Whole Body Conditioning, Muscle Strength and Size with Zercher Farmers Walks

If you want to add some size, strength and a bit of conditioning too in little time, I have a “treat” for you.

This will also activate your “core” like crazy, requires little technique and it pretty straight forward.

As shown in the video above,  you will do a farmers walk (walk while holding weight), but you will hold it in the crook of your elbows, also known as a “Zercher.”

You may have heard of the Zercher Squat which was credited to strongman Ed Zercher (1902 – 1995).

This is simply walking with weight in the zercher position.

Sounds easy right?  ha!

Seriously, you have to try this out to really get it.

Summary

The Zercher Farmer Walk is a great way to

• increase muscle
• increase strength
• add in some conditioning
• great progression to use also
• bulletproof your tissue from head to toe
• be sure to test your movement as shown in the Grip and Rip DVD

Comments

Let me know what you think by placing a comment below.

When you are doing them you will probably not like me and curse Ed Zercher, but the gains will be worth it as it will work virtually every muscle in your body at once.

Rock on
Mike T Nelson
PS
If you missed the video, be sure to check out the progressions I provide for you also.

Heretics in the High Country: Muscle Growth (Hypertrophy) Research from Dr. Lonnie Lowery

Dr Lonnie Lowery and Me

One of the great things I love about my job is that I get to talk to really smart people.  One of those uber bright guys is Dr. Lonnie Lowery.  Not only is Lonnie a PhD and an RD, he has spent a lot of time under the bar in the gym too.

Below is a great article on some brand new research on how to get bigger muscles (muscle hypertrophy),  effects of cortisol, fat burning drugs,  and set new personal records in the gym.

Be sure to check out the bio below and Dr. Lowery and friends on Iron Radio.  It is an awesome podcast that you will love.

Take it away Dr. Lowery

Heretics in the High Country: Muscle Growth (Hypertrophy) Research from Dr. Lonnie Lowery

Not all scientific conferences are of interest to strength athletes. Sometimes I find myself wading through oceans of obscure biochemistry or data with unsure applicability. Sometimes the topic matter veers too far into food and nutrition, or some clinical treatment, with no immediately apparent implications for those who are laser-focused on bigger guns or a broad back. But when I go to ski country in Barrie, Ontario in late January each year, I expect cutting edge science and an element of controversy that is sure to intrigue most bodybuilders. This year I saw some early data that seemed absolutely heretical; if the physiology and nutrition labs up there weren’t absolutely world class, I wouldn’t even have sat through some of the lectures. Some of the data and audience discussion flatly flew in the face of what many of us have long-accepted.

As a preview, here are some of the topics:

·         Cortisol: friend or foe to body fat?

·         New insight into satellite cells and muscle size

·         The optimal number of sets beyond which one is wasting time

·         The pros and cons of clenbuterol

·         Why women are tougher than men

·         Stacking stimulant drugs for maximal performance and alertness

·         The importance of insulin compared to leucine in muscle gain

·         The single best training intensity for muscle hypertrophy

If you’re interested, read on for a brief synopsis of some of the outside-of-the-box thinking I saw and what it might mean to scientific training recommendations in coming years. Of course, not every little study warrants an immediate change in your training or eating regime; nonetheless, I‘ll make some speculative or clarifying comments after each section as food for thought. Whether or not a particular study is revolutionary or game changing, having new knowledge is always good in my opinion.

Cortisol: friend or foe to body fat?

Dr Lowery and the Mighty Fortress

Glucocorticoids, as stress hormones, have long been known to increase lipolysis (fat breakdown and mobilization) and yet cause fat deposition on the torso. This study helped explain this seeming contradiction. It revealed how basal concentrations of corticosterone (think “rat cortisol”) enhance certain lipolytic enzymes in adipose tissue (which sounds good for leanness) but high concentrations induce fat cell hyperplasia (multiplication) over time. If the same holds for humans – and it probably does (consider the appearance of Cushing‘s Syndrome patients) – I personally don’t want high levels of stress causing new fat cells to slowly start appearing across my torso. Further, these researchers suggested that a high-fat diet (they weren’t specific about which type of fat) doubled corticosterone in rats. To me, this offers some insight into why stressed-out, fast food-swilling Americans (and Canadians) are sporting giant bellies and uni-pecs.

What this could mean to you: We now have even more understanding of why cortisol in excess (which is elevated by emotional stress, coffee, potentially diets high in total fat, and overtraining) is not the friend of the physique athlete. Keep in mind that the data above are from rats, not humans, but that this is indeed a valid model that offers solid information which is probably relevant to humans. It looks as though cortisol – although necessary at modest concentrations – could lead to more detriment than simply degrading muscle tissue or temporarily storing fat in certain anatomical regions; it could literally multiply one’s number of fat cells making future dieting attempts harder.

New insight into satellite cells and muscle size

Dr Lowery teaching a Staley’s Seminar 2008

Exercise,especially eccentric lifting (“negatives”) not only causes muscle soreness but is also great at activating satellite cells. Among other things, these are cells that lie among the mature muscle fibers and “wake up” to donate their nuclei to help maintain a larger muscle fiber. They can also fuse together themselves into a new entity. This research group was showing a new lab technique that can quickly count how many muscle building satellite cells get activated in response to a new anabolic stimulus. In a matter of hours this automation will offer valid results, eliminating the weeks and weeks of forcing a hapless grad student to physically count stained muscle samples under a microscope.

What this could mean to you: New training techniques can now be tested for this aspect of hypertrophy (increasing muscle cell number or muscle cell “permanent size” in a sense) at a realistic pace. This could mean less speculation and more rapid progress in the science of muscle gains. Cool.

The optimal number of sets beyond which one is wasting time

Dr Lowery looking very professosorial

A graduate student from Stu Phillips’ noteworthy lab shared insider data that three sets appears to maximize the protein synthetic response in a muscle. Earlier work from a partner lab showed that six sets were no better than three and these grad students were taking it a step further: looking at three sets versus one. Using a 70% of one-rep max (moderately heavy weight) protocol, combined with 20g whey protein immediately post-exercise, their data was such that significant elevations in fractional synthetic rate (read “anabolism”) was possible at 5 hours post-exercise from either three sets or one set, but that only the three set protocol still had anabolism kicking at 29 hours post-exercise. Note that although they’re looking at just synthesis here and not breakdown, it is muscle protein synthesis that’s largely responsible for net gains post-workout.

