High-frequency muscle contractions activate mTOR signaling independently of the IGF-I receptor pathway in skeletal muscle.
No immediate clinical implications for exercise or hypertrophy interventions; leaves open IGF-I-independent mTOR mechanisms in human muscle.
Insulin-like growth factor (IGF-I) is hypothesized to be a critical upstream regulator of mammalian target of rapamycin (mTOR)-regulated protein synthesis with muscle contraction. We utilized a mouse model that expresses a skeletal muscle specific dominant-negative IGF-I receptor to investigate the role of IGF-I signaling of protein synthesis in response to unilateral lengthening contractions (10 sets, 6 repetitions, 100 Hz) at 0 and 3 h following the stimulus. Our results indicate that one session of high frequency muscle contractions can activate mTOR signaling independent of signaling components directly downstream of the receptor.
No takes yet. Share an insight, caveat, or question.
Witkowski et al. (2010) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: