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New insight on sarcopenia Torna agli editoriali

Anna Giulia Cattaneo
Dipartimento di Scienze Biochimiche e Molecolari (DBSM), Università dell'Insubria, Varese.

The loss of mass and strength of skeletal muscle is frequently seen at all ages as a consequence of injuries and prolonged inactivation, for example following bone fractures, nerve injuries or invalidating illnesses. Nevertheless this condition dramatically rises in frequency and severity in aged people, even if still in good general health. The term sarcopenia was introduced to depict this conditions, in which a specific defect of type II myofibres and of their satellite cells has been described, not seen for example in sporadic mitochondrial myopathies. The central role of satellite cells in this condition will be discussed later.

A comprehensive description of this defect is still lacking: among the traditional methods to study muscle mass and strength, dynamometry is the most affordable and reliable, but it is not informative about the muscle mass and the physiopathology of sarcopenia. A quite large number of trials are ongoing: the, a register developed by U.S. Authorities but worldwide accessible, collect at the present 48 protocols on sarcopenia, 23 of them still recruiting patients. Most of them are both descriptive and interventional, i.e. proposing some kind of treatment. However the methods used to test muscle function are often expensive, like those using stable or radioactive isotopes, resonance imaging, and dual X-ray absorptiometry or near infrared spectroscopy. Nevertheless, these studies are very important to assess the minimal requirements for functional investigation.
More recently, histological finding associated with the assessment of skeletal muscle proteome shed new light on basic mechanisms operating during sarcopenia development and its recovery. Several proteomic predictors of recovery after resistance training (RT) have been identified: the ciliary neutrotrophic factor, the matrix metallo-proteinase-2, the TIMP-1 and the insulin-like growth factor-1, between others. Other mRNA, expressing proteins involved in immune and stress response, or in the control of cell cycle, have been found to be enhanced after a high intensity resistance loading, a type of exercise inducing a modest muscle damage. These markers were not modified, however, after RT. Resistance training (RT) instead expands the mitochondrial network in young individuals, not in aged sarcopenic subjects, in which mutations and deletions of mitochondrial DNA are observed only in type II myocytes, not in satellite cells.

Satellite cells seem to play the most important role in sarcopenia and in recovery of skeletal muscle function in elderly. These cells, also called muscle stem cells, represent a reservoir of nuclei for type II myofibres, i.e. they are responsible of regenerative responses in muscle. Their differentiation into fusion-competent myoblasts is regulated by the interplay of gene families WNT and Notch, originally identified in Drosophila but with homologs in mammals and humans. The former induces stem cell differentiation, the latter controls the proliferation and inhibiting WNT. The regulatory role of Notch influences also the expression of other genes involved in apoptosis and inflammation, and this recall the role of inflammatory and stress markers described in the previous paragraph.

Resistance training (RT) restores in older subjects both the number satellite cells and the size of type II myofibres, if sufficiently prolonged and sustained to improve skeletal muscle function. A recent, comprehensive and innovative work (EMBO Molecular Medicine 2009, doi: 10.1002/emmm.200900045) demonstrates that recovery after 2 weeks immobilization of a muscular district is near to complete after 3 weeks retraining in younger volunteers. Histology from muscle biopsies clearly shows the higher reaction of the connective and inflammatory components in muscles from older, while healthy, individuals. While still maintained and able to react normally when isolated "in vitro", satellite cells cannot repair the injured muscle. The stem muscle cells from aged persons, however, are functionally intact when isolated "in vitro" in the absence of aged muscle components, while those from young persons are inhibited in the presence of products of aged muscles. The experimental finding that aged muscle are over expressing genes products able to inhibit Notch explains, according to the Authors, their poor recovery after immobilization.

Data from this newer approach in investigating the skeletal muscle function, decline and recovery late in life seems to open not only newest and deepest explanation for a condition poorly understood until now, but they open even new perspectives to an early detection of subject at risk and prognosis. In a near future these new findings could be even of importance in posing the basis for more efficient treatment of this frequent condition.

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