Abstract Aim: Dyskinesia is a hyperkinetic abnormal involuntary movement (AIM), like chorea, dystonia, athetosis, and ballism. AIM can occur in Levodopa-induced dyskinesia (LID) in Parkinson's disease (PD), tardive dyskinesia (TD) schizophrenia, and paroxysmal dyskinesias (PxDs). This review describes the effects of physical activity and exercise adaptation (e.g., rehabilitation) in the most varied forms of dyskinesias in an attempt to provide a comprehensive understanding of the role of physical exercise on this disorder. Methods: English-language articles available in the database PubMed electronics were examined. The following indexes were adopted with different combinations: LID and exercise; TD and exercise PED and exercise. Manual searches were performed in the references of the articles related to the chosen topic. Results. The relationship between many types of dyskinesia and exercise is poorly explored. The practice of physical activity showed antidyskinetic effects in Parkinson's LID, with well-described the biological mechanisms. Conclusion: Acute exercise does not modify the abnormal respiratory patterns in TD, and it reveals a normal response to progressive training and inspiratory time. Sustained walking or running may induce a type of paroxysmal dyskinesia in the healthy subjects, which was explored by us in this review.

A atividade física é conhecida por promover saúde e bem-estar. O exercício também é responsável por aumentar a produção de Espécies Reativas de Oxigênio (ERO) pelo acréscimo do consumo de oxigênio mitocondrial nos tecidos. O desequilíbrio entre a produção de EROs e as defesas oxidantes dos tecidos pode provocar danos oxidativos a proteínas, lipídios e DNA. O dano oxidativo cerebral é um mecanismo etiopatológico comum da apoptose e da neurodegeneração. O fator de crescimento cérebro-derivado desempenha um importante papel neste contexto. Nesta revisão, apresentamos os resultados de diferentes modelos de exercício físico no metabolismo oxidativo e neurotrófico do Sistema Nervoso Central (SNC). Também revisamos estudos que utilizaram suplementação antioxidante para prevenir danos oxidativos exercício-induzido ao SNC. Os modelos de exercício físico mais comuns foram as rodas de correr, a natação e a esteira com configurações de treinamento muito diferentes como a duração e a intensidade. Os resultados do treinamento físico no tecido cerebral são muito controversos, mas geralmente demonstram ganhos na plasticidade sináptica e na função cognitiva com exercícios de intensidade moderada e baixa.

Physical activity is known for promoting health and well-being. Exercise is also responsible for increasing the production of Oxygen Reactive Species (ORS) by increasing mitochondrial oxygen consumption causing tissue oxidative stress. The imbalance between ORS production and tissue antioxidant defenses can cause oxidative damage to proteins, lipids and DNA. Brain oxidative damage is a common etiopathology mechanism of apoptosis and neurodegeneration. The brain-derived neurotrophic factor plays an important role in this context. In this review, we showed the results of different models and configurations of physical exercise in oxidative and neurotrophic metabolism of the Central Nervous System (CNS). We also reviewed studies that utilized antioxidant supplementation to prevent exercise-induced oxidative damage to CNS. The commonest physical exercise models were running wheels, swimming and treadmill with very different configurations of physical training such as duration and intensity. The results of physical training on brain tissues are very controversial, but generally show improvement in synaptic plasticity and cognition function with low and moderate intensity exercises.