The effects of age and resistance loading on skeletal muscle ribosome biogenesis

Author:

Stec Michael J.12,Mayhew David L.2,Bamman Marcas M.123

Affiliation:

1. Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama;

2. UAB Center for Exercise Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and

3. Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, University of Alabama at Birmingham, Birmingham, Alabama

Abstract

The hypertrophic response to resistance training is generally attenuated with aging; yet the mechanisms regulating this phenomenon are largely unknown. Several studies to date have shown blunted translational efficiency following acute resistance exercise in older adults; however, the effects on translational capacity (i.e., ribosome biogenesis) have not yet been examined. Thus the purpose of this study was to examine changes in markers of ribosome biogenesis following an acute bout of resistance loading (RL; 9 sets × 10 repetitions of knee extensions) in younger (Y; n = 14; 39.2 ± 4.1 yr) and older (O; n = 12; 75.7 ± 5.7 yr) adults. Vastus lateralis biopsies were taken pre- and 24 h post-RL, and muscle samples were analyzed for total RNA content, 45S pre-rRNA expression, ribosomal protein content, and levels of signaling proteins that regulate ribosome biogenesis. Before RL, O had higher total RNA content (+28%; P < 0.05), a trend toward higher 45S pre-rRNA expression (+59%; P = 0.08), and greater protein content of several ribosomal components (≈ +50–80%; P < 0.05) than Y. However, 24 h post-RL, only Y increased 45S pre-rRNA expression (+34%; P < 0.01), possibly driven by higher basal p-Rb (Ser780) (+61%; P = 0.10), and a robust transcription initiation factor (TIF)-1a response (+75%; P < 0.05). RL tended to increase protein components of the 40S ribosomal subunit in Y only (≈ +20–25%; P ≤ 0.12). Overall, the data suggest blunted ribosome biogenesis in response to RL in O, which may be a potential mechanism driving the age-related attenuation of resistance training-induced hypertrophy.

Funder

Office of Extramural Research, National Institutes of Health (OER)

HHS | NIH | National Center for Advancing Translational Sciences (NCATS)

U.S. Department of Veterans Affairs (VA)

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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