Physical Exercise Interventions for Drug Addictive Disorders

Abstract

Physical exercise physical and psychological health positive through various different avenues, as example, through affecting positively cognitive performance based upon the relocation of cortical activity which seems to advancing the brain development, connectivity and resilience [1]. Any bodily activity that enhances or maintains physical fitness implies the engagement of regular and frequent exercise thereby maintaining physical fitness and the reduction of agents associated with health problems, e.g. cortisol. With regard to the large proportion of individuals with more-or-less sedentary occupations, physical exercise offers probably the most effective health-promoting lifestyle available with positive outcomes for both neurologic and psychiatric conditions [2–10]. The expressions of disorder emerging as consequences of exposure to reward loss have been neglected in approaches to the psychobiology of substance abuse disorders. This notion emphasizes the shared characteristics reward loss and addiction are reviewed, namely, the neural circuitry involved in reward devaluation, the influence of genetic and reward history on the behavioral vulnerability and resilience, the role of competing natural rewards, and emotional selfmedication as a backdrop [11] to the consequences evolving in the “Reward Deficiency Syndrome”. The Reward Deficiency Syndrome, characterized by expressions of rewardseeking behavior and/or addictions and involving a G protein-coupled receptor located on postsynaptic dopaminergic neurons that is centrally involved in reward-mediating mesocorticolimbic pathways, originates from genetic variations, most notably resulting from those carrying the D2A1 allele implicated in addiction and abuse [12, 13]. Individuals carrying the A1 allele tend to have insufficient numbers of D2 receptors in their brain, resulting in lack of pleasure and reward from activities that would provide others with pleasure. Dopamine subtype 2 receptor (D2DR) knockdown mice fail to gain weight or exhibit elevated appetitive motivation in comparison with the wild-type mice within standard environments yet in enriched environments incorporating voluntary exercise facilities, these D2DR knockdown mice expressed markedly lower activity with a rapid increase in obesity compared with the wild-type mice without being receptive of the protective benefit from exercise contingencies [14]. Thus, an underlying mechanism for conceptualizing and