Greetings from Seattle WA. I just have a sec here due to limited internet access and more things to do yet today; but wanted to get this brand new study out to all of you.

Jodie and I just finished an amazing breakfast here by our kind hosts. Fresh espresso, pumpkin pancakes and an omelet with red pepper and roasted garlic. Yummmmmy.

ACSM was killer and tons of info coming soon (soon being early this coming week as I may not have Internet access until then). I cut down on my notes this year and only have 20 pages.

Dave Barr and I saw a killer lecture from Dr. Stu Phillips about testosterone levels and training–short version is that if you are in the normal range, being high or low will NOT accelerate or alter muscle size or strength gains (this excludes the very very low end and the very very high end–those using exogenous testosterone). Exclusive updates to my newsletter group too (thanks for your patience).

Here is the study

Am J Clin Nutr. 2009 May 27, 2009

Ingestion of a protein hydrolysate is accompanied by an accelerated in vivo digestion and absorption rate when compared with its intact protein.

Koopman R, Crombach N, Gijsen AP, Walrand S, Fauquant J, Kies AK, Lemosquet S, Saris WH, Boirie Y, van Loon LJ.

BACKGROUND: It has been suggested that a protein hydrolysate, as opposed to its intact protein, is more easily digested and absorbed from the gut, which results in greater plasma amino acid availability and a greater muscle protein synthetic response.

OBJECTIVE: We aimed to compare dietary protein digestion and absorption kinetics and the subsequent muscle protein synthetic response to the ingestion of a single bolus of protein hydrolysate compared with its intact protein in vivo in humans.

DESIGN: Ten elderly men (mean +/- SEM age: 64 +/- 1 y) were randomly assigned to a crossover experiment that involved 2 treatments in which the subjects consumed a 35-g bolus of specifically produced l-[1-(13)C]phenylal anine-labeled intact casein (CAS) or hydrolyzed casein (CASH). Blood and muscle-tissue samples were collected to assess the appearance rate of dietary protein-derived phenylalanine in the circulation and subsequent muscle protein fractional synthetic rate over a 6-h postprandial period.

RESULTS: The mean (+/-SEM) exogenous phenylalanine appearance rate was 27 +/- 6% higher after ingestion of CASH when compared with CAS (P

CONCLUSIONS: Ingestion of a protein hydrolysate, as opposed to its intact protein, accelerates protein digestion and absorption from the gut, augments postprandial amino acid availability, and tends to increase the incorporation rate of dietary amino acids into skeletal muscle protein.

Just have a few secs here before the next lecture, but check out my twitter updates on the following lower right for some cool stuff.

Gotta run to another lecture, but more coming soon!

thanks for your patience!

Rock on
Mike N

Greetings from sunny Seattle WA. Yes, it is actually sunny out here!

Jodie and I finally made it here ok and we are off to tour the Space Needle, the Experience Music exhibit and Jim Hensen’s Muppets exhibit too

I am off to ACSM tomorrow through Friday, so I will hopefully have updates here but that will all depend on my internet connection. I will have exclusive newsletter only updates for my newsletter friends too.

A few short studies on fat loss in the meantime.

Addition of aerobic exercise to a weight loss program increases BMD, with an associated reduction in inflammation in overweight postmenopausal women.

Silverman NE, Nicklas BJ, Ryan AS. University of Maryland School of Medicine, Geriatric Research, Education and Clinical Center of the Baltimore Veterans Affairs Medical Center, GRECC (BT/18/GR), 10 North Greene Street, Baltimore, MD 21201-1524, USA.

