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There is lack of clarity in the literature over whether patients with Parkinson's disease (PD) show the same post-exercise depression of corticospinal excitability as is usually observed in healthy control. This study set out to resolve the problem. Ten patients with idiopathic PD and 10 age-matched controls were included in this study. Each subject performed a submaximal sustained voluntary contraction of the right first dorsal interosseous muscle (FDI) for 10 min or until force could no longer be sustained. Resting motor threshold, motor-evoked potential (MEP), input-output curve, cortical silent period duration, interference pattern (IP) and M/F ratio were recorded at baseline, immediately after fatigue and after 20 min rest. Immediately after exercise, decreased MEP amplitude and increased cortical SP duration were observed in the control group whilst no such changes were observed in PD patients. The input-output curve was also significantly suppressed only in controls, but not in patients. The amplitude of IP was significantly reduced immediately after exercise in both PD patients and controls. Almost all these changes returned nearly to baseline values after 20 min rest. The amount of exercise was approximately equal in both groups because the effect on M-waves and EMG amplitude was similar. However, the expected decline in corticospinal excitability was absent in PD patients. The absence of this effect in PD patients may reflect reorganization of motor commands in response to basal ganglia deficit.

Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism.This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of NRF2-ARE pathway as a mechanism involved in exercise associated improvement in rotenone rat model of PD.Method: Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination) groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks.Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone model of PD. When treadmill exercise introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor co-ordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to NRF2 pathways such as TFAM, NRF2, Noq.1 mRNA expression.Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating NRF2 pathway.