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      Muscle weakness in the elderly: role of sarcopenia, dynapenia, and possibilities for rehabilitation

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      European Review of Aging and Physical Activity

      Springer Nature

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          Capitalizing on cortical plasticity: influence of physical activity on cognition and brain function.

          Given the aging populations in many countries throughout the world, there is an increasing interest in lifestyle factors and interventions that will enhance the cognitive vitality of older adults and reduce the risk for age-related neurological disorders, such as Alzheimer's disease. In this review, we evaluate the hypothesis that physical activity and exercise might serve to protect, and also enhance, cognitive and brain function across the adult lifespan. To this end, we critically review three separate literatures that have examined the influence of physical activity and exercise on cognition, brain function and brain structure of adults, including epidemiological or prospective observational studies, randomized human clinical interventions and non-human animal studies. We suggest that this literature supports the claim that physical activity enhances cognitive and brain function, and protects against the development of neurodegenerative diseases. We discuss future directions to address currently unresolved questions, such as interactions between multiple lifestyle factors on offsetting or protecting against cognitive and neural decline, and conclude that physical activity is an inexpensive treatment that could have substantial preventative and restorative properties for cognitive and brain function.
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            Mitochondrial DNA-deletion mutations accumulate intracellularly to detrimental levels in aged human skeletal muscle fibers.

            Skeletal muscle-mass loss with age has severe health consequences, yet the molecular basis of the loss remains obscure. Although mitochondrial DNA (mtDNA)-deletion mutations have been shown to accumulate with age, for these aberrant genomes to be physiologically relevant, they must accumulate to high levels intracellularly and be present in a significant number of cells. We examined mtDNA-deletion mutations in vastus lateralis (VL) muscle of human subjects aged 49-93 years, using both histologic and polymerase-chain-reaction (PCR) analyses, to determine the physiological and genomic integrity of mitochondria in aging human muscle. The number of VL muscle fibers exhibiting mitochondrial electron-transport-system (ETS) abnormalities increased from an estimated 6% at age 49 years to 31% at age 92 years. We analyzed the mitochondrial genotype of 48 single ETS-abnormal, cytochrome c oxidase-negative/succinate dehydrogenase-hyperreactive (COX-/SDH++) fibers from normal aging human subjects and identified mtDNA-deletion mutations in all abnormal fibers. Deletion mutations were clonal within a fiber and concomitant to the COX-/SDH++ region. Quantitative PCR analysis of wild-type and deletion-containing mtDNA genomes within ETS-abnormal regions of single fibers demonstrated that these deletion mutations accumulate to detrimental levels (>90% of the total mtDNA).
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              Mitochondrial function and apoptotic susceptibility in aging skeletal muscle.

              During aging, skeletal muscle undergoes sarcopenia, a condition characterized by a loss of muscle cell mass and alterations in contractile function. The origin of these decrements is unknown, but evidence suggests that they can be partly attributed to mitochondrial dysfunction. To characterize the nature of this dysfunction, we investigated skeletal muscle contractile properties, subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondrial biogenesis and function, as well as apoptotic susceptibility in young (6 months old) and senescent (36 months old) Fischer 344 Brown Norway rats. Muscle mass and maximal force production were significantly lower in the 36-month group, which is indicative of a sarcopenic phenotype. Furthermore, contractile activity in situ revealed greater fatigability in the 36-month compared to the 6-month animals. This decrement could be partially accounted for by a 30% lower mitochondrial content in fast-twitch muscle from 36-month animals, as well as lower protein levels of the transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator-1alpha. Enzyme activities and glutamate-induced oxygen consumption rates in isolated SS and IMF mitochondria were similar between age groups. However, mitochondrial reactive oxygen species (ROS) production during state 3 respiration was approximately 1.7-fold greater in mitochondria isolated from 36-month compared to 6-month animals, and was accompanied by a 1.8-fold increase in the DNA repair enzyme 8-oxoguanine glycosylase 1 in fast-twitch muscle. Basal rates of release of cytochrome c and endonuclease G in SS mitochondria were 3.5- to 7-fold higher from senescent animals. These data suggest that the age-related sarcopenia and muscle fatigability are associated with enhanced ROS production, increased mitochondrial apoptotic susceptibility and reduced transcriptional drive for mitochondrial biogenesis.
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                Author and article information

                Journal
                European Review of Aging and Physical Activity
                Eur Rev Aging Phys Act
                Springer Nature
                1813-7253
                1861-6909
                October 2012
                May 4 2012
                : 9
                : 2
                : 109-117
                Article
                10.1007/s11556-012-0102-8
                © 2012
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