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Lifelong wheel running with mild caloric restriction protects against the age‐related disruption of the dystrophin‐glycoprotein complex (DGC) in skeletal muscle
Author(s) -
Hord Jeffrey Mack,
Lee Yang,
Leeuwenburgh Christiaan L,
Lawler John M
Publication year - 2012
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.26.1_supplement.1077.8
Subject(s) - dystrophin , sarcolemma , sarcopenia , skeletal muscle , medicine , endocrinology , caloric theory , chemistry
Sarcopenia is the progressive loss of skeletal muscle mass and strength, associated with aging. Compromised integrity of sarcolemmal proteins including the dystrophin‐glycoprotein complex (DGC) are linked to dystrophic myopathies, and recent data suggest a role in sarcopenia. A critical key to compromised “mechanotransduction” of the DGC appears to be loss of neuronal nitric oxide synthase (nNOS) from the DGC and sarcolemma. Previously, we reported that life‐long wheel running (WR) and mild‐caloric restriction (CR) attenuate sarcopenia. Therefore, we tested the hypothesis that lifelong WR and CR would attenuate age‐related disruption in sarcolemmal localization of key DGC proteins in the plantaris muscle. Fischer 344 rats were assigned to four groups: young ad libitum (YAL), old ad libitum (OAL), old CR (OCR), and life‐long WR plus CR (OWRCR). OAL displayed dislocation of nNOS, α‐syntrophin, and dystrophin from the sarcolemma. nNOS and DGC disruption was attenuated in OWRCR, with lesser effect in OCR. Matrix metalloproteinase‐9 (MMP‐9), which can cleave DGC subunits, was elevated in the extramyocyte space in OAL compared with YAL, an effect diminished in OCR and OWRCR. Results are consistent with the hypothesis that lifelong exercise and mild caloric restriction may be effective countermeasures against age‐related disruption of the DGC. Supported by NIH ( AR054084 ).