What this could mean to you: If you are the kind of person who performs many many sets for each muscle group in the gym, it might be worth planning certain mesocycles to purposefully cut back on the total number of sets you do, perhaps down to just three per muscle group. This is strictly from a protein synthetic (muscle size) perspective. This is not to say that extra sets might not be good for overall leanness of other benefits. Also note that they used one particular, common intensity level (70% of max) and other intensity levels may alter the picture to some extent. I think this study does make one wonder how much time he or she might be wasting in the gym if strict bodybuilding (size gains) are the immediate goal.

The pros and cons of clenbuterol

Yes, there was actually a study on the usually taboo bodybuilding drug clenbuterol – in rodents. The inhumanly large doses often given in animal studies were again present here: 30mg per liter of drinking water. The study revealed a decrease in mitochondrial (aerobic) function, including less fat oxidation (“burning”). There was also a rise in glycolysis (carb breakdown) capability. It was all suggestive of a switch toward a faster muscle fiber type. What struck me during this session was a comment from the audience (to paraphrase): “So, this stuff is bad. If it is given clinically to patients, we need to warn them of the aerobic declines and risk of fatigue.” After witnessing hard data on increased muscle mass and a significant drop in body fat, the main conclusion from this attendee was “so this stuff is bad”? Maybe I’m biased toward bodybuilding but I for one saw a few pros among the cons.

What this could mean to you: If you are someone who has used clenbuterol or are considering it, this study suggests that you may shift toward a faster, more carb-focused muscle fiber type, possibly meaning less aerobic (endurance) capacity. Of course, this is an arena where self-administering bodybuilders and even Hollywood celebrities probably know more on a practical level than do the cautious scientists: At tolerable microgram (not milligram) doses, body fat can indeed decrease dramatically (for gross calorie expenditure reasons) and strength can climb significantly. (Sheer muscle mass is not altered very much at human-tolerated doses.) In any case, I sure hope researchers start giving clenbuterol a closer look in humans before any stigma creates a bandwagon of negativity that‘ll keep its possibilities in the dark forever.

Why women are tougher than men

Many readers know that women exhibit less post-exercise muscle damage than men. Estrogen is a big part of this. These researchers went further, showing data that exercised women also exhibit less fatigue during recovery days than men do – at least when it comes to “lighter intensity“ (lower frequency) testing. The study had an almost comical title: “The effects of sex on human skeletal muscle fatigability” and used repeated bouts of electrically-stimulated isometric knee extension exercise as the initial stressor. They concluded: “These results suggest that females are more fatigue resistant than males and are able to recover force at an accelerated rate following an acute bout of intermittent isometric exercise.” Wow.

What this could mean to you: If you’re a woman, this talk provided evidence that not only do you resist muscle damage better than guys but in some respects, you outperform them. I’ve often wondered why we don’t see a sport designed around less intense but more punishing, ongoing demands. It looks like women would dominate such an event.

Stacking stimulant drugs for maximal performance and alertness

An ironically calm student was sharing a proposal to stack caffeine (in an extra strength military gum) with a drug called modafinil to max-out alertness and performance among emergency workers and/or military personnel. Earlier work from his mentor suggested 22% increased time to exhaustion with modafinil and other data suggest around 5-30% improvements on cognitive tests of memory, reaction time, etc. after sleep deprivation. We all know caffeine has similarly energizing effects. The researchers weren’t very concerned that a dose of caffeine typically peaks at 60 min. (entry into blood is fast, starting in about 5-15 min.) while modafinil doesn’t peak until 120 minutes; both drugs have lingering improvements for a few hours.

What this could mean to you: Although at the proposal stage, this talk offered information on the pharmacokinetics (onset of action, blood levels over time) of these stimulant drugs and how they might “stack“ (additive effects). I may live under a rock, but I haven’t heard much about modafinil before. It’s cognitive and physical performance benefits are intriguing. Stay tuned for future results.

The importance of insulin compared to leucine in muscle gain

Many of us know that insulin and the amino acid leucine both stimulate the protein synthetic “mTOR pathway” in skeletal muscle. This group wants to see just how crucial the insulin aspect really is. They compared the anabolic effects of leucine in mice with and without pancreases (surgical removal in half of the animals). What happened? The normal pancreas-sporting (and thus insulin-capable) animals responded as expected to leucine, with a full anabolic response. The muscles of the insulin-lacking critters were not uniform in their ability to respond to leucine, however. It looks like different muscle groups (probably due to slow- versus fast-twitch fiber differences) react differently to leucine when insulin isn‘t around. Some can respond (at least on some level) and others cannot. Particular aspects of the mTOR pathway responded well in slow twitch muscle fibers but not in fast twitch fibers. Of course, fast twitch (and moderately fast-twitch) fibers are what strength athletes typically value for size and strength, so this suggests insulin remains an important part of the picture for us.

What this could mean to you: If you’re an endurance athlete or just interested in maintaining slow-twitch muscle fibers, leucine in a fasted state seems like an effective strategy for you. Of course it’s very preliminary (i.e. new research) but it will be interesting to see if endurance guys or those trying to hold on to endurance muscle fibers can get away with leucine-only meals at otherwise unfed times of the day. (I realize some dieting bodybuilders already try this.) If you‘re all about fast twitch muscle fibers, however, it currently looks as though regular meals throughout the day maintain insulin levels that help leucine induce fast-twitch-specific growth. A final caveat: even in a fasted state you have basal (“single digit”) concentrations of insulin and not essentially zero insulin as in the pancreas-free animals; it’s an experimental model trying to tease apart mechanisms. I for one am very interested in how important leucine is versus insulin. Perhaps one day we’ll see a consensus that humans can get away with leucine-only meals during periods of fasting.

The single best training intensity for muscle hypertrophy

This presentation from Nick Burd in Stu Phillips’ impressive lab at McMaster University was almost blasphemous. Here’s the title: “Low intensity-high volume resistance exercise promotes greater anabolic signaling and myofibrillar protein synthesis versus traditional and work-matched resistance exercise paradigms”. Come again? I’m going to get bigger with light weights? It appears so, based solely on protein synthesis data. These guys compared heavy, 90% of one-rep max lifting (subjects failed at five reps) with a work-matched set at just 30% of one-rep max (subjects were stopped at 14 reps) and finally a set to failure with 30% of one-rep max (subjects failed at 23 reps). Although protein synthesis was up at four hours-post exercise in all groups, muscle protein synthesis was still elevated at 24-hours only in the 30% to failure group. Longer periods of lingering heightened protein synthesis sound good to me.

