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Cellular aging of skeletal muscle: evidence that physical inactivity is responsible and not age (1102.14)
Author(s) -
Venturelli Massimo,
Morgan Garrett,
Donato Anthony,
Reese Van,
Tarperi Cantor,
Milanese Chiara,
Schena Federico,
Bottura Renato,
Reggiani Carlo,
Naro Fabio,
Cawthon Richard,
Richardson Russell
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1102.14
Subject(s) - telomere , skeletal muscle , sarcopenia , senescence , myocyte , biology , medicine , endocrinology , genetics , dna
Telomeres, not only provide a marker of cellular aging, but also play an essential role in maintaining chromosomal integrity in the face of physiological stressors, such as free radicals, that result in DNA damage. Although, the age‐related shortening of telomere length (TL) in highly proliferative tissue, is thought to be 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 (Y), old mobile (OM), and old immobile (OI) and by virtue of the bipedal nature of human locomotion, which declines with age, it may be possible to elucidate the mechanism responsible for cellular aging of skeletal muscle. With this approach, we revealed that TL (~15 kb) in arm skeletal muscle is unaffected by age and mobility. In contrast TL fell progressively in the legs across the young (~15 kb), the old mobile (~13 kb), and old immobile (~11 kb). Interestingly, there was a reciprocal rise in leg muscle free radical concentration across these groups that was significantly correlated with TL (r=0.7), with no such relationship in the arm (r=0.09). Our results document that chronologic age, per se, does not affect cellular aging of skeletal muscle, but reveals that physical inactivity, likely mediated by free radicals, has a profound effect upon this process. Grant Funding Source : NIH (PO1 HL, 09830), and VA (Merit Grant E6910R)