Muscle atrophy
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(Redirected from Muscle wasting)
Muscle atrophy
Classification and external resources
Prisoner of war exhibiting muscle loss as a result of malnutrition
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 results from 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. Moreover,
starvation eventually leads to muscle atrophy. Disuse of the muscles will also lead to disuse atrophy while
neurogenic atrophy is muscle atrophy that results from damage to the nerve that stimulates the muscle.
Contents
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1 Clinical settings of atrophy
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2 Quality of life
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3 Other muscles diseases, distinct from atrophy
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4 Pathophysiology
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5 Potential treatment
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6 Quantification
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7 Hibernation
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8 See also
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9 References
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10 External links
Clinical settings of atrophy [edit]
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 syndrome that is a comorbidity 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 liver disease, and starvation.
Quality of life [edit]
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 [edit]
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 [edit]
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 protein
degradation.[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-dependentubiquitin/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.
The change in synthesis during atrophy is called hypertrophy.[clarification needed]
Potential treatment [edit]
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.
In severe cases of muscular atrophy, the use of an anabolic steroid such as methandrostenolone is
administered to patients as a potential cure. A novel class of drugs, called SARM (selective adrenerge receptor
modulators) are being investigating with promising results. They would have fewer side-effects, while still
promoting muscle and bone tissue growth and regeneration. These claims are, however, yet to be confirmed in
larger clinical trials.
Quantification [edit]
A CT scan can distinguish muscle tissue from other tissues and thereby estimate the amount of muscle tissue
in the body.
Fast loss of muscle tissue (relative to normal turnover), can be approximated by the amount of urea in the
urine. The equivalent nitrogen content (in gram) of urea (in mmol) can be estimated by the conversion factor
0.028 g/mmol.[3] Furthermore, 1 gram of nitrogen is roughly equivalent to 6 gram of protein, and 1 gram of
protein is roughly equivalent to 4 gram of muscle tissue. Subsequently, in situations such as muscle wasting,
1 mmol of excessive urea in the urine (as measured by urine volume in litres multiplied by urea concentration in
mmol/l) roughly corresponds to a muscle loss of 0.67 gram.