What this could mean to you: You may benefit from (at least considering) periods of the year in which you cycle-in light, 30% of max lifting exclusively to max-out muscle size. This may be doubly true if you’re an intensity hound like me and haven’t done a set over 8 reps in ages. I was so intrigued by the protein synthesis data and with subsequent talks with Nick on www.IronRadio.org, I’m trying a “two week light (30%) / two week heavy (85-90%)” type of periodization. (A recent and timely snowboarding accident sort of forced me away from heavy lifts for a couple weeks anyway.)

I’m still trying to get my head around barbell curls with an empty Olympic bar and benching with 95-135. I’ve got to admit, this one is tough to swallow but a combined effort from universities like McMaster and Nottingham has me suspending my disbelief until their planned training study is completed. It’s then that we’ll know with more certainty whether the very light, roughly 23-rep per set protocol will be as effective or even more effective than the heavy training for mass gains.

Dr. Lonnie Lowery is a former regionally-competitive bodybuilder, exercise physiologist and nutrition professor who travels to scientific conferences often, looking for new data and new ideas that may progress the field of bodybuilding and sports nutrition. He can be reached and listened-to by way of www.IronRadio.org.

Thanks again Dr. Lowery!

Comments?  Do you want to see more research and Dr Lowery again?  If so, drop some comment love and let us know!

rock on

Mike T Nelson

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Busting Broscience: Does Increasing Testosterone and Anabolic Hormones with Exercise Equal More muscle and Strength?

Anabolic Hormones = More Muscle (Hypertrophy), Right?

You hear this in gyms everywhere,

“Dude, to get huge you need to get your test levels up higher”

or this one

“Brotha, you can’t workout any longer than 45 minutes or else you will go completely catabolic  bro!”

What? Is this true?

Have I been wasting all these years in the gym lifting longer than 45 minutes?  Do anabolic hormones from exercise matter for building muscle (hypertrophy)?

Where is the research?

I think the answer will surprise you.

In short, anabolic hormones from exercise don’t do much of anything for muscle growth.

from the study referenced below

“We report here that, despite being exposed to substantial differences in purportedly anabolic hormones such as testosterone, GH, and IGF-1, the rate of MPS (my note, this is Muscle Protein Synthesis, so adding protein to muscles to make them bigger) in identically exercised muscles was not different.

These data demonstrate that local factors are paramount in determining not only the signalling pathway activation but also the response of MPS.

Furthermore, our results indicate that increases in MPS are able to occur without increases in systemic anabolic hormone concentrations and are not enhanced by the acute elevation that can follow resistance exercise; this finding is in agreement with previous work from our lab showing that increases in circulating hormones are not necessary for hypertrophy (Wilkinson et al. 2006).”

Dave Barr from Muscle and Fitness and I geek out completely and discuss hormones and their effects in the video below.   This was filmed from the ACSM 2009 Annual Conference and I had a blast there.  I went there for a relaxing vacation (literally).

More Info!

Listen to the MP3 below for all the details and what you can do to improve your performance.  It is time to put this one to rest and there is even data going back to 1975 also (McManus et al.)

Also see this post

below

Supplements

To Naturually Increase Testosterone

More is not always better.  Better is better

Let me know what you think by posting comments as always.  Comments make me all warm and fuzzy.

Rock on

Mike T Nelson

REFERENCES

Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men

We aimed to determine whether exercise-induced elevations in systemic concentration of testosterone, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) enhanced post-exercise myofibrillar protein synthesis (MPS) and phosphorylation of signalling proteins important in regulating mRNA translation. Eight young men (20 ± 1.1 years, BMI = 26 ± 3.5 kg m^?2) completed two exercise protocols designed to mai

ntain basal hormone concentrations (low hormone, LH) or elicit increases in endogenous hormones (high hormone, HH). In the LH protocol, participants performed a bout of unilateral resistance exercise with the elbow flexors. The HH protocol consisted of the same elbow flexor exercise with the contralateral arm followed immediately by high-volume leg resistance exercise. Participants consumed 25 g of protein after arm exercise to maximize MPS. Muscle biopsies and blood samples were taken as appropriate. There were no changes in serum testosterone, GH or IGF-1 after the LH protocol, whereas there were marked elevations after HH (testosterone, P < 0.001; GH, P < 0.001; IGF-1, P < 0.05). Exercise stimulated a rise in MPS in the biceps brachii (rest = 0.040 ± 0.007, LH = 0.071 ± 0.008, HH = 0.064 ± 0.014% h^?1; P < 0.05) with no effect of elevated hormones (P = 0.72). Phosphorylation of the 70 kDa S6 protein kinase (p70S6K) also increased post-exercise (P < 0.05) with no differences between conditions. We conclude that the transient increases in endogenous purportedly anabolic hormones do not enhance fed-state anabolic signalling or MPS following resistance exercise. Local mechanisms are likely to be of predominant importance for the post-exercise increase in MPS.

Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors

The aim of our study was to determine whether resistance exercise-induced elevations in endogenous hormones enhance muscle strength and hypertrophy with training. Twelve healthy young men (21.8 +/- 1.2 y, BMI = 23.1 +/- 0.6 kg(.)m(-2)) independently trained their elbow flexors for 15 weeks on separate days and under different hormonal milieu. In one training condition, participants performed isolated arm curl exercise designed to maintain basal hormone concentrations (low hormone, LH); in the other training condition, participants performed identical arm exercise to the LH condition followed immediately by a high volume of leg resistance exercise to elicit a large increase in endogenous hormones (High Hormone, HH). There was no elevation in serum growth hormone (GH), insulin-like growth factor (IG

F-1) or testosterone after the LH protocol, but significant (P < 0.001) elevations in these hormones immediately and 15 and 30 min after the HH protocol. The hormone responses elicited by each respective exercise protocol late in the training period were similar to the response elicited early in the training period indicating that a divergent post-exercise hormone response was maintained over the training period. Muscle cross-sectional area increased by 12% in LH and 10% in HH (P < 0.001) with no difference between conditions (condition x training interaction, P = 0.25). Similarly, type I (P < 0.01) and type II (P < 0.001) muscle fiber CSA increased with training with no effect of hormone elevation in the HH condition. Strength increased in both arms but the increase was not different between the LH and HH conditions. We conclude that exposure of loaded muscle to acute exercise-induced elevations in endogenous anabolic hormones enhances neither muscle hypertrophy nor strength with resistance training in young men. Key words: testosterone, growth hormone, IGF-1, anabolism.

