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      Aging of Skeletal Muscle Fibers

      review-article
      , MD, PhD 1 , , MD, PhD 2 , , MD, PhD 3 , , MD, PhD 1 , 4 ,
      Annals of Rehabilitation Medicine
      Korean Academy of Rehabilitation Medicine
      Elderly, Sarcopenia, Myofilament

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          Abstract

          Aging has become an important topic for scientific research because life expectancy and the number of men and women in older age groups have increased dramatically in the last century. This is true in most countries of the world including the Republic of Korea and the United States. From a rehabilitation perspective, the most important associated issue is a progressive decline in functional capacity and independence. Sarcopenia is partly responsible for this decline. Many changes underlying the loss of muscle mass and force-generating capacity of skeletal muscle can be understood at the cellular and molecular levels. Muscle size and architecture are both altered with advanced adult age. Further, changes in myofibers include impairments in several physiological domains including muscle fiber activation, excitation-contraction coupling, actin-myosin cross-bridge interaction, energy production, and repair and regeneration. A thorough understanding of these alterations can lead to the design of improved preventative and rehabilitative interventions, such as personalized exercise training programs.

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          Most cited references40

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          Molecular regulation of stem cell quiescence.

          Subsets of mammalian adult stem cells reside in the quiescent state for prolonged periods of time. This state, which is reversible, has long been viewed as dormant and with minimal basal activity. Recent advances in adult stem cell isolation have provided insights into the epigenetic, transcriptional and post-transcriptional control of quiescence and suggest that quiescence is an actively maintained state in which signalling pathways are involved in maintaining a poised state that allows rapid activation. Deciphering the molecular mechanisms regulating adult stem cell quiescence will increase our understanding of tissue regeneration mechanisms and how they are dysregulated in pathological conditions and in ageing.
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            Muscle type and fiber type specificity in muscle wasting.

            Muscle wasting occurs in a variety of conditions, including both genetic diseases, such as muscular dystrophies, and acquired disorders, ranging from muscle disuse to cancer cachexia, from heart failure to aging sarcopenia. In most of these conditions, the loss of muscle tissue is not homogeneous, but involves specific muscle groups, for example Duchenne muscular dystrophy affects most body muscles but spares extraocular muscles, and other dystrophies affect selectively proximal or distal limb muscles. In addition, muscle atrophy can affect specific fiber types, involving predominantly slow type 1 or fast type 2 muscle fibers, and is frequently accompanied by a slow-to-fast or fast-to-slow fiber type shift. For example, muscle disuse, such as spinal cord injury, causes type 1 fiber atrophy with a slow-to-fast fiber type shift, whereas cancer cachexia leads to preferential atrophy of type 2 fibers with a fast-to-slow fiber type shift. The identification of the signaling pathways responsible for the differential response of muscles types and fiber types can lead to a better understanding of the pathogenesis of muscle wasting and to the design of therapeutic interventions appropriate for the specific disorders. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Copyright © 2013 Elsevier Ltd. All rights reserved.
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              Mechanisms for fiber-type specificity of skeletal muscle atrophy.

              There are a variety of pathophysiologic conditions that are known to induce skeletal muscle atrophy. However, muscle wasting can occur through multiple distinct signaling pathways with differential sensitivity between selective skeletal muscle fiber subtypes. This review summarizes some of the underlying molecular mechanisms responsible for fiber-specific muscle mass regulation. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha protects slow-twitch oxidative fibers from denervation/immobilization (disuse)-induced muscle atrophies. Nutrient-related muscle atrophies, such as those induced by cancer cachexia, sepsis, chronic heart failure, or diabetes, are largely restricted to fast-twitch glycolytic fibers, of which the underlying mechanism is usually related to abnormality of protein degradation, including proteasomal and lysosomal pathways. In contrast, nuclear factor kappaB activation apparently serves a dual function by inducing both fast-twitch fiber atrophy and slow-twitch fiber degeneration. Fast-twitch glycolytic fibers are more vulnerable than slow-twitch oxidative fibers under a variety of atrophic conditions related to signaling transduction of Forkhead box O family, autophagy inhibition, transforming growth factor beta family, and nuclear factor-kappaB. The resistance of oxidative fibers may result from the protection of peroxisome proliferator-activated receptor gamma coactivator 1-alpha.
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                Author and article information

                Journal
                Ann Rehabil Med
                Ann Rehabil Med
                ARM
                Annals of Rehabilitation Medicine
                Korean Academy of Rehabilitation Medicine
                2234-0645
                2234-0653
                April 2015
                24 April 2015
                : 39
                : 2
                : 155-162
                Affiliations
                [1 ]Department of Physical Medicine and Rehabilitation, Vanderbilt University School of Medicine, Nashville, TN, USA.
                [2 ]Department of Rehabilitation Medicine, Seoul National University College of Medicine, Seoul, Korea.
                [3 ]Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA.
                [4 ]Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico.
                Author notes
                Corresponding author: Walter R. Frontera. Department of Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Suite 1318, 2201 Children's Way, Nashville, TN 37212, USA. Tel: +1-615-322-7574, Fax: +1-615-327-9289, walter.frontera@ 123456vanderbilt.edu
                Article
                10.5535/arm.2015.39.2.155
                4414960
                25932410
                d5fe991b-4383-4107-b008-5f3487ded9b4
                Copyright © 2015 by Korean Academy of Rehabilitation Medicine

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 13 March 2015
                : 26 March 2015
                Categories
                Review Article

                Medicine
                elderly,sarcopenia,myofilament
                Medicine
                elderly, sarcopenia, myofilament

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