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Oxid Med Cell Longev. 2018 Apr 11;2018:5940748. doi: 10.1155/2018/5940748. eCollection 2018.

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

Author information

1
Department of Bioenergetics and Physiology of Exercise, Medical University of Gdansk, 80-211 Gdansk, Poland.
2
Department of Bioenergetics and Nutrition, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland.
3
Department of Neurobiology of Muscle, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland.
4
Department of Physiotherapy, Medical University of Gdansk, 80-211 Gdansk, Poland.
5
Department of Biochemistry, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland.
6
Department of Biochemistry, Nencki Institute of Experimental Biology, 02-093 Warsaw, Poland.

Abstract

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.

PMID:
29849903
PMCID:
PMC5924974
DOI:
10.1155/2018/5940748
[Indexed for MEDLINE]
Free PMC Article

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