Increased inflammation and weight loss are associated with a reduction in bone mineral density (BMD). Aerobic exercise may minimize the loss of bone and weight loss may contribute to a decrease in cytokines. We tested the hypothesis that aerobic exercise in combination with a weight loss program would decrease circulating concentrations of inflammatory markers, thus mediating changes in BMD. This was a nonrandomized controlled trial. Eighty-six overweight and obese postmenopausal women (50-70 years of age; BMI, 25-40 kg/m(2)) participated in a weight loss (WL; n = 40) or weight loss plus walking (WL + AEX; n = 46) program. Outcome measures included BMD and bone mineral content of the femoral neck and lumbar spine measured by dual energy X-ray absorptiometry, interleukin-6, tumor necrosis factor-alpha, soluble receptors of IL-6, and TNF-alpha (sTNFR1 and sTNFR2; receptors in a subset of the population), VO(2) max, fat mass, and lean mass.

Weight decreased in the WL (p

CONCLUSION: Our findings suggest that the addition of aerobic exercise is recommended to decrease inflammation and increase BMD during weight loss in overweight postmenopausal women.

My notes: Nothing earth shattering here—you need to EXERCISE (heck, even walking) for weight loss and better health (less inflammation).

Effect of calorie restriction on subjective ratings of appetite.

Anton SD, Han H, York E, Martin CK, Ravussin E, Williamson DA. Pennington Biomedical Research Center, Baton Rouge, LA, USA. santon@aging.ufl.edu

BACKGROUND: Energy or calorie restriction (CR) has consistently been shown to produce weight loss and have beneficial health effects in numerous species, including primates and humans. Most individuals, however, are unable to sustain weight losses induced through reductions in energy intake, potentially due to increased hunger levels. The effects that prolonged CR has on subjective aspects of appetite have not been well studied. Thus, the present study tested the effect of 6 months of caloric restriction on appetite in healthy, overweight men and women.

METHODS: Forty-eight overweight men and women with a body mass index (BMI; kg m(-2)) between 25-29.9 took part in a 6-month study and were randomised into one of four groups: healthy diet (control); 25% CR; 12.5% CR plus exercise (12.5% increased energy expenditure; CR + EX); low-calorie diet [LCD; 3724 kJ day(-1) (890 kcal day(-1)) until 15% of initial body weight was lost, then maintenance]. Appetite markers (i.e. hunger, fullness, desire to eat, etc.) were assessed weekly during a fasting state.

RESULTS: Body weight was significantly reduced in all three energy-restricted groups (CR = -10.4 +/- 0.9%; CR + EX = -10.0 +/- 0.8%; and LCD = -13.9 +/-0.7%), indicating that participants were adherent to their energy restriction regimen, whereas the healthy diet control group remained weight stable (control = -1.0 +/- 1.1%). Despite these significant weight losses, appetite ratings of participants in the three energy-restricted groups at month 6 were similar to the weight stable control group.

CONCLUSIONS: CR regimens with low fat diets producing significant weight losses have similar effects on appetite markers over a 6-month time period compared to a weight stable control group.

My notes: I wish they would have measured body fat instead of just using weight and BMI. You want to drop fat NOT muscle; but if you only measure weight you don’t know if you are dropping muscle and fat.

Here is a question I get a fair amount in relation to the location of pain / loss of function and where to look for a solution.

“He who treats the site of pain is lost” —Karel Lewitt, M.D., Dr.

Just because you have a chronic shoulder issue does not mean that you can SOLVE that issue by working ONLY on the shoulder! The first place I would look is the opposite joint; so for a right shoulder I would check the LEFT hip. For a right elbow issue, I would check the LEFT KNEE.

The technical term is interlimb neural coupling (see reference below).

How does this help in the real world? Keep on reading

Hey mike…you got me thinking on joint and cross joint and function. My right elbow has chronic arthritis and joint mice built up. I have full supination/pronation. But my extension is to about 130 degrees and my flexion is only at 90 degrees. It’s quite limited! So I’m always altering movement. I really don’t do much pressing anymore. In Z health should i pay extra attention to my left knee?

Just curious
Thanks a lot man
Jason Ross

The short answer is YES I have a video coming out on this soon, whenever I can steal 5 minutes to upload it.