Skeletal muscle leucine incorporation and testosterone uptake in exercised guinea pigs.

McManus BM, Lamb DR, Judis JJ, Scala J.  Eur J Appl Physiol Occup Physiol. 1975 Aug 15;34(3):149-56.

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 Hormones Needed for Muscle Hypertrophy? [12:31m]: Play Now | Play in Popup | Download

Maximizing Muscle Hypertrophy with New Research: The Application

Here is part 2 as promised!

If you missed part 1, please check it out below

How To Build Bigger Muscles (Hypertrophy) with New Research : Part 1

Last time we talked about a super cool research study that looked at muscle and connective tissue hypertrophy.   This time there will not be any of those big words and we will check out the lifting world and see if the meatheads had already figured this out years ago (like most things, the answer is yes!).

Ever notice how old school mechanics have massive forearms?

Farmers that work all day just tend to be BIG.

As Mark Ripptoes likes to say “70s Big”

70’s Big Presents: Mark Rippetoe Interview Pt. 1 from 70s Big on Vimeo.

I decide to pull the elusive professional Strongman Adam T Glass out of his cold and dark cave in Minot, ND to get his thoughts on muscle and tendon strength.   Take it away Adam

Mike, first of- great article. My thoughts will come from my direct experience and the progress of my students. So whatever that is worth here it comes

Is frequency with the lift clearly a key element for tendon development?

My first thought is absolutely. For example, the only people i see day to day whose wrist tendons look like mine are men who work with hammers and tools all day- the farmers out here.

Is load important for tendon development?

I believe load is the key. I work with some bone heads who curl literally every day. They are typical weekend warriors.  A “workout” is bench press and curl. That means 185 on the bar and the partner does all the lifting “Its all you bro” for sets of 10. The curls range from mildly good w/35-40lbs to some wild $hitty looking cleans with 50’s and 60’s. So naturally i introduce them to the plate curl.-

How To Do a Plate Curl

95% of the men i show a plate curl to are unable to curl a 25 for 1-2 reps. Only one man has ever curled a 35 in front of me– Freak show Mark Wilson- A man who has spent most of his life lifting dry wall, swinging a hammer and other stuff.  (Editor’s note, if you are in the ND Fargo area, look up Mark Wilson RKC for training HERE)

If frequency is the key element, and SO many men do curls as their primary fitness vehicle, why is the plate curl so challenging for them?

At first i though it was the thumb pinch but every time they complain their wrist tendons hurt when they try it, they are simply not strong enough to handle the force. So in my opinion, based upon what i have seen– load has to play a role in this, but i have not tested enough to have any clear data to say the extent.  –Adam T Glass

Special thanks to Adam for his words of wisdom above!  Be sure to check him out on his blog below and if you are in Minot ND, you MUST get your butt in to see him and train.

Walk the Road Less Traveled

I have noticed that on wrist curls my wrist (and others too) tend to “bend too much” and not stay straight.   This shuts down the muscles of the arm via the arthrokinetic reflex as talked about last time.  “Jammed joints = muscular weakness”

Frequency and Load

Some of you are now rolling your eyes into your head muttering “This is nothing new” and you would be correct.   To others, this is earth shattering since it is rarely talked about in the popular media.    Chad Waterbury and Jason Ferroggia had a disccusion like this one below

Build Muscle Fast

How To Do It?

To Get Big, You Need to Lift Big.  Check this out!

Amazing lift!! Raw and no belt too. Wow!!

Progress

You  need to work to add more weight over time.  Keep track of your PRs (personal records) for your major lifts.  I have PRs for rack pulls, bench, DB bench, reverse bench, kettlebell press, kettlebell snatch, etc  I have about 20+ PRs that I regularly track.  I am always looking to add more load and/or reps over time.  Just the other night I was not feeling like lifting, but I made it to the gym and after some Z-Health joint mobility work I started out on my main lifts of low rack pulls and kettlebell presses.  Everything felt good and tested good (but not great) and over time it started to get better.  I opted for an old PR on the rack pull and added 2 reps to a 1 rep max weight and also did a bottoms up kettlebell press on my left side with the 24 kg kettlebell for a PR!  I felt great after that!  Make it fun and chart progress.  You do have a training journal, right?

Frequency

Chad Waterbury has talked about this before too and if you want to bring up a lift, and easy way is to add some bodyweight drills.   Since my bench is stalling a bit and I don’t have tons of time to add more bench work in right now, I am doing 50 pushups each day for a week, and then the following week I will bump it up to 60, etc.   I also added inverted rows (from a TRX or a straight bar) to keep it balanced out.  My goal is to get to 50 per day, and that may be sets of 10, 8, 15,,and it doesn’t matter.

Advanced Only

Finger Lifting:  Note, this is advanced, which means don’t go out and try this at home right away with a heavy weight.   You may find it is the last time you do any finger lifting.   Like all things, the dose is most important and start very very light and build up the load and frequency over time.   Adam has been done this MUCH longer than you; so you are for warned.

Summary

Frequency + Load = Bigger Muscles and more strength

We have outlined some great options for you to add some size and strength around this Holiday season.

Drop me a line and let me know how it is going and what PRs you are going to break!

Rock on

Mike T Nelson

Kettlebell Snatch for a Big Chest?

What?  Listen below and let me know what you think!  Have I lost my mind completely?  Am I going to recommend kettlebell curls next?

I have used cheaper kettlebells in the past and they work, but I personally like the kettllebells from Dragon Door and you can pick them up HERE.

Throw me some comment love!

Rock on

Mike T Nelson

Nutrition Chat : Cholesterol, Protein, Muscle Growth and More!

Here I talk about the latest research on how to maximize muscle growth through nutrition based on a phone chat I had with Dr. Lonnie Lowery.

You probably know Dr. Lowery from his writings at TMuscle.com (may not be uber work friendly and also Iron Radio.  I encourage you to check out both.

