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Int J Mol Sci. 2019 Jan 9;20(2). pii: E233. doi: 10.3390/ijms20020233.

Swim Training Modulates Mouse Skeletal Muscle Energy Metabolism and Ameliorates Reduction in Grip Strength in a Mouse Model of Amyotrophic Lateral Sclerosis.

Author information

1
Department of Bioenergetics and Nutrition, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland. damian.flis@gumed.edu.pl.
2
Department of Neurobiology of Muscle, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland. kasi.dzik@gmail.com.
3
Department of Neurobiology of Muscle, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland. kaczorj@gumed.edu.pl.
4
Department of Bioenergetics and Physiology of Exercise, Faculty of Health Sciences, Medical University of Gdansk, 80-211 Gdansk, Poland. kaczorj@gumed.edu.pl.
5
School of Postgraduate Studies, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland. karol.cieminski@awf.gda.pl.
6
Department of Physiotherapy, Faculty of Health Sciences, Medical University of Gdansk, 80-211 Gdansk, Poland. malgorzata.halon-golabek@gumed.edu.pl.
7
Department of Bioenergetics and Physiology of Exercise, Faculty of Health Sciences, Medical University of Gdansk, 80-211 Gdansk, Poland. jant@gumed.edu.pl.
8
Department of Biochemistry, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland. jant@gumed.edu.pl.
9
Nencki Institute of Experimental Biology, 02-093 Warsaw, Poland. m.wieckowski@nencki.gov.pl.
10
Department of Bioenergetics and Nutrition, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland. wieslaw.ziolkowski@awf.gda.pl.

Abstract

Metabolic reprogramming in skeletal muscles in the human and animal models of amyotrophic lateral sclerosis (ALS) may be an important factor in the diseases progression. We hypothesized that swim training, a modulator of cellular metabolism via changes in muscle bioenergetics and oxidative stress, ameliorates the reduction in muscle strength in ALS mice. In this study, we used transgenic male mice with the G93A human SOD1 mutation B6SJL-Tg (SOD1G93A) 1Gur/J and wild type B6SJL (WT) mice. Mice were subjected to a grip strength test and isolated skeletal muscle mitochondria were used to perform high-resolution respirometry. Moreover, the activities of enzymes involved in the oxidative energy metabolism and total sulfhydryl groups (as an oxidative stress marker) were evaluated in skeletal muscle. ALS reduces muscle strength (-70% between 11 and 15 weeks, p < 0.05), modulates muscle metabolism through lowering citrate synthase (CS) (-30% vs. WT, p = 0.0007) and increasing cytochrome c oxidase and malate dehydrogenase activities, and elevates oxidative stress markers in skeletal muscle. Swim training slows the reduction in muscle strength (-5% between 11 and 15 weeks) and increases CS activity (+26% vs. ALS I, p = 0.0048). Our findings indicate that swim training is a modulator of skeletal muscle energy metabolism with concomitant improvement of skeletal muscle function in ALS mice.

KEYWORDS:

ALS; bioenergetics; exercise; mitochondria; neurodegeneration; oxidative stress

PMID:
30634386
PMCID:
PMC6359093
DOI:
10.3390/ijms20020233
[Indexed for MEDLINE]
Free PMC Article

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