Dumbbell Chest & Shoulder Training Shoot Out: New EMG Data from Experienced and Novice Female Lifters

Does a woman's pectoralis react the same way to dumbbell bench, incline and shoulder presses as the one of their male training partners? Does it make a difference whether you are a novice or an advanced trainee? What about light vs. heavy weights - any effect on the activation patterns of pectoralis, delts, trapezius & co? Learn the answers to these & other questions in today's SuppVersity article (photo bodybuilding.com)

The SuppVersity EMG Series is still one of the the most popular article series, here at the SuppVersity and that despite the fact that I guess most of you will already know the results by heart. Therefore I am happy to present you some additional data from a recently conducted study from the Biodynamics and Human Performance Center at the Armstrong Atlantic State University in Abercorn. The study that was published in the Journal of Sports Medicine a couple of days ago is - according to the authors - the first to investigate, whether the previously observed differences in muscular activation patterns in response to modified trunk inclination angle on muscle activation using barbells and Smith machines in men would occur in women, as well.

Another distinctive feature of the experimental protocol, Joshua Luczak, Andy Bosak, and Bryan L. Riemann devised is the use of both experienced and novice trainees and the separate analysis of the eccentric and concentric potion of the dumbbell bench press, incline bench press and shoulder press.

Who? What? How?

The researchers recruited 24 healthy college-aged (mean age 22.5 years) recreational female athletes as subjects and divided them into two groups, twelve per group, based on their experience with upper body weight training.

"One group was identified as experienced resistance trained exercisers by regularly participating in upper body resistance exercise at least 1–3 times per week for the last six months. The second group was comprised of novice resistance trained females who did not regularly participate in upper body resistance training exercises but instead were physically active in cardiovascular exercise at least 1–3 times per week." (Lukczak. 2013)

Within the 2-way repeated measures design of the study the exercise protocols were administered in a
between-subjects counterbalanced order, to ...

"[...] measure muscle activity in the anterior deltoid, pectoralis major (clavicular and sternal portions), and upper trapezius muscles by way of surface  electromyography data collection during flat bench (0° trunk inclination), incline bench (45°), and shoulder (85°) presses and then compare the muscle activation data between the novice and experienced groups as well as between the different exercises during the concentric and eccentric phases." (Lukczak. 2013)

After being familiarized with the correct execution of the exercises, the participants completed one set of five repetitions of each of the exercises with pretty light (4.5 kg) dumbbells. The order of the exercises was completed according to the counterbalanced protocol that each subject was assigned. Initiation of each set of repetitions was self-initiated and three minutes of rest were given between sets.

Figure 1: Normalized EMG activity for all subjects (no inter-group differences measured) during the dumbbell bench, inlcine and shoulder press (Lukczak. 2013)

Due to the use of the light weights I had to normalize the EMG data on a per muscle base before plotting it in figure 1. What you are seeing here are thus not the absolute values, but the EMG activity expressed relative to the mean activation pattern for a given muscle group on the concentric / eccentric potion of the exercise.... hah? I guess, I better give you an example:

• the absolute EMG value for the upper trapezius activity during the concentric phase of the bench, the incline and the shoulder press were 103.5, 374.0 and 1,164.7, respectively

It goes without saying that plotting these values would have made it very difficult to read the diagram, so I calculated the mean of these three values and plotted the ratio of the actually measured EMG value to this very mean - got it?

But didn't we know most of that already?

What we knew already: According to the study the SuppVersity EMG Series is based on, the best exercises for the pectoralis major using standard equipment are:

1. BB Bench Press
2. Cable Cross*
3. DB Bench Press
4. Pec Deck
5. DB Flys
6. DB Pullovers

* the cable cross exercise should be performed actually crossing one's arms low before your body (learn more)

Basically the way the data is displayed does not really change anything about what it's telling you and that's more or less what both previous studies and bro-science have told you as well:

"The results of this study largely confirm previous research related to performing these exercises with barbells. Specifically, the bench and incline presses produced the greatest activation for the two portions of the pectoralis major muscle, while the shoulder press elicited the greatest activation for the anterior deltoid and upper trapezius muscles." (Lukczak. 2013)

Moroever, the hypothesis that the activation patterns of novice and advanced trainees would differ was not confirmed. When the form is picture perfect and the weight light enough to keep this picture perfect form over the whole set, the activation patterns are identical. In that, it's actually important to point out that the same results have been observed in previous studies using different weights (in % of 1RM) for rookies and pros (Lagally. 2004; Schick. 2010) - so this is not a consequence of using "too little weight", guys ;-)

Ah, and lastly, the observed increased activation of the muscle during the concentric phase of pressing movements are likely related to the light weights, used in the study at hand, which did, as the scientists point out, not require "for as much stabilization of the weight during the descent" compared to what is required during the completion of the same exercise with higher weights.This hypothesis is supported by previous studies by Goodman et al. (2008) and Uribe et al. (2010), in which the subjects had to bench close to their 1RM or with still submaximal  but heavy weights and where no differences in the activation patterns between the eccentric and concentric phase were observed.

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Bottom line: I am sorry to say that, but the study at hand does not really bring anything new to the table. You want more shoulder involvement? Increase the angle! ... ah, and don't forget that the eccentric potion of the exercise has it's merits as well - specifically, when you are using practically relevant loads in the 70% 1-RM range. Now get back to the gym and rock the weights!

References:

• Goodman CA, Pearce AJ, Nicholes CJ, Gatt BM, Fairweather IH. No difference in 1RM strength and muscle activation during the barbell chest press on a stable and unstable surface. J Strength Cond Res. 2008 Jan;22(1):88-94.
• Lagally KM, McCaw ST, Young GT, Medema HC, Thomas DQ. Ratings of perceived exertion and muscle activity during the bench press exercise in recreational and novice lifters. J Strength Cond Res. 2004 May;18(2):359-64.
• Luczak L, Bosak A, Riemann BL. Shoulder Muscle Activation of Novice and Resistance Trained Women during Variations of Dumbbell Press Exercises. Journal of Sports Medicine. 2013; article ID 612650.
• Schick EE, Coburn JW, Brown LE, Judelson DA, Khamoui AV, Tran TT, Uribe BP. A comparison of muscle activation between a Smith machine and free weight bench press. J Strength Cond Res. 2010 Mar;24(3):779-84.
• Uribe BP, Coburn JW, Brown LE, Judelson DA, Khamoui AV, Nguyen D. Muscle activation when performing the chest press and shoulder press on a stable bench vs. a Swiss ball. J Strength Cond Res. 2010 Apr;24(4):1028-33.

Cannabis for Diabetes Prevention? A 1 + 5-Point Information Leaflet to Read Before Smoking Your First Medicinal Reefer

Weedy discoveries: Diabetes protection or just another addiction?

"Good news everyone! Smoking weed is going to solve all your problems." I guess, most of you will already know that, after all the results from a recent study that comes out of the leave no question: Cannabis is the answer to why we get fat... or rather, not smoking it is the reason we are becoming fatter and fatter, year after year. How the scientists know? Well, they have the cunning of the average epidemiologist who knows very well how to get publicity. And as you can see, they really know what they are doing - why else would something that's about as diametrically opposed to physical culture like smoking weed make the headlines on the SuppVersity?

Let the statistical shenanigan begin!

When you are pro Marijuana you got the support of the majority of the US citizens. Not only has smoking weed been legalized (for medical purposes, of course ;-) in 19 states and the District of Columbia following California's lean in 1996, according to a 2010 ABC poll, "81% of Americans favored medical marijuana use and its decriminalization for this purpose." In fact, "[...t]hese citizens argue that marijuana should be  regulated, sold, and taxed in a manner similar to tobacco and alcohol products." Studies saying that "cannabis is good for you" and the subtle message of "we should all smoke some weed from time to time" (Alpert. 2013) do thus fall on fertile grounds - not just in the outskirts of Hollywood.

