Abstract
Long-term voluntary resistance running has been shown to be a valid model to induce muscle growth in rodents. Moreover, the mammalian target of rapamycin complex 1 (mTORC1) is a key signaling complex regulating exercise/nutrient-induced alterations in muscle protein synthesis. How acute resistance running affects mTORC1 signaling in muscle and if resistance applied to the wheel can modulate mTORC1 activation has not yet been fully elucidated. Here, we show that both acute resistance running and acute free running activated mTORC1 signaling in the m. gastrocnemius, m. soleus, and m. plantaris, but not in m. tibialis anterior of mice when compared to sedentary controls. Furthermore, only the low threshold oxidative part in the m. gastrocnemius showed increased mTORC1 signaling upon running and acute heavy-load resistance running evoked higher downstream mTORC1 signaling in both m. soleus and m. plantaris than free running without resistance, pointing toward mechanical load as an important independent regulator of mTORC1. Collectively, in this study, we show that voluntary resistance running is an easy-to-use, time-efficient and low stress model to study acute alterations in mTORC1 signaling upon high-load muscular contractions in mice.
Highlights
Maintaining skeletal muscle mass throughout life is critical as loss of muscle mass is associated with increased mortality (Szulc et al, 2010), higher disability, loss of function (Janssen et al, 2002), and increased risk of falls (Szulc et al, 2004)
To determine if resistance exercise activates mTOR signaling within skeletal muscle, we measured the phosphorylation of downstream mammalian target of rapamycin complex 1 (mTORC1) target kinases 1 h after cessation of one night of resistance running
This study aimed to validate acute resistance running as a model of resistance exercise-induced mTORC1 activation in mouse skeletal muscle
Summary
Maintaining skeletal muscle mass throughout life is critical as loss of muscle mass is associated with increased mortality (Szulc et al, 2010), higher disability, loss of function (Janssen et al, 2002), and increased risk of falls (Szulc et al, 2004). In an attempt to elucidate these mechanisms, many resistance-based exercise models in mice have been developed (Cholewa et al, 2014), such as synergistic ablation (Goldberg, 1968), electrical stimulation (Baar and Esser, 1999), and chronic stretch (Goldspink, 1999). All valuable, they are invasive, cumbersome, and often do not mimic real life scenarios. As mouse handling and stress is minimal, the running wheel is considered an excellent model of physiological training with similar muscular adaptations as other well-accepted models
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