I can’t guarantee that, but for an elbow, the first place I would look at is the opposite knee and I would check the opposite motion too; so knee flexion (hamstring). Have you ever sprained that ankle on that side? I wold check the talocalcaneal aka subtalar joint since that corresponds to hamstring activity due to gait

Let me know what you find!

Mike N

Mike….I actually have sprained the left ankle pretty severely around 12 years ago. It has never felt as stable.

Thanks for your time man. Jason

Be sure to check out all the killer information on Jason’s blog

Train Out Pain

For a case study on how to use opposite joints and the results, see the link below

Z Health and Marathon Running

REFERENCE

Brain. 2007 Jan;130(Pt 1):159-69. Epub 2006 Oct 3.

Exaggerated interlimb neural coupling following stroke.

Kline TL, Schmit BD, Kamper DG.

Neuromechanics Laboratory, Marquette University, Milwaukee, WI, USA.

The patterns of interlimb coupling were examined in 10 stroke survivors with chronic hand impairment. In particular, the potential roles of postural state and motor tasks in promoting the flexed posture of the upper extremity were assessed. Through the use of electromyography analysis, joint angle measurements and a novel biomechanical apparatus to perturb the digits of the hand into extension, measurements of muscle activity and joint position were compared during multiple postural states, locomotion and voluntary muscle activity. The results demonstrated a significant increase in flexion of the digits (P flexion and voluntary leg extension produced significant activity in the other impaired extremity, leg and arm, respectively, in the stroke as compared with the control subjects. Thus, rectus femoris in the impaired leg was active during finger flexion of the impaired hand in the stroke survivors and all four tested muscles in the impaired arm were active during extension of the legs (P interlimb coupling related to active motor tasks, contributing to an upper extremity flexion bias following stroke.

I just have a sec as Jodie and I are off to the airport in a bit for Seattle WA for 8 days. Well, we were supposed to be on a plane now but there was a change to our flight time and the plane already left at 6:30am instead of 2:30pm today! Thanks for the great notice!
All the details will be in my newsletter that goes out tomorrow if anyone is interested (can still sign up at the bottom on this message).

Some good friends of mine were kind enough to open up their house to us (little do they know what is in store) and time for a much needed vacation. Neither of us have been to Seattle yet either and I will be a the American College of Sports Medicine (ACSM) conference this coming Wed-Fri sniffing out the latest and greatest for all of you here. I am working on some special updates and perhaps even an interview(s). Some of it will be released here and some tidbits will only be sent to my newsletter group, so be sure to sign up for my newsletter at the end of this post (it is free too).

If you are going to be at ACSM, drop me a note and we can chat live in person!

So it looks like a previous blog post I did stirred up a few comments and I got permission to post one below as this weeks “Letter to the Editor”

Read on

Ok, time for me to say something about the language you use as you may be hurting yourself and not even realize it. First, let me say, I love your blog posts, I can tell you spend a great deal of time and effort to not only “just post links to research articles”, but you take the time and effort to break down the research articles and you do an excellent job of summarizing and breaking it down to a lay person’s level, who, may be interested and intelligent enough to really “get” the article, but who may not be willing to dedicate the time to actually read the whole study, in part b/c you break it down so well!

Constructive Criticism Details below: Anytime you write on your blog or in these email updates to your blog about strength training, you refer to it as “strength training” or as training for “power/speed athletes”, but I have Never read you making Any derogatory remarks about strength training.

Except for the one blog post about “Broscience“. At the same time, I have observed, that almost anytime you write, on your blog, or in these email updates to your blog, about endurance training, you Almost Always refer to it as exercise conducted by “cardio bunnies” or as exercise conducted by (in this case) “Cardiobots“, or you may use some other derogatory word, but “Cardio bunnies” seems to be your favorite.

