Swim Training Modulates Skeletal Muscle Energy Metabolism, Oxidative Stress, and Mitochondrial Cholesterol Content in Amyotrophic Lateral Sclerosis Mice

Recently, in terms of amyotrophic lateral sclerosis (ALS), much attention has been paid to the cell structures formed by the mitochondria and the endoplasmic reticulum membranes (MAMs) that are involved in the regulation of Ca2+ signaling, mitochondrial bioenergetics, apoptosis, and oxidative stress...

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Published in:Oxidative medicine and cellular longevity 2018-01, Vol.2018 (2018), p.1-12
Main Authors: Ziolkowski, Wieslaw, Antosiewicz, J., Halon, Malgorzata, Kaczor, Jan Jacek, Dzik, Katarzyna Patrycja, Flis, Damian Jozef, Wieckowski, Mariusz R.
Format: Article
Language:English
Subjects:
Amyotrophic lateral sclerosis
Animals
Bioenergetics
Cholesterol
Disease
Endoplasmic reticulum
Ethylenediaminetetraacetic acid
Free radicals
Genetic aspects
Kinases
Metabolism
Mitochondria
Muscles
Musculoskeletal system
Mutation
Neurodegeneration
Neuromuscular diseases
Oxidative stress
Pathogenesis
Physiological aspects
Swimming
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Summary:Recently, in terms of amyotrophic lateral sclerosis (ALS), much attention has been paid to the cell structures formed by the mitochondria and the endoplasmic reticulum membranes (MAMs) that are involved in the regulation of Ca2+ signaling, mitochondrial bioenergetics, apoptosis, and oxidative stress. We assumed that remodeling of these structures via swim training may accompany the prolongation of the ALS lifespan. In the present study, we used transgenic mice with the G93A hmSOD1 gene mutation. We examined muscle energy metabolism, oxidative stress parameters, and markers of MAMs (Caveolin-1 protein level and cholesterol content in crude mitochondrial fraction) in groups of mice divided according to disease progression and training status. The progression of ALS was related to the lowering of Caveolin-1 protein levels and the accumulation of cholesterol in a crude mitochondrial fraction. These changes were associated with aerobic and anaerobic energy metabolism dysfunction and higher oxidative stress. Our data indicated that swim training prolonged the lifespan of ALS mice with accompanying changes in MAM components. Swim training also maintained mitochondrial function and lowered oxidative stress. These data suggest that modification of MAMs might play a crucial role in the exercise-induced deceleration of ALS development.
ISSN:1942-0900
1942-0994
DOI:10.1155/2018/5940748