Cellular and molecular mechanisms underlying age-related skeletal muscle wasting and weakness

  title={Cellular and molecular mechanisms underlying age-related skeletal muscle wasting and weakness},
  author={James G. Ryall and Jonathan D. Schertzer and Gordon S. Lynch},
Some of the most serious consequences of ageing are its effects on skeletal muscle. The term ‘sarcopenia’ describes the slow but progressive loss of muscle mass with advancing age and is characterised by a deterioration of muscle quantity and quality leading to a gradual slowing of movement and a decline in strength. The loss of muscle mass and strength is thought to be attributed to the progressive atrophy and loss of individual muscle fibres associated with the loss of motor units, and a… 

Sarcopenia and Age-Related Endocrine Function

The current understanding of the endocrine contribution to sarcopenia is summarized and an update on hormonal intervention to try to improve endocrine defects is provided and myostatin inhibition seems to be the most interesting strategy for attenuating sarc Openia.

Overview of Sarcopenia

This book provides the latest information on sarcopenia from leading international researchers studying the cellular and molecular mechanisms underlying age-related changes in skeletal muscle and identifying strategies to combat sarc Openia and related muscle wasting conditions and neuromuscular disorders.

Excitation-Contraction Coupling Regulation in Aging Skeletal Muscle

This chapter focuses on skeletal muscle excitation-contraction uncoupling (ECU), external calcium-dependent skeletal muscle contraction, the role of JP-45 and other recently discovered molecules of the muscle T-tubule-sarcoplasmic reticulum junction (triad), the neural influence of skeletal muscle, and the roles of trophic factors–particularly insulin-like growth factor-I (IGF-1).

Molecular mechanisms and therapeutic interventions in sarcopenia

Inflammation and age-associated skeletal muscle deterioration (sarcopaenia)

PGC-1α and Myokines in the Aging Muscle – A Mini-Review

Current discoveries about the peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α), a key exercise factor in muscle, and myokines, factors produced and secreted by active muscle fibers, expand the view of the pathological changes and the therapeutic options for sarcopenia.

The Beneficial Effects of Taurine to Counteract Sarcopenia

The aim of this review is to summarize the pleiotropic effects of taurine on specific muscle targets and to discuss its role in regulating signaling pathways involved in the maintenance of muscle homeostasis.

Role of Myokines in muscle recovery

Functional Electrical Stimulation should be prescribed in critical care units and nursing facilities, if persons are unable or reluctant to exercise, to result in less frequent hospitalizations and a reduced burden on patients’ families and public health services.

A metabolic link to skeletal muscle wasting and regeneration

Due to its essential role in movement, insulating the internal organs, generating heat to maintain core body temperature, and acting as a major energy storage depot, any impairment to skeletal muscle

Borderlines between Sarcopenia and Mild Late-Onset Muscle Disease

Muscle magnetic resonance imaging is a useful tool to help differentiate myopathies from sarcopenia and to reach the correct diagnosis also in the elderly, and is highlighted by two examples: LGMD1D and myotonic dystrophy type 2.



Emerging drugs for sarcopenia: age-related muscle wasting

This review describes a selection of the emerging drugs that have been developed during the period 1997 – 2004, relevant to sarcopenia and suggests drugs that target neurodegenerative diseases may also have important relevance for treating age-related muscle wasting and weakness.

Skeletal muscle weakness in old age: underlying mechanisms.

Much of the age-associated muscle atrophy and declining strength may be explained by motor unit remodeling which appears to occur by selective denervation of muscle fibers with reinnervation by axonal sprouting from an adjacent innervated unit.

Exercise, aging, and muscle protein metabolism.

  • K. Yarasheski
  • Biology
    The journals of gerontology. Series A, Biological sciences and medical sciences
  • 2003
Evidence is summarized that supports the notion that advancing age and physical frailty are associated with a reduction in the fasting rate of mixed and myosin heavy chain protein synthesis, which contributes to muscle protein wasting in advancing age, and this impairment can be corrected because resistance exercise acutely and dramatically increases the rate of muscle protein synthesis in men and women aged 76 years and older.

Tumor necrosis factor alpha signaling in skeletal muscle: effects of age and caloric restriction.

Caloric restriction has been shown to attenuate the age-associated adaptations in TNF-alpha signaling in skeletal muscle, which may be a possible mechanism by which CR prevents apoptosis and the loss of muscle fibers with age.

Neural control of aging skeletal muscle

The present article discusses the evidence for neural influence on age‐related impairments of skeletal muscle, including a role in excitation–contraction uncoupling, and the role of nerves in regulating the trophic actions of insulin‐like growth factor‐1 and other neurotrophic factors is considered as a novel influence on the effects of aging on the neuromuscular junction.

Modifying muscle mass - the endocrine perspective.

The molecular mechanisms associated with muscle hypertrophy are described, and the central role of the satellite cell highlighted; the increasingly recognised role of myostatin, a negative regulator of muscle function, is described, as well as its potential as a therapeutic target.

Factors contributing to neuromuscular impairment and sarcopenia during aging

Prolonged absence of myostatin reduces sarcopenia

A lack of myostatin appears to reduce age‐related sarcopenia and loss of muscle regenerative capacity in aged mice.

Involvement of the calcium-dependent proteolytic system in skeletal muscle aging