To read the first two installments please see the ALN blog page here: https://atlargenutrition.com/blog/
The Concurrent Training Effect Blog #3
As noted in our first installment, the concurrent training effect is a mitigation or cessation of the hypertrophy response to strength training when both strength and endurance training are performed concurrently. Now that we understand mTORC1 (from blog #2) is almost exclusively the driver of strength training induced hypertrophy we know that looking into how endurance training can influence it is the key to insight into how to mitigate the concurrent training effect and thus to creating a superior CrossFitter or hybrid athlete.
In this blog we are going to seek a better understanding of how endurance training can effect mTORC1. The molecular effects of endurance training on hypertrophy are much more equivocal than the molecular effects of strength training. There is no single molecular source for the manner in which endurance training can or does effect hypertrophy. This blog will focus on those sources most generally accepted to have the greatest impact.
We will begin with AMPK (adenosine monophosphate activated protein kinase). Endurance training of sufficient intensity results in metabolic and molecular responses that activate AMPK. AMPK has been shown in animal studies to be able to inhibit mTORC1. In humans its effects on mTORC1 are less certain, but overall the scientific consensus is that it (a specific form of it) likely contributes to the concurrent training effect.
Our next focus is on the sirtuin family of NAD+ dependent deacetylases with SIRT1 being of primary interest. In the previous paragraph it was noted that the intensity of endurance exercise is a controlling factor in AMPK activation. The same is true for SIRT1. The presence of SIRT1 has been clearly demonstrated to inhibit mTORC1, thus the effects on mTORC1 of relatively frequent intense endurance training may due fully, or in part, to SIRT1.
The final possible metabolic cause of the effect of endurance training on mTORC1 to be covered in this blog are unfolded proteins. Intense and frequent endurance training and high fat diets are both triggers for unfolded proteins. The body’s response to increased unfolded proteins includes the blocking of protein synthesis via a decrease in mTORC1 activity.
Hopefully you have already noted the fact that the intensity and frequency of endurance training are catalysts in each of the above possible metabolic pathways in which endurance training can effect mTORC1. This fact will be the focus of our next blog when we take the information from the first three blogs and use it to propose specific training protocols which can mitigate, and even nearly eliminate, the concurrent training effect.