Parkinson's disease (PD) is manifested by progressive motor, autonomic, and cognitive disturbances. Dopamine (DA) synthesizing neurons in the substantia nigra (SN) degenerate, causing a decline in DA level in the striatum that leads to the characteristic movement disorders. A disease-modifying therapy to arrest PD progression remains unattainable with current pharmacotherapies, most of which cause severe side effects and lose their efficacy with time. For this reason, there is a need to seek new therapies supporting the pharmacological treatment of PD. Motor therapy is recommended for pharmacologically treated PD patients as it alleviates the symptoms. Molecular mechanisms behind the beneficial effects of motor therapy are unknown, nor is it known whether such therapy may be neuroprotective in PD patients. Due to obvious limitations, human studies are unlikely to answer these questions; therefore, the use of animal models of PD seems indispensable. Motor therapy in animal models of PD characterized by the loss of dopaminergic neurons has neuroprotective and neuroregenerative effects, and the completeness of neuronal protection may depend on (i) degree of neuronal loss, (ii) duration and intensity of exercise, and (iii) time elapsed between insult and commencing of training. As the physical activity is neuroprotective for dopaminergic neurons, the question arises what is the mechanism of this protective action. A current hypothesis assumes a central role of neurotrophic factors in the neuroprotection of dopaminergic neurons, even though it is still not clear whether increased DA level in the nigrostriatal axis results from neurogenesis of dopaminergic neurons in the SN, recovery of the phenotype of dopaminergic neurons, increased sprouting of the residual dopaminergic axons in the striatum, or generation of local striatal neurons from inhibitory interneurons. In the present review, we discuss studies describing the influence of physical exercise on the PD-like changes manifested in animal models of the disease and focus our interest on the current state of knowledge on the mechanism of neuroprotection induced by physical activity as a supportive therapy in PD.

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BACKGROUND: Reduced muscle strength is one symptom of Parkinson’s disease (PD). Strength can be increased by strength training, which may cause exaggerated blood pressure (BP) rise. It is believed that exercises performed on vibrating platform can strengthen leg muscles without excessive BP increase. OBJECTIVE: To measure the pressor response to static exercises performed during whole body vibration in PD patients. METHODS: Twenty-four aged PD patients and twelve healthy young volunteers participated in the study. PD subjects performed six repetitions of deep-, semi-squat, and calves at vibration frequency of 30 Hz. Each 30 s exercise was followed by 30 s rest. The young volunteers performed two sessions of above-mentioned exercises with and without vibration. BP was measured continuously. RESULTS: In PD patients, the highest BP values were observed during deep squat; systolic blood pressure rose 10 mmHg in ‘weak responders’, and 50 mmHg in ‘strong responders’. This difference correlated with the rise in pulse pressure suggesting indirectly the role of stoke volume in individual response. In healthy subjects pressor response was also individually differentiated and not influenced by vibration. CONCLUSION: Deep and semi squat can evoke a strong cardiovascular response in some PD and healthy subjects. Low-magnitude vibrations likely did not affect pressor response.