Here we go!

Here I yap about

• Cholesterol -  Is it that Evil?

• mTOR – What the heck is that?  Why do I give a crap?

• Calories Are King!

• How Much Protein?

• Diabetics and Carbs

• Metabolic Flexibility

Let me know what you think and what questions you have!  Post away in the comments!

Rock on
Mike T Nelson

Muscle Hypertrophy (I wannna get hyooooge)

There has been some very cool studies presented recently in the literature regarding muscle hypertrophy (increase muscle size) and I thought I would take some time to see what new insights we can find to maximize your hard working time in the gym.

Hold on, as here we go!

• Most studies are about 1 year old at best by the time you read them. Presentations are the most updated, as shown by the first abstract below. I went to that session at the ACSM Annual meeting since I was there presenting some other data and it was great! Almost 1.5 years later it comes out in print form.
• The opposite condition from muscle growth (hypertrophy) is atrophy (wasting or getting smaller). If we can really understand muscle atrophy, it will help us figure out hypertrophy.

Tales of Brick Layers and Igloos

Look, Canada!

Two processes occur at the same time

1) Protein Synthesis, adding more protein to muscle tissue.  Think brick layers making a house (or snow blocks making an Igloo if you live in Canada)

2) Protein Degradation (proteolysis), taking more protein from the muscle tissue. Think of your neighbor that you don’t like stealing bricks from your house before they set up (or chipping them off in the middle of the night).  If you live in an Igloo, beware of flames.

Ideally, we want protein synthesis (commonly called an anabolic process) to be increased and protein degradation (commonly called a catabolic process) to be decreased.  End result is more muscle!

In some cases of muscle atrophy, the catabolic processes, are about the same but the anabolic process are reduced.  Some loss of bricks, but almost none being put up (lazy workers), thus resulting in an OVERALL loss of muscle.   The hole in the bucket is bigger than the water coming in. No good!

Fernando et al. found, “After 16 wk of RT, gains in muscle mass, type II
myofiber size, and voluntary strength were similar in young and old”

This is great news, since you can get better if you start training at ANY AGE! Enough with the age excuse!  If I hear one more person state that it is all downhill after age 30 I am going to scream and then chuck a kettlebell at their head.

Bezerra P et al did a cool study where they hooked up 1 leg to electrodes to zap it (youch!) and also had them do a muscle contraction.

• They found a cross educational effect (the LEFT leg got stronger) with just the zapping of the right leg.
• No change in muscle hypertrophy of the LEFT leg, but the right leg got bigger (increased size, CSA).

The nervous system is key for strength and size, but local stress (muscle contraction) is needed for a size increase!

Al Shanti et al stated “Many reviews have focused on understanding the signalling pathways of IGF-I and its receptor, which govern skeletal muscle hypertrophy. However, alternative molecular signalling pathways such as the Ca(2+)/calmodulin-dependent transcriptional pathways should also be considered as potential mediators of muscle growth.“

In English please!

Growth factors IN the muscle (not to be confused with ones just in the blood) like IGF-1 are well known to affect muscle size.

The author argues that other pathways like calmodulin-dependent pathway may be just as important.   There are MANY pathways to muscle size increases with the more popular ones also being the mTOR-1 and probably AMPK too.

Great, But What Can I Do?

• Stimulate the muscle! Go lift something as local stress is probably the biggest factor for muscle hypertrophy.
• Eat something. Increasing insulin may help decrease the protein breakdown process
• Have protein after you train. Protein is required for adding muscle size, so have about 20-30 grams after you are done training.  I prefer CFM whey protein from Protein Factory, but have some protein first and then get nit picky about exactly what type.

Any comments, let me know!

Rock on

Mike T Nelson

REFERENCES

Regulation of Muscle Atrophy: Wasting Away from the Outside In: An Introduction.

Urso ML.

US Army Research Institute of Environmental Medicine, Natick, MA.

Whereas it is clear that periods of detraining, disuse, injury and aging are marked by losses in skeletal muscle mass and function, the emerging literature suggests that there are unique molecular signaling alterations depending on the perturbation. Understanding the phenotypical adaptations in skeletal muscle and factors that are thought to promote or inhibit genes involved in the atrophy program will elucidate how the muscular system responds to decreases in activity. Recent advances in the discipline have identified specific and innovative methods to promote skeletal muscle hypertrophy including gene therapy, pharmacological, and nutritional interventions. The same success has not been met concerning attenuating skeletal muscle atrophy. If novel approaches are to be implemented in humans to mitigate disuse- and age-related skeletal muscle loss, it is imperative that we evaluate critical regulators of skeletal muscle atrophy from a system to the cellular level. The symposium “Regulation of Muscle Atrophy: Wasting Away from the Outside In” was presented at the ACSM Annual Meeting in Indianapolis on May 29, 2008, to provide an overview of the skeletal muscle atrophy literature and our current understanding of the atrophy program from the whole system to the molecular level. In addition, this symposium addressed the feasibility of intervening with specific countermeasures to attenuate atrophy. This introduction identifies the scope of the symposium, which evaluates our current understanding of the atrophy program and how this information can facilitate the development of effective countermeasures.

TRANSLATIONAL
SIGNALING RESPONSES PRECEDING RESISTANCE TRAINING-MEDIATED MYOFIBER
HYPERTROPHY IN YOUNG AND OLD HUMANS.Mayhew DL, Kim JS, Cross JM,
Ferrando AA, Bamman MM.

University of Alabama at Birmingham.

While skeletal muscle protein accretion during resistance training
(RT)-mediated myofiber hypertrophy is thought to result from
up-regulated translation initiation signaling, this concept is based on
responses to a single bout of unaccustomed resistance exercise (RE)
with no measure of hypertrophy across RT. Further, aging appears to
affect acute responses to RE but whether age differences in
responsiveness persist during RT leading to impaired RT adaptation is
unclear. We therefore tested whether muscle protein fractional
synthesis rate (FSR) and Akt/mTOR signaling in response to unaccustomed
RE differed in old vs. young, and whether age differences in acute
responsiveness were associated with differences in muscle hypertrophy
after 16 wk of RT. Fifteen old and 21 young completed the 16 wk study.
The phosphorylation states of Akt, S6K1, RPS6, 4EBP1, eIF4E, and eIF4G
were all elevated (23-199%) 24 h after a bout of unaccustomed RE. A
concomitant 62% increase in FSR was found in a subset (6 old, 8 young).
Age x time interaction was found only for RPS6 phosphorylation (+335%
in old only), while there was an interaction trend (P=0.084) for FSR
(+96% in young only). After 16 wk of RT, gains in muscle mass, type II
myofiber size, and voluntary strength were similar in young and old. In
conclusion, at the level of translational signaling we found no
evidence of impaired responsiveness among old and, for the first time,
we show that changes in translational signaling after unaccustomed RE
were associated with substantial muscle protein accretion (hypertrophy)
during continued RT. Key words: translation initiation, hypertrophy,
muscle fiber, aging.