And I get that there are people out there who “only” will do endurance training, and I can see how you may feel that strength training is not stressed enough or paid enough attention to and therefore I can see that you may be trying to make a case for why strength training is important. However, at the same time, I think there are probably just as many people out there who “only” engage in strength training and don’t see any value in endurance training. And I know, you know the value in endurance training, b/c I’ve read a number of your blog posts about how amazing you find endurance athletes like the bike race across America.

Plus, I know you are very smart and as a smart person myself (at least I like to think so), who tries to have a good balance of both endurance and strength training, I find it demeaning and simply not necessary, to almost Always make fun of people who engage in endurance training by calling them demeaning names.

This all leads to my question: Why do feel it is necessary to make derogatory remarks about endurance training or people who engage in endurance training, but you (almost) never make derogatory remarks about strength training or people who engage in it, but you in strength training?

Charles

Thanks again for the comments Charles. Much appreciated as it take cajones to actually give constructive feedback.

Yeah, I may be pissing off some cardio people although that is not my intent. I refer to a cardiobot or a cardio bunny as someone who does mindless hours of cardio normally on a treadmill or elliptical without any plan or any change in intensity–just the same thing every day hoping it will work better tomorrow. You can spot these people in big health clubs very easily (and they don’t even wear rabbit ears).

I have HUGE respect for ANY athlete (athlete is defined as anyone that trains and uses their body for a living, so that includes pretty much everyone). I totally understand why people run marathons and heck, bike across the entire US from my volunteer stint on the RAAM and I give mad props to all of them. I personally will not be signing up any time soon though.

Don’t worry, there are tons of stupid things that weight trainers do in the gym too! I tend to forget about it since the only gym I go to on occasion is at work and that is mostly cardio equipment. I do 95% of my sessions in my garage gym (aka the Xtreme Human Performance Center) and for cardio I primarily do KBs, some biking and now that summer is here more sprints, sledge hammer on the tire, push cars, etc.

I do feel the tide is turning and strength work is getting much more respect in the research community, but the reality is its much easier to study endurance training. I fully admit to falling in that camp too as part of my Monster Energy Drink study is using a bike ride to exhaustion because of previous literature (although not much) and it is easier to measure.

Yes, cardio (cardiorespiratory fitness) is very important! I actually believe that many strength athletes could benefit from more intelligent CRF work in their programs, even if strenght is their main goal. My buddy Aaron S from ND said it best, “it just helps to be ‘ft’” I will save you a lecture about HRV and work capacity.

The reality is that this blog will never be a home for die hard endurance fans, and that is fine with me. I don’t mean any disrespect to them, but I have to narrow the focus a bit to provide relevant
info to the loyal readers

Hope that helps and thanks again for the feedback as most just unsubscribe without any comments or why; which makes it very hard for me to improve them. My goal long term is to make this a trusted home for athletic performance enhancement. I agree with Dr. Cobb when he said “it is actually UNnatrual to NOT be athletic”
Rock on
Mike N
PS
If anyone else has comments on this, post away in the comments section!

PPS
If you want some cool insider scoop from ACSM, sign up to my newsletter below

Ok, just when you think you know something, another piece of evidence comes out that is 180 degrees different. While I think we all should question and test all of our assumptions, this is a bit far!

I know the fat vs fit debate has been going on for awhile, but arguing that being fat is better for survival is insane! Even a very thin person has enough fat for a long time as an energy supply. We know that fat cells are VERY active and they don’t just sit around on their fat butts all day; they are actually sending and receiving hormonal signals.

The argument that there is only ONE type of heart disease is equally insane, as I would be very surprised if this panned out to be true. Physiology is not that simple.

Just for your reading, here is the source and an article from heart wire, so judge for yourself.
Rock on
Mike T Nelson

Source
Lavie CJ, Milani RV, Ventura HO. Obesity and cardiovascular disease. Risk factor, paradox, and impact of weight loss. J Am Coll Cardiol 2009; 53:1925–1932.

