This 2nd edition of The Concurrent Training Effect blog is going to focus on the molecular underpinnings of skeletal muscular hypertrophy. Understanding the driving force behind the molecular response to strength training can provide us insight into why concurrent strength and endurance training can negatively affect muscular hypertrophy and strength. In addition, a better understanding can lead to ways to mitigate the effect and optimize progress. If you are a CrossFitter, or any other form of hybrid athlete this blog is for you. Keep reading…
A Very Cursory Overview of the Science:
The currently agreed upon molecular key to skeletal muscular hypertrophy is the mammalian target of rapamycin (mTOR). mTOR exists in two complexes with mTORC1 as the type associated with muscular hypertrophy. mTOR is most commonly activated via growth factors, but with strength training its activation is executed in an entirely different fashion. An unknown kinase gets activated causing a chemical cascade resulting in the potent stimulation of mTORC1.
Mechanical kinase activation is the not the only manner in which strength training stimulates mTOR. We have all heard of the post-workout anabolic window for nutrient consumption. The following molecular explanation is THE reason the post-workout window has been so widely touted (and misrepresented equally as often) in the fitness world.
After an intense training session (and for several hours) the skeletal muscles pull a significantly greater amount of the amino acids leucine and glutamine from the blood. The leucine individually is a potent activator mTORC1 and augments the previously mentioned kinase based mTORC1 activation. The increased glutamine yet again enhances this synergistic effect as the resultant transport of glutamine out of the muscle further up-regulates leucine intake.
The Bottom Line
Bottom line, and there is a lot more to it than described here, the end game for strength training induced muscular hypertrophy is it is almost totally dependent on mTORC1. One can thus reasonably deduct that endurance training can somehow blunt mTORC1 activation, and or its ability once activated to execute its normal spike in protein synthesis and the resultant muscular hypertrophy.
The next installment of The Concurrent Training Effect blog will focus on the manner(s) with which endurance training may effect mTORC1.