Phospholipids: Determinants of skeletal muscle hypertrophy
Cell membranes usually consist of a phospholipid bilayer. Those phospholipid bilayers contain proteins which are essential for cellular communication – in fact, (derivates of) phospholipids also directly act as second messengers.
There are some very important phospholipids:
- Phosphatidic acid
As new research suggest, phosphatidic acid is particular important for cellular communication between mechanical input (e.g. resistance training) and mTOR activation, which is essential for cellular survival and for cellular energy sensing.
Importantly, mTOR activation signals a nutrient abundance. Not so far stretched is the assumption that activation of mTOR is critical for energy consuming processes like skeletal muscle hypertrophy.
Figure 1: Growth factors and mechanoreceptors (?) mediate cellular responses to resistance training
Important is to note that PI3k means Phosphatidylinositol biphosphate 3 kinase. The crucial role of PI3k is to activate protein kinase B, normally known as Akt which interacts with mTOR. mTOR regulates a large amount of genes and modulates gene expression what induces a glycolytic hyper-mascular phenotype when there is an adequate amount of amino acids.
From this point of view, it becomes clear why phosphatidylinsositol is an important enzyme but more specifically why the consumption of inositol or phosphatidylinositol is pretty important, too.
As a matter of fact and as I mentioned above, emerging research suggest that phosphatidic acid is the most important intracellular enzyme involved in communicating with mTOR. As you can see, it mediates the response to resistance exercise via phospholipase D and mTOR.
In this issue of The Journal of Physiology, O’Neil and colleagues provide compelling evidence that activation of mTORC1 by resistance exercise requires the synthesis of phosphatidic acid by phospholipase D and is independent of PI3K–PKB signalling (O’Neil et al. 2009). Previous work by Hornberger and colleagues has shown that intermittent passive stretch in skeletal muscle activates mTORC1 by direct binding of phosphatidic acid to mTOR (Hornbergeret al.2006) and is independent of PI3K–PKB signalling (Hornberger & Chien 2006).
In vitro and in vivo studies (Joy et al., 2014) support this model of cellular responses (e.g. phosphatidic acid) to pressure overload. In fact, supplementation of phosphatidic acid lead to significant increase in lean mass gains when compared to resistance training (plus placebo) alone.
Take home: In order to “fuel” your muscle cells with these phospholipids, you have to make sure to eat adequate amounts.