity is antidepressant and addicitive.

Abstract

Physical activity has been found generally as pleasant and good for one’s health. It is known to have a positive impact on nearly every system in the body. Regular exercise will improve the cardiovascular system, facilitates weight control, will create greater bone mineral density and it will decrease the risk for cancer, stroke and diabetes. Regular exercise can enhance and protect brain function and it has been found to have an antidepressant effect. Therefore physical activity is investigated to be used as a potential treatment for depression. It was found that physical activity can increase transmission of monoamines in the brain thereby correcting any imbalances seen in depressed patients. It also has an effect on the hypothalamic pituitary adrenal axis to reduce the effects of daily stressors which can be a cause of depression. In addition, it can increase the expression of BDNF in the hippocampus to facilitate neuronal growth and dendritic sprouting. Many other genes are activated important for regulating plasticity, metabolism, immune function and degeneration processes. Physical activity and anti-depressant drugs seem to have most prominent effect when used together. However, physical activity has traditionally been seen as having only positive influence for all people, but when taken to extremes, physical activity can become addictive and compulsive-like behaviour. This behaviour is called exercise dependence (ED). Traditionally, definitions of dependence were only restricted to ingestion of psychoactive substances stated in the DSM-IV. However, the concept of addiction is changing. There is becoming more emphasis on how certain behaviours may cause long-term damage to the brain the same way as drugs of abuse do, resulting in addiction. This is for instance seen when physical training causes neurochemical and morphological adaptations in brain reward pathways and hippocampus that are also shared by addictive drugs. In addition, physical activity can cause tolerance and withdrawal symptoms which are behaviours comparable to the DSM-IV of substance abuse. Neurochemically similar long term effects are seen, showed for instance with the activation of ∆FosB. Also positive reinforcement of addiction is seen in for instance when regular runners experience the runner’s high and negative reinforcement is indicated by several withdrawal symptoms. Therefore ED should be seen as a clinical disorder in its own right as almost 3% off all active people exhibit this extreme behaviour. A better understanding of the neurochemical and morphological effects of physical activity in the brain could constitute a basis for developing novel treatments for depression and drug addiction. Linking molecules to mood and physical activity should continue to be investigated in the future and the research field of depression and addiction should increasingly work together.