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      Age-related changes in skeletal muscle mitochondria: the role of exercise

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          Abstract

          Aging is associated with mitochondrial dysfunction, which leads to a decline in cellular function and the development of age-related diseases. Reduced skeletal muscle mass with aging appears to promote a decrease in mitochondrial quality and quantity. Moreover, mitochondrial dysfunction adversely affects the quality and quantity of skeletal muscle. During aging, physical exercise can cause beneficial adaptations to cellular energy metabolism in skeletal muscle, including alterations to mitochondrial content, protein, and biogenesis. Here, we briefly summarize current findings on the association between the aging process and impairment of mitochondrial function, including mitochondrial biogenesis and reactive oxygen species in skeletal muscle. We also discuss the potential role of exercise in the improvement of aging-driven mitochondrial dysfunctions.

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          Effects of exercise on mitochondrial content and function in aging human skeletal muscle.

          E Menshikova, V B Ritov, L. Fairfull … (2006)
          Skeletal muscle mitochondria are implicated with age-related loss of function and insulin resistance. We examined the effects of exercise on skeletal muscle mitochondria in older (age = 67.3 +/- 0.6 years) men (n = 5) and women (n = 3). Similar increases in (p <.01) cardiolipin (88.2 +/- 9.0 to 130.6 +/- 7.5 microg/mU creatine kinase activity [CK]) and the total mitochondrial DNA (1264 +/- 170 to 1895 +/- 273 copies per diploid of nuclear genome) reflected increased mitochondria content. Succinate oxidase activity, complexes 2-4 of the electron transport chain (ETC), increased from 0.13 +/- 0.02 to 0.20 +/- 0.02 U/mU CK (p <.01). This improvement was more pronounced (p <.05) in subsarcolemmal (127 +/- 48%) compared to intermyofibrillar (56 +/- 12%) mitochondria. NADH oxidase activity, representing total ETC activity, increased from 0.51 +/- 0.09 to 1.00 +/- 0.09 U/mU CK (p <.01). In conclusion, exercise enhances mitochondria ETC activity in older human skeletal muscle, particularly in subsarcolemmal mitochondria, which is likely related to the concomitant increases in mitochondrial biogenesis.
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            Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production.

            F Muller, Wook Song, L. Y. Jang … (2007)
            Reactive oxygen species (ROS), especially mitochondrial ROS, are postulated to play a significant role in muscle atrophy. We report a dramatic increase in mitochondrial ROS generation in three conditions associated with muscle atrophy: in aging, in mice lacking CuZn-SOD (Sod1(-/-)), and in the neurodegenerative disease, amyotrophic lateral sclerosis (ALS). ROS generation in muscle mitochondria is nearly threefold higher in 28- to 32-mo-old than in 10-mo-old mice and is associated with a 30% loss in gastrocnemius mass. In Sod1(-/-) mice, muscle mitochondrial ROS production is increased >100% in 20-mo compared with 5-mo-old mice along with a >50% loss in muscle mass. ALS G93A mutant mice show a 75% loss of muscle mass during disease progression and up to 12-fold higher muscle mitochondrial ROS generation. In a second ALS mutant model, H46RH48Q mice, ROS production is approximately fourfold higher than in control mice and is associated with a less dramatic loss (30%) in muscle mass. Thus ROS production is strongly correlated with the extent of muscle atrophy in these models. Because each of the models of muscle atrophy studied are associated to some degree with a loss of innervation, we were interested in determining whether denervation plays a role in ROS generation in muscle mitochondria isolated from hindlimb muscle following surgical sciatic nerve transection. Seven days post-denervation, muscle mitochondrial ROS production increased nearly 30-fold. We conclude that enhanced generation of mitochondrial ROS may be a common factor in the mechanism underlying denervation-induced atrophy.
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              Skeletal Muscle Mitochondria and Aging: A Review

              Courtney M. Peterson, Darcy L. Johannsen, Eric Ravussin (2012)
              Aging is characterized by a progressive loss of muscle mass and muscle strength. Declines in skeletal muscle mitochondria are thought to play a primary role in this process. Mitochondria are the major producers of reactive oxygen species, which damage DNA, proteins, and lipids if not rapidly quenched. Animal and human studies typically show that skeletal muscle mitochondria are altered with aging, including increased mutations in mitochondrial DNA, decreased activity of some mitochondrial enzymes, altered respiration with reduced maximal capacity at least in sedentary individuals, and reduced total mitochondrial content with increased morphological changes. However, there has been much controversy over measurements of mitochondrial energy production, which may largely be explained by differences in approach and by whether physical activity is controlled for. These changes may in turn alter mitochondrial dynamics, such as fusion and fission rates, and mitochondrially induced apoptosis, which may also lead to net muscle fiber loss and age-related sarcopenia. Fortunately, strategies such as exercise and caloric restriction that reduce oxidative damage also improve mitochondrial function. While these strategies may not completely prevent the primary effects of aging, they may help to attenuate the rate of decline.
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                Author and article information

                Contributors
                Jin Han
                Journal
                Journal ID (nlm-ta): Integr Med Res
                Journal ID (iso-abbrev): Integr Med Res
                Title: Integrative Medicine Research
                Publisher: Elsevier
                ISSN (Print): 2213-4220
                ISSN (Electronic): 2213-4239
                Publication date PMC-release: 22 July 2016
                Publication date (Print): September 2016
                Publication date (Electronic): 22 July 2016
                Volume: 5
                Issue: 3
                Pages: 182-186
                Affiliations
                [a ]National Research Laboratory for Mitochondrial Signaling, Department of Physiology, BK21 Plus Project Team, College of Medicine, Inje University, Busan, Republic of Korea
                [b ]Department of Health Science and Technology, Graduate School, Inje University, Busan, Republic of Korea
                [c ]Cardiovascular and Metabolic Disease Center, Inje University, Busan, Republic of Korea
                Author notes
                [* ] Corresponding author. Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, 633-165, Bokji-ro 75, Busan jin-gu, Busan, 47392, Republic of Korea. phyhanj@ 123456inje.ac.kr
                Article
                Publisher ID: S2213-4220(16)30072-5
                DOI: 10.1016/j.imr.2016.07.003
                PMC ID: 5390452
                PubMed ID: 28462116
                SO-VID: c83c7d2b-1c6f-4c50-a074-96a0705dbf15
                Copyright © © 2016 Korea Institute of Oriental Medicine. Published by Elsevier.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 1 July 2016
                Date revision received : 8 July 2016
                Date accepted : 14 July 2016
                Categories
                Subject: Review Article

                Keywords: aging,exercise,mitochondria,skeletal muscle
                Data availability:
                Keywords: aging, exercise, mitochondria, skeletal muscle

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