From Heartwire
Obesity Paradox Probed in New Review
Shelley Wood

Despite being a key cause of heart disease, obesity appears to be protective in a range of cardiovascular problems, a new review concludes [1]. But that doesn’t mean people shouldn’t try to lose weight, lead author on the paper, Dr Carl J Lavie (Ochsner Medical Center, New Orleans, LA), told heartwire . Indeed, patients who fare the best seem to be obese patients who manage to lose some weight, he said.

“First, obesity is a very strong risk factor and increases all types of heart disease, but second, once you get heart disease, the obese patients do better, so their prognosis is not doomsday,” Lavie explained. “In fact, if you have obese patients with congestive heart failure or coronary heart disease or other heart disorders, those patients actually have a pretty good prognosis if they are treated well. But third, the ones who lose weight do even better.”

According to Lavie, there is solid evidence to suggest that being overweight or obese may improve survival, not just in heart failure, but also in diseases like hypertension, coronary artery disease, and peripheral artery disease.

“There are a large number of cardiologists who don’t even recognize that this is the case, and they are confused about it, too. It is honestly a confusing topic because if obesity is so bad, and it contributes to all cardiovascular risk factors and markedly increases the prevalence of developing heart disease of almost every type, then why, once they get it, do obese patients do better?”

The new review appears in the May 26, 2009 issue of the Journal of the American College of Cardiology (JACC) [1].

Obesity Likely Protects Through Various Mechanisms

The protective effects of excess weight have been best documented in heart-failure patients, where patients with higher body weight or percent body fat have demonstrated better event-free survival. In this setting, says Lavie, extra weight may function much the same way it does with cancer and other chronic diseases, by providing the body with additional fuel to help fight the disease.

Less well known is the relationship between obesity and hypertension, Lavie et al note. While people who are obese do have more hypertension, five papers spanning almost 20 years also point to the fact that obese people with hypertension seem to have lower mortality and/or lower stroke risk, despite less effective blood-pressure control, than do normal-weight people. In this setting, obese patients “may have a better prognosis in part because of having lower systemic vascular resistance and plasma renin activity compared with more lean hypertensive patients,” Lavie et al write.

Also incompletely understood is the paradoxical relationship of obesity and coronary and peripheral artery diseases. Obesity is believed to play a causal role in the development of a number of major risk factors for arterial disease, among them hypertension, dyslipidemia, and diabetes, and is believed to be, in and of itself, a risk factor for atherosclerosis. But according to the JACC authors, there is also literature to suggest that overweight and obese coronary heart disease patients have a lower risk for mortality compared with under- and normal-weight coronary heart disease patients who have undergone revascularization procedures. A similar contradictory relationship has been seen in patients with peripheral artery disease.

Speaking with heartwire , Lavie emphasized that the protective effects of excess weight and excess fat likely function in different ways in different diseases. “We know that fat cells do a lot of bad things, but it’s certainly conceivable that in advanced disease, the fat cell could have some beneficial effects. There’s still a lot that needs to be known about this process.”

Weight Loss Still Key

A key new piece of the puzzle that emerged in Lavie et al’s review, however, is that weight loss, often touted as a way to reduce cardiovascular risk, appears to be a good thing in spite of the protective effects of extra weight.

“For people who follow this field, these kinds of findings have led them to question whether weight loss is good for heart-disease patients. . . . We found that the patients who do the best are the obese patients who lose weight.”

This additional contradiction may be explained in part by the theory that heart disease in obese patients is likely “a different disease” than heart disease in lean people, in whom genetic factors are probably more important. “It may be that the obese person wouldn’t have even gotten blocked arteries if [he] hadn’t gained 70 pounds over a 30-year period,” Lavie said. “The thin person who gets blocked arteries or congestive heart failure or high blood pressure is probably different from the obese patient who got the disease from becoming obese.”

For now, he says, it’s important particularly for the general public to appreciate that the “protective” effects of obesity in no way provide a rationale for weight gain. “Very clearly,” he said, “if no one in our country became overweight or obese, heart-disease rates would go down dramatically.”

