The Concurrent Training Effect Blog #4

The Concurrent Training Effect Blog #4

The first three blogs of this series provided a basic understanding of the molecular underpinnings of the concurrent training effect (the blunting/elimination of the hypertrophy and strength response when both strength and endurance training are performed concurrently).  This edition is going to take that knowledge and use it to recommend specific training protocols focused on mitigating, and potentially even eliminating it.

The primary training factor which seems to drive the concurrent training effect is the intensity of the endurance exercise being performed.  Closely following intensity is frequency, and when high intensity is combined with high frequency the effect is maximized.

Recommendation 1:

As noted in blog #3 both AMPK and SIRT1 are activated by high intensity endurance exercise.  As both can inhibit mTORC1 one clearly does not want them activated when strength training is performed.  What has not yet been noted is that both will return to baseline levels roughly three hours after activation from intense endurance exercise.  The simple conclusion is that there should be at least three hours between an intense endurance session and a strength training session.  CrossFitters take note, if you are going to do an intense endurance session, and can only train once that day, skip the strength training afterwards (or prior to).  If you can do more than one session, intense endurance in the morning followed by strength training in the evening would be ideal.

This couple needs to wait at least 4 hours before any endurance work...
This couple needs to wait at least 3 hours before any endurance work…

Recommendation 2:

As noted above, frequency of high intensity endurance training is a factor in the concurrent training effect.  The molecular reason for this effect is unknown, but empirical evidence and personal experience indicate that no more than three sessions at greater than 70% of VO2max are best for mitigation of the concurrent training effect.

Recommendation 3:

Blog #2 focused on the molecular machinations relative to the hypertrophy response to strength training.  It was noted that mTORC1 is the driver of hypertrophy.  It was also noted that the mechanical stimulation of strength training was not the only manner in which mTORC1 is potently activated post workout.  A huge skeletal muscular spike in the uptake of the BCAA leucine occurs immediately after strength training.  Leucine itself is a potent stimulator of mTORC1.  The recommendation is thus to make sure plenty of blood-borne leucine is available.  Below are some specific recommendations using ALN products:

1) Take one serving of ALN Finish immediately after strength training.  Within 30 minutes, and preferably as soon as possible, take one serving of Recover as well.
2) If fat loss is the primary goal replace Recover above with Nitrean, or take two servings of Finish and skip either Recover or Nitrean to minimize total caloric intake.

ALN's Finish
ALN’s Finish

Recommendation 4:

Strength training immediately after an endurance session of low to moderate intensity (no more than 69%) is fine.  In fact, strength training immediately following a low intensity endurance session positively influences the endurance adaptation while simultaneously not impairing the hypertrophy and strength adaptations.

We aren’t done yet.  I am going to do more research and we are going to learn even more about the concurrent training effect and how to control it.  

Chris Mason
Owner
AtLarge Nutrition, LLC

The Concurrent Training Effect Blog #3

To read the first two installments please see the ALN blog page here: http://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.

marathon

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.

The Concurrent Training Effect Blog #2

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…

Mike Mentzer - knew a thing or two about muscular hypertrophy.
Mike Mentzer – knew a thing or two about muscular hypertrophy.

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.

Start and Finish provide both leucine and glutamine (as well as other great stuff).
Start and Finish provide both leucine and glutamine (as well as other great stuff).

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.