During early “non-addicted” stages, such as when drug use is initiated, dopamine signaling in the reward pathway (i.e., nucleus accumbens, NAc ventral tegmental area, prefrontal cortex, PFC) is believed to be a primary mechanism motivating drug use (for reviews see Gardner, 2011 Kalivas and Volkow, 2005 Koob and Volkow, 2010 Pierce and Kumaresan, 2006 Willuhn et al., 2010). New and more effective treatments are critically needed, but developing treatments for drug addiction is challenging because its underlying neurobiology varies over time as the disease progresses. We conclude with future directions, including the development of exercise-based interventions alone or as an adjunct to other strategies for treating drug addiction.ĭrug addiction is the leading cause of preventable death in the United States followed closely by obesity ( Mokdad et al., 2004).
During drug use initiation and withdrawal, its efficacy may be related to its ability to facilitate dopaminergic transmission, and once addiction develops, its efficacy may be related to its ability to normalize glutamatergic and dopaminergic signaling and reverse drug-induced changes in chromatin via epigenetic interactions with BDNF in the reward pathway. While exercise generally produces an efficacious response, certain exercise conditions may be either ineffective or lead to detrimental effects depending on the level/type/timing of exercise exposure, the stage of addiction, the drug involved, and the subject population. Potential neurobiological mechanisms are also discussed focusing on interactions with dopaminergic and glutamatergic signaling and chromatin remodeling in the reward pathway.
In this review, we discuss clinical and preclinical evidence for the efficacy of exercise at different phases of the addiction process. Physical activity, and specifically exercise, has been suggested as a potential treatment for drug addiction.
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