For physicians, the data today are sufficiently comprehensive for them to encourage their overweight
and obese patients to stay motivated to reduce their risk factors. That wasn’t always the case, he added. “When people were finding this in their data, five and six years ago, they probably had some trouble getting their papers published, because it didn’t make any sense.”

Here is a great video to give you an inside look at the RKC done in my back yard (ok, not literally but a few miles down the road).

I will be assisting at the RKC I in June, so please come up and say hi to me if you are going to be there. I also have a limited number of Z Health sessions available on Thurs, so email at me at michaelTnelson@yahoo.com Right now I think I only have 2 slots open—first come first serve.

Hope to see you all soon and enjoy the video
Rock on
Mike T Nelson

Effects of Creatine Monohydrate and Polyethylene Glycosylated Creatine Supplementation on Muscular Strength, Endurance, and Power Output.

Herda TJ, Beck TW, Ryan ED, Smith AE, Walter AA, Hartman MJ, Stout JR, Cramer JT. 1Department of Health and Exercise Science, University of Oklahoma, Norman, Oklahoma; and 2Department of Exercise Science and Health Promotion, Florida Atlantic University, Davie, Florida.

Herda, TJ, Beck, TW, Ryan, ED, Smith, AE, Walter, AA, Hartman, MJ, Stout, JR, and Cramer, JT.

Effects of creatine monohydrate and polyethylene glycosylated creatine supplementation on muscular strength, endurance, and power output.

The purpose of this study was to examine the effects of a moderate dose of creatine monohydrate (CM) and two smaller doses of polyethylene glycosylated (PEG) creatine on muscular strength, endurance, and power output. Fifty-eight healthy men (mean +/- SD: age, 21 +/- 2 years; height, 176 +/- 6 cm; body mass [BM], 75 +/- 14 kg) volunteered and were randomly assigned to 1 of 4 groups: (a) placebo (PL; 3.6 g of microcrystalline cellulose; n = 15), (b) CM (5 g of creatine; n = 13), (c) small-dose PEG creatine (1.25 g of creatine: PEG1.25; n = 14), or (d) moderate-dose PEG creatine (2.50 g of creatine: PEG2.50; n = 16).

Testing was conducted before (pre-) and after (post-) a 30-day supplementation period. Measurements included body mass, countermovement vertical jump (CVJ) height, power output during the Wingate test (peak power [PP] and mean power [MP]), 1 repetition maximum bench press (1RMBP), 1RM leg press (1RMLP) strength, and repetitions to failure at 80% of the 1RM for bench press (REPBP) and leg press (REPLP). BM and MP (W) increased (p<!–= 0.05) from pre- to postsupplementation for the CM group only, whereas 1RMBP and 1RMLP increased (p </= 0.05) for the CM, PEG1.25, and PEG2.50 groups. CVJ height (cm and cm.kg), MP (W.kg), PP (W and W.kg), REPBP, and REPLP increased (p </= 0.05) for all groups.

<!–= 0.05) from pre- to postsupplementation for the CM group only, whereas 1RMBP and 1RMLP increased (p </= 0.05) for the CM, PEG1.25, and PEG2.50 groups. CVJ height (cm and cm.kg), MP (W.kg), PP (W and W.kg), REPBP, and REPLP increased (p </= 0.05) for all groups.
CONCLUSION These findings indicated that the recommended safe dose of 5 g.d of CM increased BM and improved muscle strength (1RMBP and 1RMLP). Smaller doses of PEG creatine (1.25 and 2.50 g.d) improved muscle strength (1RMBP and 1RMLP) to the same extent as 5 g.d of CM, but did not alter BM, power output, or endurance. When compared to the PL group, neither CM nor PEG creatine supplementation improved peak power output (CVJ or PP), MP, or muscle endurance (REPBP or REPLP).

Thus, PEG creatine may have ergogenic effects that are comparable to those of CM, but with a smaller dose of creatine.

