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Skeletal muscle remodeling during hypertrophy involves the coordinated expression of growth and atrophy genes
Author(s) -
Nader Gustavo A.,
Adams Phoebe,
Pistili Ed,
Guttman Laurie,
Gordon Paul,
Hoffman Eric
Publication year - 2006
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.20.4.a392-a
Subject(s) - muscle hypertrophy , skeletal muscle , atrophy , gene expression , protein degradation , gene , muscle atrophy , biology , messenger rna , medicine , endocrinology , microbiology and biotechnology , genetics
To better understand the mechanisms underlying human skeletal muscle hypertrophy, we carried out a genome‐wide analysis of gene expression in response to an acute bout of resistance exercise (RE). Subjects trained the non‐dominant elbow flexors for 12 weeks resulting in a 21.5 +/‐ 5.5 % increase in muscle cross sectional area and a 64.2 +/‐ 23.2% increase in 1RM strength. Six days after the last exercise session, an acute bout of RE was performed and bilateral biopsies taken 4 hr post‐exercise from both trained and untrained arms. RNA was extracted and prepared for expression profiling using the Affymetrix Human Genome U133 Plus 2 chips. Absolute expression values were calculated using MAS.5 and dChip and data analysis carried out in Gene Spring. Statistical significance was determined for those genes that changed >1.5 fold and were significantly different at p<0.05. Genes significantly different from control were analyzed for gene networks using Ingenuity Pathways. Our results revealed the coordinated induction of a molecular signature comprising genes involved in both cell growth and protein degradation. The initial response to acute RE was characterized by a growth network including IGF‐1, c‐myc, EGR‐1, and eIFs 4E and 4A while the “protein degradation” network included FOXO3a, FBXO32 ( atrogin ), RNF28 ( MURF‐1 ), NEDD4 and NEDL2. In summary, muscle growth and protein degradation processes may be simultaneously active to support skeletal muscle remodeling, thus previously characterized atrophy genes may be important for muscle adaptation as they may have remodeling functions associated with exercise‐induced muscle hypertrophy.