Format

Send to

Choose Destination
Clin Sci (Lond). 2014 Sep;127(6):415-21. doi: 10.1042/CS20140051.

Cellular aging of skeletal muscle: telomeric and free radical evidence that physical inactivity is responsible and not age.

Author information

1
†Mons Mazzali Foundation, Mantova, Italy.
2
‡Department of Neurological, and Movement Sciences, University of Verona, Verona, Italy.
3
¶Department of Biomedical Sciences, University of Padova, Padova, Italy.
4
**DAHFMO Unit of Histology and Medical Embryology, Sapienza University, Rome, Italy.
5
††Department of Human Genetics, University of Utah, Salt Lake City, Utah, U.S.A.

Abstract

Telomeres play an essential role in maintaining chromosomal integrity in the face of physiological stressors. Although the age-related shortening of TL (telomere length) in highly proliferative tissue is predominantly due to the replication process, the mechanism for telomere shortening in skeletal muscle, which is minimally proliferative, is unclear. By studying TL in both the upper and lower limbs of the young, old-mobile and old-immobile subjects and by virtue of the bipedal nature of human locomotion, which declines with age, it may be possible to elucidate the mechanism(s) responsible for cellular aging of skeletal muscle. With this approach, we revealed that TL (~15 kb) in arm skeletal muscle is unaffected by age. In contrast TL fell progressively in the legs across the young (~15 kb), the old mobile (~13 kb) and old immobile (~11 kb) subjects. Interestingly, there was a reciprocal increase in leg muscle free radicals across these groups that was correlated with TL (r=0.7), with no such relationship in the arm (r=0.09). Our results document that chronological age does not affect the cellular aging of skeletal muscle, but reveals that physical inactivity, probably mediated by free radicals, has a profound effect upon this process.

PMID:
24708050
PMCID:
PMC4757470
DOI:
10.1042/CS20140051
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center