My Notes: Once again, creatine monohydrate wins again! True, the new form here may need a smaller dose, but who gives a hairy rat’s butt—that won’t get me to switch.

Remember the Public Enemy quote “Don’t believe the hype” on all the new forms of creatine—stay with the old standard of creatine monohydrate. It is cheap, has tons of data behind and it works.

Any comments, let me know as they make me feel warm and fuzzy inside.
Rock on
Mike T Nelson

Greetings everyone!

I apologize for the delays here as Jodie and I were at a marketing conference this past weekend in CT. It was crazy as we did not get much sleep, but learned a ton! We also got to meet TONS of great people and connect with old friends too. I hope to have an update soon, but our flight was delayed last night so I got a whole 5 hours of sleep and 6 the night before and 7 the night before—blah blah blah.

Changes Coming
Tons of changing coming as I am working on a new website, blog, and lots of really cool stuff–all to better serve you and keep providing killer information. Keep that dial (er, mouse?) here for all the latest and greatest.

Tips for KB Pressing Power

Just wanted to let everyone know I have a new article up at Dragon Door entitled “Tips for Kettlebell Pressing Power” so click on the link above to read it. Feel free to leave comments here and I will answer them as soon as I can.

Off to finish some last minute research for a nutrition teleseminar I am doing tonight.

Rock on!
Mike T Nelson

Greetings! Some very cool studies below for yas and I apologize that I don’t have time to add my comments per normal, but if there are any questions post them in the comments and I will get back to you as soon as I can.

Jodie and I are headed out super early tomorrow AM for Ryan Lee’s Ozworth conference on business stuff for 3 days. It should be very interesting and I am looking forward to learning as much as I can so I can better help all of you! If you are there, please come up and say hi! If I miss you, email me at my normal address with the title URGENT and my assistant will call me with your contact information.

If you have sent an email, I will get back to you soon, but it probably won’t be until next week. I know I probably said that last week too, but I will get back to you at some point.

The first study I need to send a huge congrats out to Layne Norton for getting it published! If you have not checked out his website, click on it below.

Biolayne
(for some reason my computer spits at me about the link, but it worked earlier today)

I know first hand how much effort goes into publishing studies! You can listen to Layne himself and a great discussion about protein on Super Human Radio below. Excellent info and interview

Super Human Radio Show – # 273 – BREAKING NEWS – Which Protein Source Builds More Muscle
Monday, March 16, 2009 1:00 PM

From http://www.superhumanradio.com/rss/show_podcast.xml

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

The Leucine Content of a Complete Meal Directs Peak Activation but Not Duration of Skeletal Muscle Protein Synthesis and Mammalian Target of Rapamycin Signaling in Rats1,2
Layne E. Norton3,*, Donald K. Layman3, Piyawan Bunpo5, Tracy G. Anthony5, Diego V. Brana4 and Peter J. Garlick3,4

J. Nutr. (April 29, 2009)

3 Division of Nutritional Sciences, Department of Food Science and Human Nutrition 4 Department of Animal Sciences University of Illinois at Urbana-Champaign, Urbana, IL 61801 5 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Evansville, IN 47712

This study examined the impact of leucine (Leu) derived from complete meals on stimulation of skeletal muscle protein synthesis (MPS). Expt. 1 examined time course changes in translation initiation and MPS after a meal. Male rats (~300 g) were trained for 5 d to eat 3 meals/d providing 20, 50, and 30% of energy from whey protein, carbohydrates, and fats, respectively. Plasma and skeletal muscle were collected at time 0 (baseline) after 12 h of food deprivation and then at 45, 90, 135, 180, and 300 min after a 4-g meal.

Plasma Leu increased at 45 min and remained elevated through 180 min. MPS peaked at 45–90 min and returned to baseline by 180 min.

Plasma Leu correlated with phosphorylation of ribosomal protein p70 S6 kinase (r = 0.723; P CONCLUSION These studies demonstrate that peak activation but not duration of MPS is proportional to the Leu content of a meal.

