Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
Poster Board Number: E611
Andrew Smith (Brigham Young University), Kole Brodowski (Brigham Young University), Shalene Wilcox (Brigham Young University), Tyler Darrington (Brigham Young University), David Thomson (Brigham Young University)
Many fields of study have grappled with the challenge of decelerating the effects of aging. Physical exercise plays a vital role in attenuating the impact of the aging process. While many exercise-induced chemical signaling pathways are not fully understood, AMP-activated protein kinase mediates many beneficial adaptations to exercise training. AMPK is activated by the accumulation of AMP (and ADP) during muscle contraction-induced ATP breakdown. The prodrug AICAR mimics AMP accumulation and leads to AMPK activation by increasing the concentration of the AMP analog, ZMP. The primary purpose of the present study is to determine the effect of chronic (31 days) AICAR treatment on muscle anabolic signaling in old (24 mo.) mice. AICAR improved treadmill running performance and attenuated muscle atrophy in the aged mice. Surprisingly, given its known acute effects on muscle anabolism, AICAR treatment increased the skeletal muscle concentrations of insulin-like growth factor-1 and apelin, both of which are known to activate anabolic signaling through the mechanistic target of rapamycin complex 1 (mTORC1). Accordingly, ribosomal protein S6 phosphorylation was also elevated in AICAR-treated muscles. Our results suggest that in addition to its other well-established metabolic effects, chronic AICAR treatment may enhance anabolism in sarcopenic muscle and potentially in other muscle-wasting conditions.
This work was funded by National Institute of Arthritis and Musculoskeletal and Skin Diseases Grant R01 AR-051928 and a BYU Gerontology Program Grant.