I guess that was about enough sarcasm for the day, so let's get to the facts, or rather statistics the scientists derived from a re-analysis of the data from theh National Health and Nutrition Survey between 2005 and 2010. Penner et al. studied data from 4657 patients, of whom 579 were current users of cannabis, 1975  used cannabis in the past, but were now - according to what they told the scientists - "clean" and 2013 bores who had never inhaled or ingested marijuana. The researchers measured the patients fasting insulin and glucose levels and tested their subjects insulin resistance and what they found made the headlines:

Figure 1:Adjusted mean/percent differences in measures of glucose metabolism & BMI/WC according to marijuana use among participants from the national health and nutrition examination survey, 2005 to 2010(Penner. 2013)

Fasting insulin levels were reduced in current cannabis users but not in former or never users. Furthermore, the waist circumference of the users was lower, the high density lipoprotein cholesterol (HDL) levels were higher and the insulin sensitivity was slightly improved.

As Joseph S. Alpert, Professor of Medicine University of Arizona College of Medicine in Tucson and the Editor-in-Chief of The American Journal of Medicine, obviously a highly influential man who says about himself that he was "pleased" (his own words) to finally see the little we we know about cannabis from folktales and limited clinical observation, points out in his editorial (still ahead of print), "these are indeed remarkable observations that are supported [...] by basic science experiments that came to similar conclusions" (Alpert. 2013)

But Alpert is already thinking one step further. Well-versed as he obviously must be how the pharma industry functions, he is already foreseeing a great future for THC-based drugs, which

"will be commonly prescribed in the future for patients with diabetes or metabolic syndrome
alongside antidiabetic oral agents or insulin for improved management of this chronic illness" (

Now at first this may sound hilarious, but after reading the rest of the article you may well realize that the synthesize of pure or slightly modified spin-offs of "regular" THC could in fact turn out to be a viable and not that side-effect ridden tool in the battle against the obesity epidemic. 

Even if all that is true, there are still a couple of strings attached...

Now that the good news are delivered let's come to the not so good and actually not so new stuff about smoking weed:

• Marijuana makes you dumb - The evidence for the detrimental effects of chronic cannabis consumption on cognition is overwhelming, particularly in younger weed-headz. Examples?
  

  "Marijuana users demonstrated poorer verbal learning (p<.01), verbal working memory (p<.05), and attention accuracy (p<.01) compared to controls. Improvements in users were seen on word list learning after 2weeks of abstinence and on verbal working memory after 3weeks. While attention processing speed was similar between groups, attention accuracy remained deficient in users throughout the 3-week abstinence period." (Hanson. 2010)

  In adolescents the cognitive impairments appear to be particularly pronounced and last for at least 6 weeks (Schweinsburg. 2008) The longer the chronic exposure to cannabis, the more severe the changes will become (Meier. 2012)

• Cannabis increases the incidence of psychotic episodes - Obviously psychotic episodes are part of the kick, users expect from cannabis consumption. I am yet not sure if the following items with the highest frequencies of occurrence in a 2007 study (frequency in brackets), i.e.
  

  "Items with highest frequencies were unusual thought content (100%), excitement (75%), grandiosity (75%), hallucinatory behavior (70%) and uncooperativeness (65%). The least common symptoms were anxiety (5%), guilt feeling (5%), depressive mood (10%), motor retardation (10%) and blunted affect (30%). Nine subjects (45%) presented with cognitive dysfunction " (Kulhalli. 2007)

  ... is something anyone looking to improve his / her glucose metabolism would be happy about - what about you? And what about the voices you are hearing already (cf. Ruiz-Veguilla. 2013)

• 

  If you are deciding to smoke weed, you better make sure avoid at least all the other anti-androgens on the SuppVersity exclusive "Natural Hormone Optimization Cheat Sheet" Otherwise you may well be in trouble soon. What are you waiting for - go learn them by heart your fertility and sexual satisfaction will depend on it!

  Smoking weed will mess with your endocrine health - THC dose-dependently reduces testosterone levels (-57% in heavy users; Kolodney. 1974)
  

  "Data from human and nonhuman species converge on the ephemeral nature of THC-induced testosterone decline."  (Gorzolka. 2010)

  From rodent studies we also know that the consumption of low levels of marijuana lead to shrinkage of tubular diameter and detrimental changes in seminiferous epithelium of testis with resulting lowered serum testosterone and pituitary gonadotropins (follicular stimulating [FSH] and luteinizing hormones [LH]) levels (Mandal. 2010). It also reduces sperm count and induces infertility (Banerjee. 2011)

• Cannabis causes endothelial dysfunction and a lame dick- And as if that was not already enough it can also lead to anorgasmia, which is - as you have probably already guessed - the inability to achieve an orgasm irrespective of your erectile function, by the way  (Saso. 2002; Aversa. 2008; Shamloul. 2011)

• 

  Learn more about other factors involved in the development of gynecomastia and how to battle it.

  Marijuana will give you breast cancer, gyno and germ cell / testicular tumors  -The growth promoting effects of cannabis are mediated by THC directly at a cellular level via COX-2 (Dardick. 1993; Takeda. 2009).
  
  In men cannabis use is associated with the development of gynecomastia (Harmon. 1972). The mechanisms are not fully elucidated, but they possibly involve elevated prolactin levels (Olusi. 1980) and in the end you are probably better off with gyno than with a malignant germ cell tumor, which is something frequent marijuana users are 2x more prone to develop than their non-smoking peers (Trabert. 2010; Lacson. 2012) .

I guess, I could find a couple of dozen additional references and continue this list of potential unwanted side effects, but I am not going to waste any further time I could invest on relevant SuppVersity news...

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The 70s, that was a time! A time, when the average American still had a 20% lower BMI, being normal weight was still the norm and models like those in the photo above did not have to be anorexic all because of the weed?

Bottom line: While you may escape becoming a dumb, impotent home to various forms of cancer as a consequence of developing diabetes, you better be careful with your cannabis use or you just take another route towards the same detrimental outcomes - a route from which you cannot escape by healthy dieting and working out. If that's a risk you are willing to take - go ahead, but don't forget that the "cannabis vs. diabetes" study does not provide any evidence for a causal relationship between the reduced incidence of insulin resistance and obesity and smoking weed. It's the same statistical shenanigan that will tell you that eggs cause heart disease (learn that they don't) and that eating fat will make you fat.

In the end, cannabis is a drug - a drug with effects and side effects... or, as we should finally admit for "regular" drugs as well dietary supplements with effects we classify as desirable (classic effects) and undesirable (side effects). Against that background you may consider today's SuppVersity article as the patient information leaflet that goes with the "diabetes drug cannabis". Now you decide if you feel that the potential advantages outweigh the way better researched potential side effects.

References:

• Aversa A, Rossi F, Francomano D, Bruzziches R, Bertone C, Santiemma V, Spera G. Early endothelial dysfunction as a marker of vasculogenic erectile dysfunction in young habitual cannabis users. Int J Impot Res. 2008 Nov-Dec;20(6):566-73. 
• Banerjee A, Singh A, Srivastava P, Turner H, Krishna A. Effects of chronic bhang (cannabis) administration on the reproductive system of male mice. Birth Defects Res B Dev Reprod Toxicol. 2011 Jun;92(3):195-205. 
• Dardick KR. Holiday gynecomastia related to marijuana? Ann Intern Med. 1993 Aug 1;119(3):253.
• Gorzalka BB, Hill MN, Chang SC. Male-female differences in the effects of cannabinoids on sexual behavior and gonadal hormone function. Horm Behav. 2010 Jun;58(1):91-9.
• Hanson KL, Winward JL, Schweinsburg AD, Medina KL, Brown SA, Tapert SF. Longitudinal study of cognition among adolescent marijuana users over three weeks of abstinence. Addict Behav. 2010 Nov;35(11):970-6. 
• Harmon J, Aliapoulios MA. Gynecomastia in marihuana users. N Engl J Med. 1972 Nov 2;287(18):936. 
• Kolodny RC, Masters WH, Kolodner RM, Toro G. Depression of plasma testosterone levels after chronic intensive marihuana use. N Engl J Med. 1974 Apr 18;290(16):872-4.  
• Kulhalli V, Isaac M, Murthy P. Cannabis-related psychosis: Presentation and effect of abstinence. Indian J Psychiatry. 2007 Oct;49(4):256-61. 
• Lacson JC, Carroll JD, Tuazon E, Castelao EJ, Bernstein L, Cortessis VK. Population-based case-control study of recreational drug use and testis cancer risk confirms an association between marijuana use and nonseminoma risk. Cancer. 2012 Nov 1;118(21):5374-83.
• Mandal TK, Das NS. Testicular toxicity in cannabis extract treated mice: association with oxidative stress and role of antioxidant enzyme systems. Toxicol Ind Health. 2010 Feb;26(1):11-23.
• Meier MH, Caspi A, Ambler A, Harrington H, Houts R, Keefe RS, McDonald K, Ward A, Poulton R, Moffitt TE. Persistent cannabis users show neuropsychological decline from childhood to midlife. Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):E2657-64.
• Olusi SO. Hyperprolactinaemia in patients with suspected cannabis-induced gynaecomastia. Lancet. 1980 Feb 2;1(8162):255.
• Penner EA, Buettner H, Middleman MA. The impact of marijuana use on glucose, insulin, and insulin resistance among US adults.Am J Med. 2013;126:XX-XX
• Ruiz-Veguilla M, Barrigón ML, Hernández L, Rubio JL, Gurpegui M, Sarramea F, Cervilla J, Gutiérrez B, James A, Ferrin M. Dose-response effect between cannabis use and psychosis liability in a non-clinical population: Evidence from a snowball sample. J Psychiatr Res. 2013 May 16. 
• Saso L. Effects of drug abuse on sexual response. Ann Ist Super Sanita. 2002;38(3):289–96 .
• Schweinsburg AD, Brown SA, Tapert SF. The influence of marijuana use on neurocognitive functioning in adolescents. Curr Drug Abuse Rev. 2008 Jan;1(1):99-111.
• Shamloul R, Bella AJ. Impact of cannabis use on male sexual health. J Sex Med. 2011;8(4):971–5.
• Takeda S, Yamamoto I, Watanabe K. Modulation of Delta9-tetrahydrocannabinol-induced MCF-7 breast cancer cell growth by cyclooxygenase and aromatase. Toxicology. 2009 May 2;259(1-2):25-32.
• Trabert B, Sigurdson AJ, Sweeney AM, Strom SS, McGlynn KA. Marijuana use and testicular germ cell tumors. Cancer. 2011 Feb 15;117(4):848-53. doi: 10.1002/cncr.25499. Epub 2010 Oct 5.

Peri-Workout Hydro-Whey Supplementation: Tried & Proven Muscle Builder Will Also Increase Tendon Size & Strength

Squats are by no means the only exercise that requires strong muscles and tendons.

In a way you could argue that today's SuppVersity article serves two purposes. Firstly, it provides direct evidence for my outrageous claim that the VPX Shotgun + Synthesize study from Saturday's installment of On Short Notice has little to no practical value, because the use of 2x17g of maltodextrin as a control has little to do with the real-world supplementation regimen the potential consumers of respective products are ingesting. I mean, you can safely assume that people who are willing to spend the money on expensive peri-workout kitchen sink supplements will - just like most of you - be ingesting a whey (or other fast acting) protein source after their workouts, anyways.

It goes without saying that it would not have needed a new study to prove this point, so that informing you about another observation Farup et al. made in their most recent study is not just the second, but actually the main purpose of today's SuppVersity article.

A new whey to build tendons of steel

The training protocol: The subjects completed 33 training sessions during the 12 weeks of training. The training program was primarily designed to induce hypertrophy and to a lesser extent maximal muscle strength highlighted by a large number of sets and repetitions and by moderate high intensity. Training frequency was three times per week with a progressive increase in volume and intensity throughout the 12 weeks.

The resistance training exercise consisted of isolated knee extensions in a Technogym knee extensor machine. All repetitions were performed by lifting the load with the concentric leg (while extending the

eccentric leg unloaded). Then, with aid from a training supervisor, an additional load was released onto the weight stack and then lowered with the eccentric leg.

Both the eccentric and concentric leg training program consisted of isotonic knee extensions (TUT 2-0-2s; rest between sets 2min) and applied the following progression in volume and intensity: 6 x 10-15RM (sessions 1–4), 8 x 10-15RM (S 5–10), 10 x 10-15RM (S 11–20), 12¥6–10 RM (S 21–28), and 8 x 6-10RM (S 29–33).

The actual paper is going to be published in one of the future issues of The Scandinavian Journal of Medicine & Science in Sports and deals with the outcomes of a 12-week double-blinded resistance training intervention in the course of which the 22 male subjects (healthy, young, recreationally active height 181.5+/- 1.5 cm, weight 78.1 1.8 kg, age 23.9 +/-0.8 years, fat% 16.0+/- 0.9%) consumed either

• a high leucine whey protein hydrolysate + carbohydrate group (WHD; 19.5 g whey protein hydrolysate +19.5 g) or 
• an isoenergetic carbohydrate only supplement for the placebo group (PLA, 36g of carbohydrates)

Regardless of supplementary intake, all subjects performed eccentric training with one leg and concentric training with the other.

"This within-subject design was used to minimize the potential differences in the hypertrophy response that are inherent with group designs (e.g. initial training status, habitual nutritional intake,and/or hormonal status). Eccentric leg was randomly chosen to be either the dominant (preferred kicking leg) or the nondominant leg to exclude any potential pre-training difference between the two." (Farup. 2013)

Overall, we are thus comparing not two, but rather four different training modalities, namely eccentric+WHD, eccentric+PLA, concentric+WHD and concentric+PLA.

Maximal standardization, reliable measuring methods

In the two weeks before commencing the training program, magnetic resonance image (MRI) scans of both thighs and patellar tendons and isometric strength test were taken. In conjunction with the before and after tests that were standardized up to the time of the day, pre- and post-training, "to control for potential effects of diurnal rhythm" (Farup. 2013)

The training sessions were closely supervised and monitored by qualified training instructors to ensure proper execution and loading. The same goes for the ingestion of the supplements, 19.5 g whey protein hydrolysate +19.5 g of carbohydrate (both equal to 4% solution) and the placebo drink consisting of 39 g of carbohydrate, which were handed to the trainees at the beginning of the training sessions and were to be consumed before and after the training (50/50).

Even the intake of additional plain water was standardized, so that the subjects would not ingest and fluids 1 1/2 h prior to and 1 h after completion of an exercise session, "to ensure and standardize the conditions for digestion/absorption and within the range typically applied" (Farup. 2013)

The only methodologically lapse was the absence of dietary control. While the subjects of previous studies in which the participants were advised to "maintain their normal habitual dietary intake throughout the study" (Farup. 2013), did not register any differences in habitual total energy or protein intake (Andersen. 2005; Hartman. 2007; Hulmi. 2009; Erskine. 2012) and the accuracy of food logs is generally questionable, this is kind of awkward in view of the lengths to which the scientists went to exclude any other confounding factors.

Enough of the prelude, what about the results?

So, while we cannot exclude that the subjects in any of the two groups may have skewed the overall results by consuming an additional steak on top of their regular diets, it is quite unlikely that these counfounding factors would have been group specific, so that the overall effects on quadriceps cross-sectional area I plotted in figure 1 are unquestionably reliable.

Figure 1: Relative changes in quadriceps and patella tendon CSA in concentrically and eccentrically trained leg of the subjects in the whey protein hydrolysate and placebo groups (Farup. 2013)

The same obviously goes for the strength increases and the initially mentioned increase in patella tendon CSA. All good and reliable evidence supporting the current "standard" in periworkout supplementation.

Apropos, in conjunction with the recent revelations about the unique glucose-sensitizing effects of the short-chain peptides in whey hydrolysate, it may even be worth to consider adding a "hyrolysate" to the current recommendation to ingest 30g of whey protein in the vicinity of your workouts. Convincing evidence from studies that were specifically designed to elicit the marginal benefits of replacing a regular whey protein with the less tasty (you won't notice that with the tons of flavoring agents, though) and still more expensive "pre-digested" form of whey is yet - at least as far as I know - still missing.

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Bottom line: Actually, I already mentioned the most important findings of the study at hand in the introduction:

Figure 2: Whether the effects observed in the study are "hydrolysate specific" and related to the amino acid or peptide composition of the supplement that was used in the study at hand cannot be said without a "regular" whey control. The same goes for the general superiority or inferiority of hydrolysates vs. whey isolates or concentrates.