Effects
of unilateral electromyostimulation superimposed on voluntary training
on strength and cross-sectional area.Bezerra P, Zhou S, Crowley Z,
Brooks L, Hooper A.

Department of Exercise Science, Southern Cross University, P.O. Box 157, Lismore, NSW 2480, Australia. j.bezerra.10@scu.edu.au

In this study we investigate the effects of unilateral voluntary
contraction (VC) and electromyostimulation superimposed on VC (EV)
training on maximal voluntary (MVC) force and cross-sectional area
(CSA), as assessed by magnetic resonance imaging of knee extensors.
Thirty young men were randomly assigned to either a control group (CG),
VC group (VG), or EV group (EVG). The VG and EVG trained the right leg
isometrically three sessions per week for 6 weeks. After training, MVC
increased in the right leg in the VG and in both legs in the EVG, and
EVG was significantly different from CG (all P < 0.01). increased
CSA was found only in the right leg in the VG and EVG (P < 0.01),
and correlated with improvements of MVC (r = 0.49, P = 0.01). It
appeared that the EV training was equally effective as VC at increasing
MVC and CSA, while having a greater cross-education effect. Increased
strength without muscle hypertrophy in the unexercised leg of the EVG
indicated that neural adaptation was responsible for the
cross-education effect.

Ca(2+)/calmodulin-dependent
transcriptional pathways: potential mediators of skeletal muscle growth
and development.Al-Shanti N, Stewart CE.

Institute for Biomedical Research into Human Movement and Health,
Manchester Metropolitan University, John Dalton Building, Oxford Road,
Manchester, M1 5GD, UK.

ABSTRACT The loss of muscle mass with age and disuse has a
significant impact on the physiological and social well-being of the
aged; this is an increasingly important problem as the population
becomes skewed towards older age. Exercise has psychological benefits
but it also impacts on muscle protein synthesis and degradation,
increasing muscle tissue volume in both young and older individuals.
Skeletal muscle hypertrophy involves an increase in muscle mass and
cross-sectional area and associated increased myofibrillar protein
content. Attempts to understand the molecular mechanisms that underlie
muscle growth, development and maintenance, have focused on
characterising the molecular pathways that initiate, maintain and
regenerate skeletal muscle. Such understanding may aid in improving
targeted interventional therapies for age-related muscle loss and
muscle wasting associated with diseases. Two major routes through which
skeletal muscle development and growth are regulated are insulin-like
growth factor I (IGF-I) and Ca(2+)/calmodulin-dependent transcriptional
pathways. Many reviews have focused on understanding the signalling
pathways of IGF-I and its receptor, which govern skeletal muscle
hypertrophy. However, alternative molecular signalling pathways such as
the Ca(2+)/calmodulin-dependent transcriptional pathways should also be
considered as potential mediators of muscle growth. These latter
pathways have received relatively little attention and the purpose
herein is to highlight the progress being made in the understanding of
these pathways and associated molecules: calmodulin, calmodulin kinases
(CaMKs), calcineurin and nuclear factor of activated T-cell (NFAT),
which are involved in skeletal muscle regulation. We describe: (1) how
conformational changes in the Ca(2+) sensor calmodulin result in the
exposure of binding pockets for the target proteins (CaMKs and
calcineurin). (2) How Calmodulin consequently activates either the
Ca(2+)/calmodulin-dependent kinases pathways (via CaMKs) or
calmodulin-dependent serine/threonine phosphatases (via calcineurin).
(3) How calmodulin kinases alter transcription in the nucleus through
the phosphorylation, deactivation and translocation of histone
deacetylase 4 (HDAC4) from the nucleus to the cytoplasm. (4) How
calcineurin transmits signals to the nucleus through the
dephosphorylation and translocation of NFAT from the cytoplasm to the
nucleus.

Muscle Hypertrophy (bigger muscles!)

Below is a great brand new review of what makes a muscle bigger! Sweet! Here are some take aways to keep in mind.

In general, muscle types can be broadly defined as Type I or Type II.

Slow Twitch (Type I)
These guys are slow muscles and they are more efficient at using oxygen (aerobic) for continuous, extended muscle contractions over a long time. They are a friend to all the cardio bunnies. As the name states, they contract more slowly than fast twitch fibers too.

Fast Twitch (Type II)
Fast twitch fibers use anaerobic metabolism (think NO oxygen) and work best to created short bursts of strength or speed as compared to the Type Is. The downside is that they get tired (fatigue) more quickly. Think of sprinting—you can go very fast, but you can’t go fast AND long distances.

Type IIs are almost more prone to hypertrophy (increasing in size) and are a friend to weight trainers and power/speed athletes. I would argue they are a friend to all since they keep you more “functional” as you age.

Study Highlights
The study also states, “Eccentric resistance training has been shown to be highly efficient in inducing sarcomeric protein assembly in the longitudinal orientation of muscle cells.”

What? Eccentric (lowering of weight) may help you increase muscle size! It also may make you crazy sore too. I once (er, I mean I heard about a guy) in college that did too much calf work and included heavy eccentrics for too many reps and walked like a friggin penguin for a week. Those crazy college kids!

So don’t just go crazy on the ecentrics as the study states, “concentric contractions lead to a hypertrophic response (increased fiber diameter) in muscle which can still be activated in old age.”

Yep, you can to be strong as you age!

Last key point, “The central signaling pathway to mediate the elevation of protein synthesis in response to training is the mTOR pathway, which is also stimulated by free amino acids.”

mTOR is the pathway stimulated by protein. So protein by itself is very anabolic (building) in nature.

Stimulate the muscle + protein and calories= increased muscle size! Viola.

