Abstract
IntroductionThe lipid messenger phosphatidic acid (PA) plays a critical role in the stimulation of mTOR signaling. However, the mechanism by which PA stimulates mTOR is currently unknown. Therefore, the purpose of this study was to compare the effects of various PA precursors and phospholipids on their ability to stimulate mTOR signaling and its ability to augment resistance training-induced changes in body composition and performance.MethodsIn phase one, C2C12 myoblasts cells were stimulated with different phospholipids and phospholipid precursors derived from soy and egg sources. The ratio of phosphorylated p70 (P-p70-389) to total p70 was then used as readout for mTOR signaling. In phase two, resistance trained subjects (n = 28, 21 ± 3 years, 77 ± 4 kg, 176 ± 9 cm) consumed either 750 mg PA daily or placebo and each took part in an 8 week periodized resistance training program.ResultsIn phase one, soy-phosphatidylserine, soy-Lyso-PA, egg-PA, and soy-PA stimulated mTOR signaling, and the effects of soy-PA (+636%) were significantly greater than egg-PA (+221%). In phase two, PA significantly increased lean body mass (+2.4 kg), cross sectional area (+1.0 cm), and leg press strength (+51.9 kg) over placebo.ConclusionPA significantly activates mTOR and significantly improved responses in skeletal muscle hypertrophy, lean body mass, and maximal strength to resistance exercise.
Highlights
The lipid messenger phosphatidic acid (PA) plays a critical role in the stimulation of mechanistic target of rapamycin (mTOR) signaling
Winter and colleagues [15] have demonstrated that the exogenous addition of PA to fibroblasts results in the activation of mTOR signaling via an indirect mechanism that is dependent on PA being metabolized to lysophosphatidic acid (LPA) and activating LPA family receptors
Elevated mTOR signaling was observed at all tested concentrations of S-PS (529, and 558%), egg-derived PA (E-PA) (206, and 221%), S-LPA (638, and 694%), and S-PA (658, and 636%; p < 0.05)
Summary
The lipid messenger phosphatidic acid (PA) plays a critical role in the stimulation of mTOR signaling. You et al [14] have shown that passively stretching skeletal muscles leads to an increase in intracellular PA and mTOR signaling and that the activation of mTOR signaling occurs through an ERK-independent mechanism. These findings suggest that the exogenous provision of PA and mechanical stimuli can activate mTOR signaling through distinct pathways, and it is possible that the activation of these distinct pathways could have additive effects on mTOR signaling
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