(a) Whey proteins alone will amplify the effects of regular strength training to a degree that is hard to surpass by the more expensive "advanced muscle builders" - no wonder the producers are reluctant to use anything but an isocaloric carbohydrate supplement as their yardstick. (b) Increases in tendon CSA are a novel benefit to be added to the comprehensive list of benefits of a supplement I suspect most of you are using anyway.

Whether the hydrolyzed whey proteins are actually worth the extra bucks is yet still not 100% certain. As previously mentioned, the number of practically relevant direct comparisons is still scarce. We know that they create a more rapid increase of the amino acid levels in the blood, that they are more insulinogenic and we that some of the short peptides have favorable physiological effects (learn more). A long-term study comparing the muscle and (that's new) tendon building effects of the three commonly available varieties of whey, i.e. concentrate, isolate and hydrolysate, has not yet been conducted. But don't worry, as soon as the pertinent data is going to be available, you'll find all the information you need, as well as the practical implications of the results right here, at the SuppVersity - your #1 source for the latest on exercise, nutrition and supplementation research on the Internet.

References:

• Farup J, Rahbek SK, Vendelbo MH, Matzon A, Hindhede J, Bejder A, Ringgard S, Vissing K. Whey protein hydrolysate augments tendon and muscle hypertrophy independent of resistance exercise contraction mode. Scand J Med Sci Sports. 2013 May 7.

A Bomb Calorimeter You Are Not! And That's Why Even the "Adjusted" Energy Values on Food Labels Are 5% Off

How productive are you?

A couple of you will probably remember the SuppVersity news from ~1 year ago in which I discussed the revelation that nuts (pistachios and almonds) effectively deliver much less energy (-25%) than the "label" or databases on the Internet will tell you. In other words, while these healthy snacks are still extremely calorie dense, our bodies are not exactly as well equipped as a bomb calorimeter to use that energy.... "bomb calorimeter"? That reminds me of a study I read about a week ago and remembered, today, when I was thinking about writing an article on a topic that is not the 10214124x study on how aerobic exercise is good for elderly obese diabetics, or how extract XYZ from whatever TCM medicine ameliorates the weight gain in obese rodents.

The study, I was thinking of was conducted at the Department of Nutrition and Dietetics, VU University Medical Centre in Amsterdam (Wierdsma. 2013) and with it investigating the practically highly relevant ability of our tummy to extract and digest (=make bioavailable) the energy from the foods, we eat, it is truely one of a kind. After all, corresponding ...

"[...] reference values for energy and macronutrient absorption are scarce, especially for adults in an outpatient ambulatory setting, which forms the usual circumstances for dietetic and nutritional interventions or therapy." (Wierdsma. 2013)

That may seem hilarious in view of the bazillions of money we are spending year by year to figure out "why we are fat", but believe it or not, due to the lack of data we (=science) simply estimate the ‘standard’ energy absorption to be at a level of 95%.

"We use 95% of the energy we eat" - says who?

What's the significance of the data? It goes without saying that measuring the energy that is not absorbed is only one of the things that will eventually be necessary to elucidate "how much calories the average dietary carbohydrate-, fat- and protein calorie effectively delivers. This information would yet still have been something we'd have to have before the dozens of studies on the thermic and other metabolically relevant effects of foods had been conducted. Why? Well, at least in those cases (a non-negligible part of the currently available research), where this effect was estimated by simply monitoring the weight gain of the subject over longer time periods, the result critically depends on the amount of energy from carbs, fats and protein that did even make it into the participants organism. If the latter is not 95%, but only 90% and differs from macronutrient to macronutrient, all previous results would be skewed.

This assumption is based on a single study from the 1970s, in which the amount of non-absorbed healthy adults is reported to be approximately 5% when digesting a standard diet (Southgate. 1970). A study like the one at hand, which was designed to

"[...] assess faecal energy, subdivided in its major contributors of fat, protein and carbohydrate losses, to quantify standard intestinal absorption capacity in healthy adults on a Western European diet in an ambulatory setting in The Netherlands by using a feasible and unique methodology of intestinal absorptiometry reflecting routine practice." (Wierdsma. 2013)

Put differently, the scientists wanted to find out (a) whether a calorie is a calorie or maybe just half a calorie and (b) whether this relation is different for the three main macronutrients, carbohydrates, fat and protein. What? Yeah, you'd think we'd know that all along, but aside from certain experts who know exactly "why we are fat", we obviously don't.

So what did the scientists do?

The Dutch researchers recruited 25 healthy subjects who had been deliberately picked from the staff of institutional healthcare workers at the facilities the authors are working at all had specific dietetic and healthcare knowledge and were thus skilled in adequately registering nutrient intake and meticulously collecting stools. Yep, you read me right: Over the course of 4 subsequent days, the study participants did not just have to track everything they ate and drink, they also had to collect specimen from what left their bodies "undigested" (=stool samples ;-).

"All faeces were collected during 72 h (day 2–4), as per the protocol, in specifically designed 5-L buckets. Faeces were weighed (faecal wet weight in g/day ), homogenised and immediately stored at <4°C until analysis. To measure faecal macronutrient content and to calculate intestinal absorption capacity of the healthy subjects, the faeces were analysed for energy, fat and nitrogen content." (Wierdsma. 2013)

Based on the nutrition data and the stool samples, which had been recorded and collected by all, but two male lazi-a**es who failed to comply to the rigorous requirements of the study protocol the scientists determined the intestinal absorption capacity and the faecal production and composition of male and female subjects separately:

Figure 1: Relative energy and nutrient absorption in male and female subjects (Wierdsma. 2013)

As you can see in my plot of the data in figure 1, the mean (SD) intestinal absorption capacity (as a percentage of nutritional intake) was different for fats, proteins and carbohydrates, so that the average subject digested only

• 89.4% (3.8%) of the total energy their meals provided,
• 92.5% (3.7%) of the "fat calories",
• 86.9% (6.4%) of the energy from protein and
• 87.3% (6.6%) of the calories from the carbohydrates

in their meals (the values in the brackets denote the corresponding standard deviations). Accordingly, fats are not only the most energetically dense macronutrient, they are also the one healthy individuals digest best an with the lowest inter-personal differences. Overall, ...

"[w]omen had a statistically significantly lower energy absorption capacity compared to men (88.0% versus 91.8%, respectively, P=0.02). A similar trend was seen for fat and carbohydrate absorption, although this was not statistically significant (P=0.19 and 0.06, respectively)" (Wierdsma. 2013)

The latter may be surprising, after all, it's usually the women who complain they'd only have to 'look at a piece of cake to gain weightÄ and how unfair it was that men 'can eat whatever they want and still stay relatively lean' (obviously, the latter is not only a function of how much you eat, but also of how much energy you expend and the symbolic piece of cake may well satify 50% of a woman's, but only 25-30% of a man's daily energy requirements).

What goes in must go out again ;-)

Figure 2: Daily faecal production (g/day; x-axis) negatively correlated with intestinal energy absorption capacity (% of the energy intake; y-axis) (n = 23) (Pearson’s r = 0.46, P < 0.05 for the total group, r = 0.65, P < 0.05 for women and r = 0.71, P = 0.05 for men; Wierdsma. 2013).

The mean daily stool production for both sexes was 141 (49) g (29% dry weight) and amounted to an energy loss of 891 (276) kJ, while the individual contribution of  fats, protein and carbohydrates was 5.2 (2.2) g, 10.0 (3.8) g and 29.7 (11.7) g, respectively. Accordingly, the average nutrient contribution to faecal energy content was

• 23% (10%) for fat,
• 20% (8%) for proteins and 
• 57% (23%) for carbohydrates.

With the stools of the female study participants containing a lower percentage of water than those of men (P<0.05), the energy content per gram of wet faeces was higher in women than in men (P<0.05), while the daily faecal nutrient losses were not statistically significantly different between men and women. Moreover, the scientists observed that ...

