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Effect of Exercise on Oxidative Stress in Neurological Disorders

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Inflammation and Oxidative Stress in Neurological Disorders

Abstract

Overproduction of ROS and RNS produces oxidative and nitrosative damage to biomolecules (lipids, proteins, and DNA) eventually leading to many chronic neurological disorders such as stroke, SCI, TBI, AD, PD, and depression in humans. Exercise produces beneficial effects in patients with stroke, SCI, TBI, AD, PD, and depression. Regular moderate exercise improves cardiovascular and cerebrovascular fitness in normal older subjects and in patients with stroke, SCI, TBI, AD, PD, and depression by increasing blood flow. In addition, exercise improves cognition and support learning and memory by promoting neuroplasticity, facilitating angiogenesis, protecting blood brain barrier permeability, and inducing BDNF-mediated neurogenesis. Neurochemically, exercise increases the synthesis and release of protein chaperones (heat shock protein 70, Hsp70) and glucose regulated protein 78 (GRP78); antioxidant enzymes (heme oxygenase-1), and the regulator of mitochondrial biogenesis PGC-1α. In skeletal muscles exercise also increases intracellular Ca2+ as well as alters energy status (i.e. ATP/ADP ratio) and the consequent activation of downstream kinases such as AMP kinase and Ca2+-calmodulin-activated kinases. These kinases activate transcription factors that bind DNA to modulate the gene transcription along with biochemical changes that occur during the post-exercise recovery period when energy metabolism is directed toward anabolism, rather than contractile activity.

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    Akhlaq A. Farooqui

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Farooqui, A. (2014). Effect of Exercise on Oxidative Stress in Neurological Disorders. In: Inflammation and Oxidative Stress in Neurological Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-04111-7_10

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