Stimulation of muscle anabolism by resistance exercise and ingestion of leucine plus protein.

Tipton KD, Elliott TA, Ferrando AA, Aarsland AA, Wolfe RR. Metabolism Unit, Shriners Hospitals for Children, University of Texas Medical Branch, Galveston, TX 77555, USA.

Leucine is known to stimulate muscle protein synthesis and anabolism. However, evidence for the efficacy of additional leucine to enhance the response of muscle anabolism to resistance exercise and protein ingestion is unclear. Thus, we investigated the response of net muscle protein balance to ingestion of additional leucine with protein in association with resistance exercise. Two groups of untrained subjects performed an intense bout of leg resistance exercise following ingestion of 1 of 2 drinks: flavored water (PL); or 16.6 g of whey protein + 3.4 g of leucine (W+L). Arteriovenous amino acid balance across the leg was measured to assess the anabolic response of muscle in each group.

Arterial amino acid concentrations increased in response to ingestion of W+L. Amino acid concentrations peaked between 60 and 120 min after ingestion, and then declined to baseline values. Valine concentration decreased to levels significantly lower than baseline. Net balance of leucine, threonine, and phenylalanine did not change following PL ingestion, but increased and remained elevated above baseline for 90-120 min following W+L ingestion. Leucine (138 +/- 37 and -23 +/- 23 mg), phenylalanine (58 +/- 28 and -38 +/- 14 mg), and threonine (138 +/- 37 and -23 +/- 23 mg) uptake was greater for W+L than for PL over the 5.5 h following drink ingestion.

CONCLUSION: Our results indicate that the whey protein plus leucine in healthy young volunteers results in an anabolic response in muscle that is not greater than the previously reported response to whey protein alone.

My notes: Ok, I could not resist. Looks like if you are using protein high in BCAAs and leucine, that EXTRA leucine may not be beneficiail (although does not appear to be harmful, unless you count money going out of your wallet as harmful)

The balancing act between the cellular processes of protein synthesis and breakdown: exercise as a model to understand the molecular mechanisms regulating muscle mass.

Rasmussen BB, Richter EA. Univ. of Texas Medical Branch, Dept. of Physical Therapy. Div. of Rehabilitation Sciences, 301 Univ. Blvd., Galveston, TX 77555-1144. blrasmus@utmb).

No Abstract Available.

Nutritional and contractile regulation of human skeletal muscle protein synthesis and mTORC1 signaling.

Drummond MJ, Dreyer HC, Fry CS, Glynn EL, Rasmussen BB. Univ. of Texas Medical Branch, Dept. of Physical Therapy, Div. of Rehabilitation Sciences, 301 Univ. Blvd. Galveston, TX 77555-1144. blrasmus@utmb.edu).

In this review we discuss current findings in the human skeletal muscle literature describing the acute influence of nutrients (leucine-enriched essential amino acids in particular) and resistance exercise on muscle protein synthe
sis and mammalian target of rapamycin complex 1 (mTORC1) signaling. We show that essential amino acids and an acute bout of resistance exercise independently stimulate human skeletal muscle protein synthesis.

It also appears that ingestion of essential amino acids following resistance exercise leads to an even larger increase in the rate of muscle protein synthesis compared with the independent effects of nutrients or muscle contraction. Until recently the cellular mechanisms responsible for controlling the rate of muscle protein synthesis in humans were unknown. In this review, we highlight new studies in humans that have clearly shown the mTORC1 signaling pathway is playing an important regulatory role in controlling muscle protein synthesis in response to nutrients and/or muscle contraction.

CONCLUSION: We propose that essential amino acid ingestion shortly following a bout of resistance exercise is beneficial in promoting skeletal muscle growth and may be useful in counteracting muscle wasting in a variety of conditions such as aging, cancer cachexia, physical inactivity, and perhaps during rehabilitation following trauma or surgery.