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Muscle atrophy
Classification and external resources
ICD-10 M62.5
ICD-9 728.2
DiseasesDB 29472
MedlinePlus 003188
MeSH D009133

Muscle atrophy is defined as a decrease in the mass of the muscle; it can be a partial or complete wasting away of muscle. When a muscle atrophies, this leads to muscle weakness, since the ability to exert force is related to mass. Muscle atrophy is a co-morbidity of several common diseases, including cancer, AIDS, congestive heart failure, COPD (chronic obstructive pulmonary disease), renal failure, and severe burns; patients who have "cachexia" in these disease settings have a poor prognosis.

Contents

Clinical settings of atrophy

There are many diseases and conditions which cause a decrease in muscle mass, known as atrophy, including: Dejerine Sottas syndrome (HSMN Type III), inactivity, as seen when a cast is put on a limb, or upon extended bedrest (which can occur during a prolonged illness); cachexia - which is a "body-wasting" syndrome that is a co-morbidity of cancer and Congestive Heart Failure; Chronic Obstructive Pulmonary Disease; burns, liver failure, etc. Other syndromes or conditions which can induce skeletal muscle atrophy are congestive heart failure, liver disease, and starvation.

Quality of life

Muscular atrophy decreases quality of life as the sufferer becomes unable to perform certain tasks or worsen the risks of accidents while performing those (like walking). Muscular atrophy increases the risks of falling in conditions such as IBM (inclusion body myositis). Muscular atrophy affects a major number of elderly.

Other muscles diseases, distinct from atrophy

During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass. This condition is called "sarcopenia". The exact cause of sarcopenia is unknown, but it may be due to a combination of the gradual failure in the "satellite cells" which help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted growth factors which are necessary to maintain muscle mass and satellite cell survival.

In addition to the simple loss of muscle mass (atrophy), or the age-related decrease in muscle function (sarcopenia), there are other diseases which may be caused by structural defects in the muscle (muscular dystrophy), or by inflammatory reactions in the body directed against muscle (the myopathies).

Pathophysiology

Muscle atrophy occurs by a change in the normal balance between protein synthesis and protein degradation. During atrophy, there is a down-regulation of protein synthesis pathways, and an activation of protein breakdown pathways[1]. The particular protein degradation pathway which seems to be responsible for much of the muscle loss seen in a muscle undergoing atrophy is the ATP-dependent ubiquitin/proteasome pathway. In this system, particular proteins are targeted for destruction by the ligation of at least four copies of a small peptide called ubiquitin onto a substrate protein. When a substrate is thus "poly-ubiquitinated", it is targeted for destruction by the proteasome. Particular enzymes in the ubiquitin/proteasome pathway allow ubiquitination to be directed to some proteins but not others - specificity is gained by coupling targeted proteins to an "E3 ubiquitin ligase". Each E3 ubiquitin ligase binds to a particular set of substrates, causing their ubiquitination.

Potential treatment

Muscle atrophy can be opposed by the signaling pathways which induce muscle hypertrophy, or an increase in muscle size. Therefore one way in which exercise induces an increase in muscle mass is to downregulate the pathways which have the opposite effect.

One important rehabilitation tool for muscle atrophy includes the use of functional electrical stimulation to stimulate the muscles. This has seen a large amount of success in the rehabilitation of paraplegic patients. [2]

Since the absence of muscle-building amino acids can contribute to muscle wasting (that which is torn down must be rebuilt with like material), amino acid therapy may be helpful for regenerating damaged or atrophied muscle tissue. The branched-chain amino acids or BCAAs (leucine, isoleucine, and valine) are critical to this process, in addition to lysine and other amino acids.

See also

References

  1. ^ Sandri M. 2008. Signaling in Muscle Atrophy and Hypertrophy. Physiology 23: 160-170.
  2. ^ D.Zhang et al., Functional Electrical Stimulation in Rehabilitation Engineering: A survey, Nenyang technological University, Singapore

External links

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Simple English

Muscle atrophy or “muscle wastage” is a decrease in the mass of the muscle. It leads to muscle weakness, since the ability to exert force is related to mass. Muscle atrophy can be a partial or complete wasting away of muscle. Muscular atrophy affects a major number of elderly. It also develops in several common diseases, including cancer, AIDS, congestive heart failure, Chronic obstructive pulmonary disease, renal failure. It may be observed in Dejerine Sottas syndrome, inactivity, as seen when a cast is put on a limb, or upon extended bed rest (which can occur during a prolonged illness or hostel research); cachexia, burns, liver failure and starvation. Muscular atrophy decreases quality of life as the sufferer becomes unable to perform certain tasks or worsen the risks of accidents while performing those (like walking). It also increases the risks of falling in conditions such as IBM (inclusion body myositis).

The exact cause of muscular atrophy is unknown, but it may be due to the gradual failure in the "satellite cells" which help to regenerate skeletal muscle fibres, and a decrease in sensitivity to or the availability of secreted growth factors which are necessary to maintain muscle mass and satellite cell survival.

In muscle atrophy, the normal balance between protein synthesis and protein degradation changes. There is a down-regulation of protein synthesis pathways, and an activation of protein breakdown pathways[1]. In the ATP-dependent ubiquitin/proteasome pathway, particular proteins are targeted for destruction by the ligation of at least four copies of a small peptide called ubiquitin onto a substrate protein. The substrate is later targeted for destruction by the proteasome.

Muscle atrophy can be treated

  • by exercise which induces an increase in muscle mass. The exercise downregulates the pathways which induce muscle hypertrophy, or an increase in muscle size.
  • by the use of functional electrical stimulation to stimulate the muscles. This has seen a large amount of success in the rehabilitation of paraplegic patients. [2]
  • by therapy with muscle-building amino acids for regenerating damaged or atrophied muscle tissue. The branched-chain amino acids or BCAAs (leucine, isoleucine, and valine) are critical to this process, in addition to lysine and other amino acids.

See also

  • Muscle weakness

References

  1. Sandri M. 2008. Signaling in Muscle Atrophy and Hypertrophy. Physiology 23: 160-170.
  2. D.Zhang et al., Functional Electrical Stimulation in Rehabilitation Engineering: A survey, Nenyang technological University, Singapore

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