"[...]"the daily faecal production was positively correlated with faecal energy loss in kcal (Pearson’s r =0.80, P<0.001) [and negatively] correlated with intestinal energy absorption capacity (%) (Pearson’s r = 0.46, P<0.05)." (Wierdsma. 2013)

- an observation that means nothing else, but "the more you eat, the more inclined your body will be to have some energy pass through undigested"... or, in other words: Once you starve yourself, your body will try it's best use each joule of energy it can get! 

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Bottom line: With the main results of the study at hand being that the average calculated standard for energy absorption in healthy Dutch adults is 90% and thus 5% less than it was previously assumed, it should be obvious that the already skewed "energy in vs. energy out" calculations you may have been conducting (against my explicit recommendation!) based on food labels and co are even less reliable than previously assumed.

"Accept There is No Magic Macronutrient Ratio" (read more)

On the other hand, the 5% more or less energy won't make a difference anyway, after all a main characteristic of our bodies is that they are no overtly simplistic bomb calorimeters, and their energy demands, as well as uptake depend on the total amount and composition (macronutrients, vitamins, minerals and other co-factors) of what we eat. If you want to gain or lose weight you will therefore not be able to forebear doing a 2-week food-log. Record all the foods and energy containing drinks you consume, sit down and (a) re-evalute the food quality, (b) take stock of the macronutrient ratios and (c) add / subtract foods, not calories or "energy" to establish a 20% caloric defict or 10% caloric surplus as a starting point for your diet / bulk. It's easy, it's bullet proof, but it's less convenient than relying on unreliable formula and databases.

References:

• Southgate DA, Durnin JV. Calorie conversion factors. An experimental reassessment of the factors used in the calculation of the energy value of human diets. Br. J. Nutr. 1970; 24:517–535.
• Van de Kamer JH, Ten Bokkel Huinink H,. Weyers HA. Rapid method for determination of fat in feces. J. Biol. Chem. 1949; 177: 347–355.
• Wierdsma NJ, Peters JH, van Bokhorst-de van der Schueren MA, Mulder CJ, Metgod I, van Bodegraven AA. Bomb calorimetry, the gold standard for assessment of intestinal absorption capacity: normative values in healthy ambulant adults. J Hum Nutr Diet. 2013 May 6.

11% Increase in Type I Fiber Cross Sectional Area During 12 Weeks of KHCO3 Supplementation: Are Alkali Supplements Fiber-Type Specific Anabolics W/ Add. Metabolic Benefits?

Muscle toning with bicarbonate? Without weight gain? For some women probably a dream come true ;-)

I guess, you will be hard-pressed to find another website with a similar amount of information the effects of alakali (mostly sodium bicarbonate) supplementation on exercise performance and metabolism as the SuppVersity. Irrespective of the previous posts on "baking soda" or the recent elaborations on the importance of a well-controlled acid base ratio (learn more), I am quite sure that the results of a recently published study from the Tufts Medical Center and the Bone Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University will come as a surprise even for the most regular visitors among you - to be honest, I was and am still surprised myself ;-)

So what's the surprise?

In their 12-week rodent study that was devised to elucidate whether the addition of a neutralizing amount of potassium bicarbonate (KHCO3) to purified diet designed to match the standard acid forming Western way of eating would ameliorate the urinary nitrogen loss and affect the muscle fiber size and number, as well as the levels of circulating and muscle-specific IGF-1 in thirty-six vitamin D sufficient or deficient, 20-month-old, Fischer rats, Lisa Ceglia and her colleagues did not only observe (relative changes in brackets are expressed for vitamin D sufficient / insufficient animals)...

• higher urinary pH (33% / 34%, after only 6 weeks),
• lower urinary nitrogen losses (-28% / -42%) and
• increased circulating 25OHD levels (3% and 15%);

they also observed significant increases in the cross-sectional area of the soleus muscles of the animals that did not depend on the vitamin D status of the animals.

Figure 1: Vitamin D levels, 24h urinary Nitrogen / Creatine ratio, cross sectional area of soleus (type I fibers; CSA1) and extensor digitorum longus (EDL; type II fibers, CSA2) after 12 weeks in rodents on KHCO3 supplemented diets with / without adequate vitamin D, data expressed relative to unsupplemented control (Ceglia. 2013)

As the data in figure 1 goes to show you, this effect was fiber-type specific and was not observed in the extensor digitorum longus (EDL), which is - contrary to the soleus - type II (fast twitch, glycolytic; learn more) fiber dominant. What is surprising though is the fact that the researchers did not observe corresponding increases in muscle weights (p > 0.05).

Unfortunately, the scientists don't address the "growth vs. weight" discrepancy in the discussion of the results, so that we are left to come up with our own hypotheses to explain why this may have been the case. We know that it cannot be the mere result of decreased food intakes or total body weight - both were virtually identical in all groups (just a note: the muscle weight per total body weight did not differ either). Moreover, the scientists explicitly state that "the lower UNi/Cr could be considered an indicator of reduced muscle proteolysis" - so that common sense would dictate an increase in muscle size and mass as it was in fact observed in previous human studies from the same laboratory:

"In a 6-week study in 19 healthy adults (average age 62 years), KHCO3 supplementation attenuated a protein-induced rise in UNi/Cr excretion by over 50 % compared to placebo (Ceglia. 2009). A larger study in 162 adults (average age 62 years) given a lower bicarbonate supplement dose or no bicarbonate, also demonstrated a 6 % decline in UNi/Cr excretion (Dawson-Hughes. 2009)." (Ceglia. 2013)

In fact, the provision of the bicarbonate supplement in the latter of the two studies did also increase the lower extremity power of the healthy older women who participated in the study by 13%; an observation that speaks in favor of the practical relevance of bicarbonate supplements - at least in the context of a normal / low vegetable and correspondingly low dietary alkali intake and that irrespective of the presence / absence of increases in skeletal muscle mass.

So what's the general mechanism here?

What about the muscle fiber specificity? The scientists speculate that the difference may simply be mediated by the "size difference of type II fiber subtypes (IIa, IIb, IIx) in rat EDL muscle and an inadequate [study] duration to detect a significant fiber size effect." This alone would, warrant a "larger and longer-term" at the end of which it may be possible to "fully characterize effects of this dietary
intervention on muscle morphology." (Ceglia. 2013)

If we simply discard the (as of now inexplicable) absence of increases in muscle weight and focus on the increases in muscle cross-sectional area it would in fact appear as if the alkali-induced improvements in nitrogen retention are the primary cause for the "muscle building" effects, the New Yorker researchers observed.

The latter appears all the more likely, in view of the fact that neither the provision of vitamin D nor the addition of bicarbonate (or a combination of both) resulted in significant reductions in the catabolic signaling molecules E3 ubiquitin ligases, MURF1 and MAFbx. Still, if we don't assume that the rodents expended much more energy and simply burned off the extra protein it must have gone somewhere, so that the most likely explanation for the inconsistencies would actually be the time-point at which the signaling molecules were measured. After all, a pre- vs. post comparison doesn't tell us what happened during the 12-week supplementation period. Neither do we know whether the acid-base balance does not target a completely different set of anabolic molecules than exercise or protein nutrition so that the scientists may simply have missed measuring the "correct" markers of anabolism / catabolism to be able to fully explain their observations.

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Bottom line: There is still much to be learned about the effects and detailed mechanisms of alkali supplementation. So much, in fact, that the addition of large boluses of potassium bicarbonate to a whole foods diet that includes large amounts of net alkalizing vegetables and fruits (funny how difficult it was to write that this way around and not "fruits and vegetables" ;-) as a means to increase your gains appears to be unwarranted or at least unnecessary at the moment.

Latent acidoses can set you up to become obese (learn more)

For someone following a typical Western and or high meat + fat / high grain or otherwise acid forming diet without adequate "vegetable buffer" a medium dose alkali supplement providing ~67.5 mmol of bicarbonate (~647mg of KHCO3 or 800mg NaHCO3/baking soda, which was the dose that has been used in the previously mentioned human study by Dawson-Hughes et al.) ingested twice a day, could yield all sorts of metabolic benefits, of which you have learned in previous posts on sodium bicarbonate and the acid base balance here at the SuppVersity that they go way beyond increases in muscle strength and cross-sectional area and reach into the realms of metabolic disease and even cancer.

