| Popis: |
Addiction involves functional changes to brain circuits that are involved with reward, stress, and self-control. Studies estimate that 20-60% of athletes suffer from stress due to excessive exercise and inadequate recovery. This research addresses certain neuroadaptations in the striatum of the brain that renders elite athletes more vulnerable to addictive behavior, particularly as a result of an increased tolerance to dopamine. Dopamine receptors in the striatum are crucial to the addiction process. Dopamine receptor type 2 (D2) receptors have a 10-to-100-fold greater affinity for dopamine (DA) than dopamine receptor type 1 (D1) receptors. The intense exercise that elite athletes must complete on a day-to-day basis can increase D2 receptor expression and binding in the striatum, until tolerance to the elevated levels of dopamine is eventually developed. In animal models, studies show that consistent, moderate aerobic exercise amplifies the availability and processing of dopamine neurotransmitters in the striatal region of the brain. In MPTP-induced mice models of Parkinson’s disease, intense daily exercise for 28 days (four weeks) resulted in higher levels of dopamine neurotransmission compared to non-exercise mice, through an increase in D2 receptor expression and binding in the dorsolateral striatum. Using a fast-scan cyclic voltammetry technique on mice, studies show that treadmill exercise increased stimulus-evoked DA release in MPTP-induced PD mice while also decreasing the decay of DA in the dorsal striatum. Additionally, positron emission tomography (PET) validated that treadmill exercise upregulates striatal D2 receptors. These increases in dopaminergic levels due to exercise can consequently increase motivation for rewards. Taken together, evidence supports the hypothesis that long-term, intense exercise modulates dopamine receptor expression. These changes may render elite athletes more vulnerable to addictive behavior, mainly due to an increased tolerance to dopamine. Tolerance leads to increased risk-taking behavior to compensate for the decrease in D2 receptor expression. |
