The effects of enforced running on the gastrocnemius muscle in aging mice

Ludatscher, Ruth M.; Silbermann, Michael; Gershon, David; Reznick, Abraham Z.

doi:10.1016/0531-5565(83)90004-9

Cited by 27 publications

(13 citation statements)

References 24 publications

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“…Genome-wide transcriptional profiling data revealed an age-related decline in expression levels of genes involved in mitochondrial biogenesis, mtDNA maintenance, ATP synthase, and mitochondrial protein folding in mouse skeletal muscle [88]. These data are in agreement with previous findings that mitochondrial dysfunction occurs in aged animals [92]. Interestingly, this age-dependent decline in mitochondria-related gene expression is completely or partially prevented by DR begun in early adulthood [88].…”

Section: Dietary Restriction and Mitochondriasupporting

confidence: 84%

Mitochondria and Organismal Longevity

Hwang

Jeong²,

Lee³

2012

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Mitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-dependent decline in biological function. However, recent studies show that increased levels of ROS or inhibition of mitochondrial function can actually delay aging and increase lifespan. The aim of this review is to summarize recent findings regarding the role of mitochondria in organismal aging processes. We will discuss how mitochondria contribute to evolutionarily conserved longevity pathways, including mild inhibition of respiration, dietary restriction, and target of rapamycin (TOR) signaling.

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Section: Dietary Restriction and Mitochondriasupporting

confidence: 84%

Mitochondria and Organismal Longevity

Hwang

Jeong²,

Lee³

2012

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“…Forced short-term exercise on these animals resulted in an increase in T tubule systems of the sarcoplasmic reticulum. Overall, the conclusion of most researchers is that most of the architecture of aging muscle is well preserved in old age with some minor but probably significant changes characteristic of old age (42).…”

Section: Changes In Muscular Apparatus With Agingmentioning

confidence: 99%

The Physiology and Biochemistry of Skeletal Muscle Atrophy as a Function of Age

Carmeli¹,

Reznick²

1994

Experimental Biology and Medicine

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The skeletal muscles are an important entity in the proper function of aging animals and humans. Studies have shown that until humans are 60-70 years old, age-related changes in muscle function and structure are relatively small, while after 70 years, these alterations are accelerated considerably. Factors responsible for the "aging" of skeletal muscles are complex and include intrinsic biochemical changes in muscle metabolism, changes in the distribution and size of muscle fibers, and a general loss of muscle mass. In addition, other factors like the control of muscle contraction by the motor neural system and the influence of external conditions such as exercise, immobility, nutrition and others may also contribute to the age-related decrease in muscle functions. Studies have shown that with age there is some loss of peripheral motor neurons, reduction in the number of motor units, alterations in the neuromuscular junctions, and selective denervation of Type II muscle fibers. These findings led to the concept of denervation atrophy of skeletal muscles as one of the major mechanisms for muscle degeneration in old age. However, it should be emphasized that the extent of age-related changes varies from muscle to muscle, and some do not seem to be affected by age. For example, it has been shown recently, in animal studies, that weight-bearing muscles are much more susceptible to senescent processes than non-weight-bearing muscles. More work is needed to clarify the contributions of the various factors, especially the role of muscle training in alleviating the symptoms of age-related muscle atrophy.

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“…One of the most significant effects of aging is loss of muscle mass, known as sarcopenia, a process that may be triggered by reactive oxygen species (ROS) that are generated throughout an organism's lifespan [6,7]. Aging of muscle is also characterized by muscle cell atrophy, presence of lipofuscin deposits, mitochondrial abnormalities, and increase in oxidative damage to proteins, lipid, and DNA [8][9][10].…”

Section: The Gene Expression Profile Of Aging and Cr In Mouse Skeletamentioning

confidence: 99%

Gene expression profiling studies of aging in cardiac and skeletal muscles

Prolla¹

2005

Cardiovascular Research

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To examine transcriptional alterations associated with aging in skeletal muscle and the heart, we and others have used DNA microarrays to compare the gene expression profile of young and old animals. Aging results in a differential gene expression pattern specific to each tissue, and most alterations can be completely or partially prevented by caloric restriction (CR) in both heart and skeletal muscle. Transcriptional patterns of tissues from calorie-restricted animals suggests that CR retards the aging process by reducing endogenous damage and by inducing metabolic shifts associated with specific transcriptional profiles. These studies demonstrate that DNA microarrays can be used in cardiovascular aging research to generate panels of hundreds of transcriptional biomarkers, providing a new tool to measure biological age of cardiac and skeletal muscles and to test interventions designed to retard aging in these tissues.

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The effects of enforced running on the gastrocnemius muscle in aging mice

Cited by 27 publications

References 24 publications

Mitochondria and Organismal Longevity

Mitochondria and Organismal Longevity

The Physiology and Biochemistry of Skeletal Muscle Atrophy as a Function of Age

Gene expression profiling studies of aging in cardiac and skeletal muscles

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