Suggested reads:

• Calcium, Magnesium, Potassium & Co in Food, Water & Supps - Getting Enough is Easy, Knowing How Much Is Not! (read more)
• SuppVersity Science Round-Up on Sodium, Potassium, Alkalinity & Co (listen now)
• Science Round-Up Seconds: The Macro-Mineral Alphabet & the Potential Health Hazards of Diet-Induced Latent Acidosis (read more)
• Previous SuppVersity posts on sodium bicarbonate (browse all)

References:

• Bailey JL, Zheng B, Hu Z, Price SR, Mitch WE. Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt pathway: implications for muscle atrophy. J Am Soc Nephrol. 2006 May;17(5):1388-94. Epub 2006 Apr 12.
• Ceglia L, Harris SS, Abrams SA, Rasmussen HM, Dallal GE, Dawson-Hughes B. Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption. J Clin Endocrinol Metab. 2009 Feb;94(2):645-53. 
• Ceglia L, Rivas DA, Pojednic RM, Price LL, Harris SS, Smith D, Fielding RA, Dawson-Hughes B. Effects of alkali supplementation and vitamin D insufficiency on rat skeletal muscle. Endocrine. 2013 May 11. 
• Dawson-Hughes B, Castaneda-Sceppa C, Harris SS, Palermo NJ, Cloutier G, Ceglia L, Dallal GE. Impact of supplementation with bicarbonate on lower-extremity muscle performance in older men and women. Osteoporos Int. 2010 Jul;21(7):1171-9.

Detrimental Effects of Aerobic & High Oxygen Packaging on Meat Quality: 2x Higher Lipid & Cholesterol Oxidation, Less Tender, More Drip Loss, Less Juicy... but More Convenient!

Rosy, but rusty: "Fresh" meat packaged with 70% oxygen.

I don't know about the US, but most of the "fresh" meat, you buy at the Supermarket here in Germany is packaged in what the label calls a "Schutzatmosphäre". Literally translated this means nothing but a "protective atmosphere" and it refers to the supposedly bacteria-free high oxygen air that's pumped into the airtight packaging in which the chicken breasts and beef steaks, the pork and lamb and all the other appetizingly looking meats are stored for up to a week in the fridges of the meat counter.

Good to now it's protected! Right?

If you ever bought a product like that you will have realized that you can easily store it for the whole 7day+ period in you fridge and - as long as the airtight plastic container is not broken - it will look and smell almost as it did on day one, when you rip the container open and take a closer look, whether the meat you are about to prepare is still good to eat; Looking good!

What you cannot see though, is that the "protective atmosphere" protects, may have protected the looks of the meat, but not its nutritional quality. 

I mean think about it: What happens when you put metal into a wet high oxygen environment? Right! It starts to oxidize. Now guess what has happened to your appetizing piece of chicken, beef, pork or lamb while it was (highly conveniently, obviously) waiting for you in your fridge. Right it began to rust.

Figure 1: Content of cholesterol oxidation products (COPs) in non-irradiated raw chicken/turkey leg and raw beef with packaging, and storage time; data expressed relative to baseline (Nam. 2001)

As the data in figure 1 goes to show aerobic packaging (this is not yet a high oxygen environment) accelerates the rate of lipid and protein oxidation, so that the content of potentially hazardous cholesterol oxidation products (COPs) in your turkey legs, raw beef on day 7 is anywhere between 20-100% higher than on day one.

"Although the packaging conditions of meat during storage were critical for the oxidation of cholesterol in raw meat, irradiation synergistically increased it." (Nam. 2001)

And as Nam et al. point out this effect is even more pronounced if the meat has been irridated before packaging. The vacuum packaging, most producers and vendors are reluctant to use, because the meat does not look anywhere as fresh as the one that's packaged with highly oxygenated air (in fact it's the oxidized oxyhaemoglobin MbO2 that's responsible for the rosy color, cf. Rennere. 1999), on the other hand, "was enough to protect cholesterol and fatty acids from oxidation regardless of irradiation dose." (Nam. 2001)

Red deception in the "fresh" food corner

Figure 2: T-bar levels (a marker of lipid oxidation) in air, high oxygen and vacuum packaged pork during refrigeration for 0-20 days (Cayuela. 2004)

Now, with normal air, the nice red color will at some time give way to a brownish one, with extra high oxygen air that's used in high oxygen packaging, it will prevail, but at the same time,

"[t]he use of modified atmospheres with a high oxygen concentration (70%) act[s] as a pro-oxidation factor both for fatty acids and for cholesterol (an increase of 86.4% on the initial COPS content)." (Cayuela. 2004)

And that's a plus of almost 90% on top of what you would see with "regular" air packaging, as it was used in the Nam study.

Ah, and did I mention that this "meat" will also be less tender, less juicy and will have a 4-6x higher drip loss than "regular" packaged meat, when it's stored at 4°C for several days (Lund. 2004).

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Vacuum + Irridation = Plastimeat 2.0 According to a 2012 paper the phtalate DEHP content of vacuumed meats increases "dramatically" by 2.55, 2.75, 2.18 and 2.16 times in comparison to that in control samples having a fat content of 10%, 20%, 30% and 40%, respectively, when it is exposed to 20 h of UV irradiation at an intensity 900µW/cm² (Zhang. 2012).

Bottom line: As inconvenient as it may sound, the lipid and cholesterol oxidation meat undergoes, when it is packaged surrounded by a "protective atmosphere" of highly oxygenated air is just another example of how our urge for "convenience" and immediate 365 x 24/7 availability of whatever we want to eat can contribute to the overall burden of dietary-related diseases.

Don't get me wrong, you certainly won't die when you eat meat from the supermarket and still - the oxidized fats and cholesterol from the gas packaged meats from the supermarket are another on its own probably negligible piece to the puzzle that holds the answer to the complex question why we are fat and sick. One thing appears to be relatively certain, though, the terms "convenience" and "revenue" relate to almost every item on the never ending list of causative and confounding factors of the obesity epidemic in one or the other way.

References:

• Cayuela JM, Gil MD, Bañón S, Garrido MD. Effect of vacuum and modified atmosphere packaging on the quality of pork loin. European Food Research and Technology. 2004; 219(4), 316-320.
• Lund MN, Lametsch R, Hviid MS, Jensen ON, Skibsted LH. High-oxygen packaging atmosphere influences protein oxidation and tenderness of porcine longissimus dorsi during chill storage. Meat Sci. 2007 Nov;77(3):295-303. 
• Nam KC, Du M, Jo C, Ahn DU. Cholesterol oxidation products in irradiated raw meat with different packaging and storage time. Meat Sci. 2001 Aug;58(4):431-5.
• Rennere, M. Factors involved in the discoloration of beef meat. International Journal of Food Science & Technology. 1990; 25: 613–630.
• Zhang SL. Effect of UV Irradiation on the Migration of DEHP from Food-Grade PVC Film into Packaged Ground Meat . Advanced Materials Research. 2012; 601(94).

Cod Liver Oil vs. URTI. 2x Higher Fat Oxidation W/ Optimal Workout Timing, Aggressive Diabesity Control, Seaweed & Breast Cancer and NO Supplements Superior to Sugar

Self-proclaimed experts will say: "No cod liver! It's poison! It has way too much vitamin A... you better pop a kg of vitamin D pills if you want to do something for your health." Really? How do you explain the results of the Robertson study, then?

"Grandma was right" - That's if you will the statement of the week - a statement that is verified by the SuppVersity Figure of the Week which is p = 0.04 and describes the probability that the association between the consumption of cod liver oil and a decreased occurrence of upper respiratory tract infects (URTI) Swedish researchers observed in a cohort of 6350 middle-aged and elderly participants in the Tromsø Study 6, of which Robertsen et al. had actually expected that it would finally confirm the protective effects of high(er) vitamin D levels / intake against respiratory disease. As it turned out, however, neither vitamin D (25-OHD), nor the intake of fish, n-3 capsules or vitamin and/or mineral supplements were significantly associated. Shamed be he who thinks of vitamin A now ;-)

• 2-Fold Increase in Fat Oxidation W/ Correct Workout Timing (Darvakh. 2013) -- If we assume that you want to burn the maximal amount of fat during a workout, timing could be a more important factor than previously thought.