Converting Type IIs to Type Is?
They also talk about doing some endurance training at a low intensity and for longer than 30 minutes to help convert Type IIs to Type Is. Yikes! Personally, I want to keep as many Type II fibers as possible; so based on this study you would want to keep your “cardio” work to UNDER 30 minutes and do more high intensity work. Yet another reason for Kettlebell CRF (cardiorespiratory fitness) work instead of jogging. Keep off that darn treadmill too. You can even push your car, pick up something heavy and walk around with it, get a sledge hammer and pound away on a tire, etc.

Any questions, comments, post away! Let me know what you think
Rock on
Mike T Nelson

[Exercise and cellular adaptation of muscle.]

Tegtbur U, Busse MW, Kubis HP. Institut für Sportmedizin, Medizinische Hochschule Hannover , Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland, tegtbur.uwe@mh-hannover.de.

Resistance training and to a lesser extent endurance training are capable of enhancing protein synthesis in skeletal muscle via various signaling pathways. Additionally, the expression of muscle fiber types responds to different regimes of training stimuli and immobilization as characterized by changes in myosin heavy chain isoforms (IIIAIIX). Eccentric resistance training has been shown to be highly efficient in inducing sarcomeric protein assembly in the longitudinal orientation of muscle cells. However, concentric contractions lead to a hypertrophic response (increased fiber diameter) in muscle which can still be activated in old age. The central signaling pathway to mediate the elevation of protein synthesis in response to training is the mTOR pathway, which is also stimulated by free amino acids.

Moreover, adaptation to endurance training is mediated by the calcium-calcineurin-NFATc1 pathway which is strongly activated by the calcium transients involved in the muscle contraction process. High contraction frequency and long duration of training sessions are essential for activation and maintenance of fiber type I expression as well as for induction of transformation of type II into type I fibers. Endurance training sessions should therefore be longer than 30 min and dominated by periods of high frequency contractions. A further factor in the muscular response to training includes the recruitment and integration of satellite cells into muscle fibers. Satellite cells can respond to muscular stretch, activity and injury with increased proliferation and can later be integrated into muscle fibers.

CONCLUSION: Therefore, new myonuclei are available to enhance mRNA synthesis and protein expression in muscle cells. New understanding of the cellular mechanisms of signal transduction in muscle in response to training, bed rest and ageing will help to optimize training and interventions in an ageing population.

Coming at ya with another Random Friday since all the cool people are doing! Actually it is a good way to get out some thoughts running around in my head that I am not sure what to do with or don’t have time to expand on.

If you are reading this at the butt crack of dawn, I will be starting or finishing up my 4th to last (fingers crossed) battery of tests in the Energy Drink study!! Getting close to the end of data collection and a HUGE thanks to everyone that has participated so far! I could not do it without you.

Here we go!

1) Minnesota NSCA clinic later today and tomorrow

It is an honor for me to be presenting later tonight and tomorrow with Brad “No Relation” Nelson from Kinetic Edge Performance on the topic “Speed: Walk Before You Run: How Neuroscience Affects Speed by Two Closet Geeks” I can’t speak for Brad, but I burned my closet for kindling years ago–hahaha.

We will be covering some ways to make you faster using that big brain on your head and efficient foot work. The player/athlete that can minimize the number of unnecessary steps he/she takes will be faster.

One simple example is how to start out going straight ahead (or to slight angle).

Some coaches tell their athletes to “fall” forward to get that first step and go from there.

Lee Taft has been saying this for years (and Dr. Cobb covers it in Z Health S Phase too) that if you watch the fastest players, they take a very quick step BACKWARDS to propel them forward and the don’t fall forward—it is too slow. Don’t take my word for it–try it!

They don’t rock back like slingshot, they step back (plyo step) and use that foot/leg to DRIVE them forward fast.

Be careful doing this, as there is a ton of stress applied to the driving (plyo) foot–that does not mean it is bad, just go slow and get the proper form down and ease into full speed drills and do NOT rush it. Most need more mobility work on both of their feet/ankles too.

Is there any research to support this? Glad you asked!

Starting from standing; why step backwards?

Reference Kraan GA e al. J Biomech. 2001 Feb;34(2):211-5.

3 different positions

• an athletic stance with no step back
• athletic stance allowing a step back (plyo step)
• a standing track start with one foot in front of the other
• Found that the Plyo Step had a greater impact on an athlete’s acceleration in terms of force and impulse time
• Also referenced by Lee Taft in “Coaching Away an Athlete’s Speed”

Stepping backward can improve sprint performance over short distances (2008)

“…utilizing a step forward to initiate movement resulted in significantly slower sprint times to both 2.5 and 5 m (6.4% and 5.3%, respectively)

“…adopting a starting technique in which a step backward is employed may result in superior performance.”

Reference: Strength Cond Res. 2008 May;22(3):918-22.

2) NSCA clinic, come talk to me and say hi

Seriously, come on over and at minimum say hi, argue or throw stale muffins at me. I look forward to meeting many of you there and talking shop for 1.5 days—–yeahhhh ha!

Super stoked to see the presentations and one of the Gillinghams and pro strong man from Minnesota Dave Ostlund. Dave is also a brand new dad, so congrats to him!

3) Remodeling your body

Thinking out loud here about the remodeling process of the body due to weight training (more strength, more muscle and perhaps less fat). Here are my thoughts

Stimulus (weight training) + protein (calories with sufficient protein) = more muscle!

Stimulus (weight training, jumping, etc) + calcium and minerals = more bone!

If the raw materials (calcium, protein, etc) are not present in your diet you will have less than optimal remodeling, and it will also be associated with a “higher cost”

Think of it this way, it would be like trying to fix your toilet downstairs by stealing part off the one upstairs. Yep, the downstairs one works great now, but you have another issue.

If you look in the literature, there are some older cool studies on rats where they cut the tendons in the calf area to completely overload the other muscle (soleus). They could stave them, cut their nuts off (youch, I am all for rat studies now!!), and lots of other things and the little buggers still had LOCALIZED muscle hypertrophy, since the stimulus was so large.

The take away
For muscle hypertrophy, the stimulus and protein (probably more calories too) are extremely important. You could argue that the stimulus is the most important thing.

