Maximizing Muscle Hypertrophy with New Research (aka How to Lift and Eat)

Updation

Sorry for the delays here as I have been swamped and the last two days it feels like I got hit by a truck. Ugh.  So after lots of sleep I am back on track now.

Jodie and I had a blast in S. Padre Island kiteboarding and I will have an update soon.  I am working on TONS of great content coming up here.  As always, drop me a line on what YOU want to see.

Maximize Muscle Growth

Very cool new study today on what may be the best combination of lifting and eating for performance.  I am a huge geek and spend hours per week (literally) combing the literature to see if there are any new research gems that will help guide on how to increase muscle size and strength to make you a freaky athlete!    I am happy to report I found an AMAZING study.  Don’t worry, as I will break it down into terms even the most novice can understand and those who have been around for a bit will probably pick up some new things too.  Here we go!

We know that connective tissue (collagen) is a key component in strength since it is literally holding everything together (along with a specialized form called fascia).

Strong Connective Tissue + Bigger Muscle = Crazy Strength

A Tangent on “Jammed Joints = Muscular Weakness“

This is not a new thought, but it is rarely talked about and there has been really a big hole in the literature regarding any direct data to support this idea.  It makes sense that just like if you have a buggered up joint, it will start to decrease strength (”shut down”) the muscles around it.

I can say that first hand this is true when I messed up my ankle in a snowboarding incident about 5 years ago to this very day.   It swelled up to the size of a large softball, I had a walking cast, crutches, the whole 9 yards (hardcore all the way—haha).  I could not even MOVE my ankle, let alone generate any strength.   My body had shut every thing down there and increased fluid to the ankle (massive swelling) to further immobilize the ankle.

Now this is an extreme example, but it happens to a lesser degree with a joint that does not have optimal mobility (called the arthrokinetic reflex and taught in Z Health).

So we know the nervous system has a MASSIVE influence on strength.  It would only make sense that if we thought our connective tissue was not up to the task, our smart brains would limit our strength.

While we don’t have direct data on that point yet, we are getting closer and this study below holds some HUGE keys to muscle growth for you!

Contraction intensity and feeding affect collagen and myofibrillar protein synthesis rates differently in human skeletal muscle

This study looked at any changes to

1) connective tissue (collagen synthesis rates) and

2) muscle protein synthesis rates (FSR) which tells us how much protein is being added to muscles.

More protein added to muscles = bigger muscles (hypertrophy)

The great part is they looked a feeding them also to see if it helped out.  As you know, I highly recommend some protein around the time of your lifting session.

(from wikipedia)

Intramuscular total collagen protein synthesis rate (more connective tissue)

The heavy black is a direct quote from the study and the blue is my translation

“There was a clear effect of prior exercise on  skeletal muscle collagen FSR whether studied in the fasted or fed state (p<0.05)”

Even if you lift in a fasted state (no food before), there is still an increase in connective tissue formation.  Lifting BY ITSELF ALONE is highly anabolic for connective tissue.

“These changes in collagen FSR were unaffected by contractile intensity (p>0.10). Feeding did not increase  resting nor post exercise collagen protein synthesis rate and nor was the post exercise temporal response different compared with fasting”

It did not matter if you lifted a lighter load or heavier load, as there was still an increase in connective tissue.  This effect was NOT changed by eating.

Myofibrillar protein synthesis rate (bigger muscles)

“Fasting myofibrillar protein FSR was influenced by the contraction intensity of a prior exercise bout (interaction: p<0.05,).   Myofibrillar FSR was 303 0.08±0.01 %?hr-1 at rest and LL contractions was not sufficient to enhance the myofibrillar FSR  level significantly above that level (early: 0.11±0.01 and late: 0.09±0.02%hr-1; NS).

In contrast, HL contractions resulted in a delayed improvement (late: 0.14±0.02 %?hr-1, 2.0±0.4 fold, p<0.05).”

Lifting heavier (70% of max) was better than a very light load (16% of max) for bigger muscles.

Oral feeding elevated myofibrillar protein FSR at rest 2.3±0.3 fold up to 0.18±0.03 %?hr-1 (p<0.05,) and this elevated level was maintained at all post exercise time points irrespective of prior contraction intensity.

WOW!  If you eat protein after training, you can maximize your gains by over 2Xs as much as skipping it.  Very cool and simple to do!

When food was provided, LL contractions kept the myofibrillar protein  FSR elevated above fasting conditions at the late time point (p<0.05). Similarly, HL  contractions tended to increase the myofibrillar FSR at the late time point (p<0.10).

You are still building muscle HOURS after you leave the gym!  Simulate and then recover

What Did We Learn Today

Today we learned

Have a protein shake (I like a whey protein isolate from Protein Factory) after training to more than DOUBLE your gains.

Connective tissue increases are primarily only from lifting, even at a light load

Muscle growth needs a higher load and food help a ton!

Stay Tuned

Come back tomorrow for some tips on how you directly use this information to maximize your muscle gains in the gym with some novel methods

The full abstract is below

Any questions/thoughts let me know in the comments!  I want to know if you think this is helpful or not.  What do you want to see?

Rock on

Mike T Nelson

PS

You can also easily retweet any of my articles now!  Just hit the “retweet” symbol on the top right of any post.  Go crazy and thanks in advance for your help in spreading the good word!   Information needs to be shared.

Contraction intensity and feeding affect collagen and myofibrillar protein synthesis rates differently in human skeletal muscle

Exercise stimulates muscle protein fractional synthesis rate (FSR) but the importance of contractile intensity and whether it interplays with feeding is not understood. This was investigated following two distinct resistance exercise (RE) contraction intensities using an intra-subject design in the fasted (n=10) and fed (n=10) states. RE consisted of ten sets of knee-extensions. One leg worked against light-load (LL) at 16% of 1-repetition maximum (1RM), the other leg against heavy-load (HL) at 70% 1RM, with intensities equalized for total lifted load. Males were infused with (13)C-leucine and vastus lateralis biopsies were obtained bi-laterally at rest as well as 1/2, 3, and 51/2 hr after RE. Western blots were run on muscle-lysates and phospho-specific antibodies used to detect phosphorylation status of targets involved in regulation of FSR. The intramuscular collagen FSR was evenly increased following LL- and HL-RE and was not affected by feeding. Myofibrillar FSR was unaffected by LL-RE, whereas HL-RE resulted in a delayed improvement (0.14+/-0.02%xhr(-1), p<0.05). Myofibrillar FSR was increased at rest by feeding (p<0.05) and remained elevated late in the post-exercise period when compared with the fasting condition. The Rp-s6k-4E-BP1- and the MAPk-pathways were activated by the HL intensity and were suggested to be responsible for regulating myofibrillar FSR in response to adequate contractile activity. Feeding predominantly affected Rp-s6k and eEF2 phosphorylations in correspondence with the observed changes in myofibrillar FSR, whereas 4E-BP1 remained to respond only to the heavy load contraction intensity. Thus, the study design allows us to conclude that the MAPk and mTOR dependent signaling responds to contractile activity, whereas elongation mainly was found to respond to feeding. Further, although functionally linked, the contractile and the supportive matrix structures upregulate their protein synthesis rate quite differently in response to feeding and contractile-activity and -intensity.