  

  Figure 1: Maximal fat oxidation, intensity necessary to achieve the maximal fatty acid oxidation and total fat oxidation per minute; all values expressed relative to absolute mean in each category (Darvakh. 2013)

  In a recent study from the Department of Physical Education and Sport Sciences at the Shahid Chamran University of Ahvaz in Iran the maximal rate of fatty acid oxidation in healthy, but untrained subjects was 2x higher in the afternoon compared to both the morning and evening conditions.
  
  What's likewise interesting to observe is the fact that the exercise intensity that was required to achieve maximal fatty acid oxidation was higher in the morning. No wonder that the total fatty acid oxidation per minute in all three trials was the highest, when the participants worked out in the morning!

  ---

  Bottom line: It's not just the missing dietary control, but also the mere idea that "burning fat for fuel" during a workout would have beneficial effects on long-term weight loss - let alone help you shed weight, when you are not in a caloric deficit that renders the results of the study at hand interesting, but more or less irrelevant. My personal advice would thus be: Work out, whenever you can muster the time and whenever you got the choice, base your decision on when to work out on performance measures, not results from studies like these (learn more about planning your workouts here).

• Is the time ripe for aggressive diabesity cures?! (Belsare. 2010) -- Everyone who has listened to the Wednesday episode of Super Human Radio, when Carl Lanore interviewed the Indian researcher Milind G. Watve, co-author of the paper at hand, will already be familar with the concept:
  

  

  Table 1: Molecules that affect aggressive behavior as well as insulin resistance (Belsare. 2010)

  Physical aggression is known to increase secretion of epidermal growth factor (EGF) in anticipation of injuries and EGF is important in pancreatic beta cell regeneration too. In anticipation of injuries aggression related hormones also facilitate angiogenesis and angiogenesis dysfunction is the root cause of a number of co-morbidities of insulin resistance syndrome.
  
  Reduced injury proneness typical of ‘diplomat’ life style would also reorient the immune system resulting into delayed wound healing on the one hand and increased systemic inflammation on the other. Diabetes is negatively associated with physically aggressive behaviour."

  These and the unquestionably striking associations the researchers collected in the tabular overview I used as a basis for table 1 to the right of this post (you read it a follows: arrows indicate up-/down-regulation or pos-/neg. correlation; "A"/"B" causation / reverse causation shown in A1/B1 = mutant or knockout experiment; A2/B2 = pharmacological/physiological exp. based on infusion or use of agonists/antagonists); C indicates only statistical association w/out direct evidence for causality), would unquestionably justify the hypothesis:
  

  "[...]that suppression of physical aggression is the major behavioural cue for the development of metabolic syndrome."

  However, despite the fact that "preliminary trials of behavioural intervention indicate that games and exercises involving physical aggression reduce systemic inflammation and improve glycemic control" - the same is true for "unagressive" types of exercise, so that I can't but vouch my doubts about the causative nature of aggression in this game of convenient laziness.

  ---

  

  Sugg. Podcast: Doves, Diplomats & Diabetes: A Darwinian Interpretation Of the Obesity Epidemic (listen)

  Bottom line: Irrespective of the causative or correlative nature of the lack of aggression or its presence in the etiology and resolution of the obesity epidemic.
  
  In the end, I am with Dr. Watve and his Indian colleagues: the non-pharmacological and in my humble opinion only viable solution to our problem are lifestyle changes - and as far as the "aggressiveness" is concerned, I guess, we'd just have to enforce these more aggressively. At least as aggressively as the Australians are leading their "war against" cigarette smoking - maybe a "war against" and not as a quest for revenue-generating pharmacological solutions to behavioral problems as we are still doing it by now.

• The breast cancer protective effects of seaweed - proof of principle (Teas. 2013) -- Researchers from the South Carolina Cancer Center at the University of South Carolina state in their recently published paper in the Journal of Applied Physiology that the consumption of seaweed (Undaria) in the form of a capped supplement (5g/day, total) decreases the urinary human urokinase-type plasminogen activator receptor (uPAR) concentrations in15 healthy postmenopausal women (5 had no history of breast cancer, 5 were breast cancer surivors) during a 3-month single-blinded placebo controlled clinical trial.

  ---

  What to make of these results? With the well-established increase in uPAR in post-menopausal and it's highly significant correlation with unfavorable breast cancer outcomes. The scientists argue that this controlled experiment would provide the hitherto missing "proof of principle" to confirm the epidemiologically observed anti-breast cancer effects of seaweed.

• Pre- & Post-workout supplementation with VPX' flagship products NO Shotgun & Synthesize promote fat free gains more than pure sugar (Ormsbee. 2013) -- Actually I did not even want to post this study, but it's so hilariously funny that I could not resist informing you about the marginal edge the provision of the VPX pre- & post-workout supplements NO Shotgun & NO Synthesize had in a sponsored study from the Florida State University that's been published in provisional form on Friday afternoon.
  
  When the researchers analyzed the effects the provision of the said supplements before and after each of the workouts the 29 healthy resistance trained men had compared to a maltodextrin [yeah, that's protein, BCAA, creatine, caffeine, beta alanine & more in the "multi-ingredient performance supplements (MIPS) vs. plain sugar as "control" placebo)] they found

  • 

    Figure 2: Body composition of previously resistance trained subjects after 6 weeks of standardized thrice weekly progressive strength training in participants ingesting one serving of NO Shotgun and Synthesize (MIPS) vs. 2x17g maltodextrin (placebo) pre / post workout; values expressed relative to group baseline (Ormsbee. 2013)

    no group time  interaction  for  HR,  BP,  blood  glucose,  lipids,  NOx,  hs-CRP,
    cortisol  concentrations  or  body  fat
  • significant decrease in body fat in both groups (mean ± SD; MIPS: -1.2 ± 1.2%; Placebo: -0.9  ± 1.1%), android fat (MIPS: -1.8 ± 2.1%; Placebo: -1.6 ± 2.0%), and gynoid fat (MIPS: -1.3 ± 1 .6%; Placebo: -1.0 ± 1.4%) and *drum rolls please* 
  • a  group × time interaction  for the increases in fat-free mass which were significantly  higher (4.2% vs. 1.9%) after the ingestion of the kitchen sink supplements compared to the 21g of pure maltodextrin
  What? Yeah, I know that VPX has had a very similar study done in the past (read up on the details, here) and obviously nobody read my comment back in the days that it's nice to spend some money to prove that your supplements works, but basically useless if the study protocol is designed in a way that ensures that your product will come as the more or, as in this case, rather less glorious winner.
  

  ---

  Bottom line: I wonder when the first supplement company dares doing a study comparing their product to a basic comination of creatine + whey and a cup of coffee before the workouts... what? Oh, you suspect that this could hamper their sales? Well, I guess you could be right.

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That's it for this installment of "On Short Notice"!  If you still have to kill some time before you start into the weekend, I suggest you take a peek at one of the following Facebook news:

• 

  I hope you did not already forget that. The isoleucine-containing peptides in hydro-whey can also ramp up GLUT-4 expression and increase skeletal muscle glucose uptake - a true repartitioning effect (learn more)

  Endurance boosting effects of hydro whey -- Whey protein hydrolysate aka "low molecular weight whey" has superior effects on the endurance of rodents compared to regular whey isolate (read more)
• Influenza: marketing vaccine by marketing disease -- Young Harvard scientists speaks out about the hilariousness of the flu vaccine (learn more)
• Further evidence androgens program fat-cells-to-be to become bone, not fat -- "[O]ur results suggest androgens promote an osteogenic gene program at the expense of adipocyte differentiation." (read more)
• Metabolic IN-flexibility is a characteristic feature of PCOS in women -- That's corroborated by both insulin resistance and androgen excess (learn more)
  

If that's still not enough to satisfy your cravings, just "like" the SuppVersity on Facebook and keep on par with the latest news of which I am sure there will be more to come before the next full article is going to be published tomorrow.