REFERENCES
: Experientia. 1971 Sep 15;27(9):1039-40.Links
‘Compensatory’ muscle hypertrophy in the rat induced by tenotomy of synergistic muscles.”
Macková E, Hník P.

Cell Tissue Res. 1975 Jul 16;160(3):411-21.Links
Satellite cells of the rat soleus muscle in the process of compensatory hypertrophy combined with denervation.
Hanzlíková V, Macková EV, Hník P.

4) New Quote on Beliefs
I was talking to Frankie Faires the other night and the quote we came up with

“All beliefs are limited”

The mind is incredibly powerful and if you truly believe a new weight training program will help you, then it will (and there is nothing wrong with that). The power of belief is huge, but limited. I can try as hard as I want to believe that I can fly all by myself, but in the end gravity will win.

5) A shout out to all my friends kiteboarding in South Padre
Pete Koski shot thi
s cool kite view video. I am so jealous……. if anyone in SPI is reading this, have some sweet rides and airs for me. Jodie and I will be down in Nov this year for sure.
Ride on

SPI #2 from Pete Koski on Vimeo.

Even more data for all you on how to stay “functional” and add muscle.

Off to the U of MN for some early morning testing on subject in my Energy Drink study.

Aging, exercise and muscle protein metabolism.

Koopman R, van Loon LJ. NUTRIM, Maastricht University.

Aging is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk of developing chronic metabolic disease. The age-related loss of skeletal muscle mass is attributed to a disruption in the regulation of skeletal muscle protein turnover, resulting in an imbalance between muscle protein synthesis and degradation. As basal (fasting) muscle protein synthesis rates do not seem to differ substantially between the young and elderly, many research groups have started to focus on the muscle protein synthetic response to the main anabolic stimuli, i.e. food intake and physical activity. Recent studies suggest that the muscle protein synthetic response to food intake is blunted in the elderly.

The latter is now believed to represent a key factor responsible for the age-related decline in skeletal muscle mass. Physical activity and/or exercise stimulate post-exercise muscle protein accretion in both the young and elderly. However, the latter largely depends on the timed administration of amino acids and/or protein prior to, during, and/or after exercise. Prolonged resistance type exercise training represents an effective therapeutic strategy to augment skeletal muscle mass and improve functional performance in the elderly. The latter shows that the ability of the muscle protein synthetic machinery to respond to anabolic stimuli is preserved up to very old age.

CONCLUSION: Research is warranted to elucidate the interaction between nutrition, exercise and the skeletal muscle adaptive response. The latter is needed to define more effective strategies that will maximize the therapeutic benefits of lifestyle intervention in the elderly.

My Notes: A very astute reader of my newsletter (seriously, I would put the average IQ of my newsletter readers up against anyone in an IQ Battle and day of the week), pointed out that in my previous blog (see link below) that the response of protein in older athletes is not the same. He was exactly correct and this is a great review of what may be going on.

Research Review: Do You Only Need 20 Grams of Protein Post Workout?

As you age, you really want to keep as much muscle as possible since it is muscle/strength that allows you to function on a day to day basis and enjoy a higher quality of life.

Differential stimulation of myofibrillar and sarcoplasmic protein synthesis with protein ingestion at rest and after resistance exercise.

Moore DR, Tang JE, Burd NA, Rerecich T, Tarnopolsky MA, Phillips SM. McMaster University.

We aimed to determine whether there is a differential stimulation of the contractile myofibrillar and the cellular sarcoplasmic proteins after ingestion of protein and how this is affected by resistance exercise. Fasted (FAST) muscle protein synthesis was measured in seven healthy young men with a primed constant infusion of L-[ring-(13)C6]phenylalanine. Participants then performed an intense bout of unilateral resistance exercise followed by the consumption of 25 g of whey protein to maximally stimulate protein synthesis. In the rested (FED) leg myofibrillar (MYO) protein synthesis was elevated (P0.05).

In contrast, MYO protein synthesis in the exercised (FED-EX) leg was stimulated above FAST at 1, 3, and 5 h (~100, 216, and 229%, respectively; Phe synthesis of muscle contractile proteins is stimulated by both feeding and resistance exercise early (1 h) but is still elevated at 5h after resistance exercise. In contrast, sarcoplasmic (SARC) protein synthesis was similarly elevated (P

CONCLUSION: In conclusion, myofibrillar and sarcoplasmic protein synthesis are similarly, but transiently, stimulated with protein feeding. In contrast, resistance exercise rapidly stimulates and sustains the synthesis of only the myofibrillar protein fraction after protein ingestion. These data highlight the importance of measuring the synthetic response of specific muscle protein fractions when examining the effects of exercise and nutrition.

My notes: Interesting to note that it was still elevated at 5 hours, but 5 hours was the last measurement they took, so it could be going on even longer. Keep this in mind the next time you hear that the ‘anabolic window is only 2 hours long’

Maximizing muscle protein anabolism: the role of protein quality.

Tang JE, Phillips SM. Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.

PURPOSE OF REVIEW: Muscle protein synthesis (MPS) and muscle protein breakdown are simultaneous ongoing processes. Here, we examine evidence for how protein quality can affect exercise-induced muscle protein anabolism or protein balance (MPS minus muscle protein breakdown). Evidence is highlighted showing differences in the responses of MPS, and muscle protein accretion, with ingestion of milk-based and soy-based proteins in young and elderly persons.

RECENT FINDINGS: Protein consumption, and the accompanying hyperaminoacidemia, stimulates an increase in MPS and a small suppression of muscle protein breakdown.

Beyond the feeding-induced rise in MPS, small incremental addition of new muscle protein mass occurs following intense resistance exercise which over time (i.e. resistance training) leads to muscle hypertrophy. Athletes make use of the paradigm of resistance training and eating to maximize the gains in their skeletal muscle mass. Importantly, however, metabolically active skeletal muscle can offset the morbidities associated with the sarcopenia of aging such as type II diabetes, decline in aerobic fitness and the reduction in metabolic rate that can lead to fat mass accumulation.

CONCLUSION: Recent evidence suggests that consumption of different proteins can affect the amplitude and possibly duration of MPS increases after feeding and this effect interacts and is possibly accentuated with resistance exercise.

My Notes: Wow, they are cranking out the killer studies up in Canada there eh! So the type of protein you take in appears to affect the response. While still debatable, I would go with a high quality whey protein per and post training (ab
out 20-40 grams).