Aim: 

During aging humans lose gradually muscle mass, a process defined sarcopenia. One of the main factors that could play a key role in the genesis and maintenance of this status is the presence of oxidative stress of muscle resident satellite cells which became unable to repair muscle damage present in sarcopenic muscle. The aim of this work is to investigate "in vitro" the effects of aging on myogenesis utilising satellite cells derived from human donors, characterizing them morphologically, and functionally utilising also the contribute of their transcriptional gene profile, to check the presence of deregulated genes and/or pathways to justify the aging-related alterations.

Methods: 

Satellite cell populations were isolated from biopsies of young and elderly healthy subjects and grown so as to obtain fuse myotubes. [Ca²⁺]_i measurements were performed as test of functional maturation by using a fast imaging system. A microarray technique was utilized to identify deregulated genes in the early myogenesis phases.

Results: 

We found that myoblasts from elderly show an altered ability to fuse and to differentiate in myotubes. We also check the functionality of DHPR and RyR, Ca-channels involving in E-C coupling mechanism, and we found the probable existence of a uncoupling status in myotubes derived from elderly, that could be due to a probable disorganization of the DHPR-RyR system. The presence in elderly myotubes, of a increase in lipid peroxidation could be (by alteration of membrane fluidity) and one of the causes, of the altered myogenesis program. These possibility is also supported by data carried out from transcriptional profile, that show the presence of several genes differentially expressed whose trascripts code for different pathways directly linked to oxidative stress, cytoskeletal organization, extracellular matrix deposition, atrophy, etc..

Conclusions: 

These data suggest that in elderly, morphological and functional alteration of myogenesis process could be one of the causes for their reduced ability to repair muscle damage and as consequence of this the decrease of the capacity to counteract the muscle mass loss.