References:

• Belsare PV, Watve MG, Ghaskadbi SS, Bhat DS, Yajnik CS, Jog M. Metabolic syndrome: aggression control mechanisms gone out of control. Med Hypotheses. 2010 Mar;74(3):578-89.
• Darvakh H, Nikbakht M, Shakerian S, Mousavian AS.  Effect of Circadian Rhythm on Peak of Maximal Fat Oxidation on Non-Athletic. Zahedan J Res Med Sci. 2013; 15 [epub ahead of print].
• Ormsbee MJ, Thomas DD, Mandler WK, Ward EG, Kinsey AW, Panton LB, Scheett TP, Hooshmand S, Simonavice E, Kim JS. The effects of pre- and post-exercise consumption of multi-ingredient performance supplements on cardiovascular health and body fat in trained men after six weeks of resistance training: a stratified, randomized, double-blind study. Nutr Metab (Lond). 2013 May 16;10(1):39.
• Robertsen S, Grimnes G, Melbye H. Association between serum 25-hydroxyvitamin D concentration and symptoms of respiratory tract infection in a Norwegian population: the Tromsø Study. Public Health Nutr. 2013 May 9:1-7.  
• Teas J, Vena S, Cone DL, Irhimeh M. The consumption of seaweed as a protective factor in the etiology of breast cancer: proof of principle. J Appl Phycol. 2013 Jun;25(3):771-779.

Science Round-Up Seconds: Breast Cancer, GH Induced Insulin Resistance, Stretch + Contraction Increase Molecular Hypertrophy Signals and Probiotics & the Obesity Pandemic

When we are talking about the extinction of endangered species such as the Siberian tiger, we are adopting a perspective that will also help us to understand such things as the pitfalls of probiotic supplementations as a "solution" to the diabesity epidemic

It's Friday the day after the SuppVersity Science Round-Up (download the podcast) and you all know what that means: Right! Time to summarize the stuff that did not make it into the show and provide you with a couple of thoughts, as well as additional information on the topics, Carl Lanore and I did already cover (this does also imply that you have to listen to the show if you want the info on the genetic and non-genetic underpinnings of breast cancer).

If I had to come up with a motto, something that connects the topics in the show and thus obviously also the ones that will be discussed in this article, I guess it would be "ecosystems". I have repeatedly pointed out in the past that I am not a believer in the "back in the good old days everything was better" interpretation of "Paleo". What I do believe in, however, is the notion that exposition entails adaptation.

You can't control the adaptation, but you can control the exposition

Now, these adaptation processes whether they be negative such as the growth of cancerous tissue in the breast or ovaries of a woman like Angelina Jolie are beyond our reach: The environment that triggers them, on the other hand, can be manipulated - whether that's by getting your breasts and ovaries removed to rid yourself of the 50-80% (you heard me right! the "real" chance carriers of a defect BRCA1/2 gene to develop cancer ranges from 50% to 80%, by the age of 70) or - and this is obviously a pretty drastic change of subjects, by emphasizing peak contractions in a semi-stretched position to benefit from the upregulation of the proteins p-Akt, p70S6K, p38 MAPK and ERK 1/2, i.e. the driving forces of protein synthesis, it's always your manipulation of the environment that will bring about "adaptation" (used in the broadest sense).

Figure 1: Graphical summary of the main results, i.e. the stretch initiated activation (+, ++, +++) of the signaling molecules on different conditions with either short, long (at maximal peak contraction) or slightly longer (+25%, but still way from lockout) positions and the corresponding tension on the soleus muscle of the rodents (Van Dyke. 2013)

If I was successful, the above introduction should have set the scene and thus provided an environment for your perspective on things to change / align with mine. I've manipulated the "cognitive environment" that determines or at least influences the way you are about to understand what follows, i.e. the missing side-kick on the recently observed negative effects of growth hormone on insulin sensitivity and glucose uptake in healthy men and the comprehensive discussion of the (imho) misunderstood role of the gut microbiome as both, a trigger and solution to the obesity epidemic.

Can exogenous growth hormone trigger insulin resistance?

Within our new cognitive framework you will probably have transformed the above question as follows, by now: "How does the exogenous administration of growth hormone change the the endocrine environment and why does this entail an adaptive response of which most people would say that it's highly detrimental?" From this "mini-evolutionary perspective", as you may call it, it's surprisingly easy to understand what exactly has happened in a recent study from the University of Aarhus in Denmark (Vestergaard. 2013).

In their effort to probe the hypothesis that there was a connection between ghrelin, growth hormone and the increases in retinol-binding hormone (RBP4, to be specific) that are observed in patients with developing and/or full-blown metabolic syndrome, Vestergaard et al. conducted two studies of which only the second one, which involved nine totally healthy young men in their twenties (23y; BMI 23kg/m²), will - without major qualifications - transfer to you me or other healthy physical culturists.

The men received a course of daily 2mg GH injections while consuming a previously standardized diet containing 50–60 % carbohydrates, <30 % fat, and roughly 10–15 % of protein (in % of total energy intake). Before and after the intervention period, the participants had to report to the lab at fasted and thus optimally prepared for the hyperinsulinemic euglycemic clamp test.

Figure 2: Basal fasting glucose and insulin concentrations, as well as M-value (=marker of insulin resistance) in healthy young men after eight days of placebo and GH administration, respectively (left; p-values over bars); glucose infusion rates (GIR) indicated by during hyperinsulinemia after placebo / GH administration (right, Vestergaard. 2013)

The selected results I plotted in figure 2 are quite unambiguous. As expected there was a huge increase in the IGF-I concentrations in response to the 8-day course of 2mg GH per day.

The 8% increase in fasting plasma glucose and even more so, the doubling of the insulin levels that were required to keep these elevated glucose levels stable, certainly come as a surprise, if you're thinking about it from an broscientifically influenced mechanistic point of view. I mean, doesn't broscience tell us that GH is the good guy that's going to make you lean and ripped?

How come we are seeing a -34% reduction in glucose sensitivity (this is actually what's measured as the so-called "M value" in the euglycemic clamp studies).

Within our previously established cognitive framework, the answer to this question is actually quite straight forward. To get to the bottom of the counter-intuitive effects of GH we just have to think about the "natural" environment that will trigger the release of GH from the somatotropic cells within the lateral wings of the anterior pituitary gland.

Did you know that the normal GH response to hypoglycemia is blunted in the obese and the reduced obese (Ball. 1972)? Without GH to get their blood sugar back up, overweight individuals and formerly obese will thus have to resort exclusively to corticosteroids (cortisol) to regulate their blood sugar levels.

In this context, it's also worth mentioning that insulin induced hypoglycemia is still considered a valid - yet maybe not optimal - in children who are suffering from retarded growth. With the injection of exogenous insulin and the kids becoming hypoglycemic the body should compensate for that by secreting growth hormone. If that's not the case, this is a good indicator of a general malfunction of the pituitary gland.

Hah? Right! Hypoglycemia or borderline hypoglycemia is among the primary triggers of somatotropin aka GH release. Now, think about it - would it make sense that a hormone that's supposed to increase fatty acid oxidation to supply your body with glucose would at the same time increase insulin sensitivity and thus have your muscles suck up all the precious glucose your brain is longing for?

On the contrary, it is only logical that GH - just like it's falsely vilified potent cousin cortisol (yeah, you heard me right, you won't see both at the scene on the same time, because they serve a similar purpose at least wrt to glucose metabolism) - will decrease the insulin sensitivity of your muscles in order not to "waste" the precious glucose which should be scarce once GH goes up.

In the study at hand, the environment in which the high growth hormone levels occur are totally different: Once you plug people to a euglycemic clamp, there is a mismatch between the actual environment, which is normal / high glucose, and the natural (if you will "evolutionary) expected environment for elevated GH levels - and what you see in figure 2 is the inevitable consequence of this mismatch: a significantly lowered glucose sensitivity... quite cool, how a small change in the way we are looking at things allows us to understand phenomena that do initially appear totally inexplicable, right?

Lifestlye changes, not probiotic supplements are the solution to the diabesity epidemic

Now that we have first-hand evidence for the explanatory power of our new perspective let's stick to it and apply it to the false expectations studies such as the recently released investigation into the "anti-obesity" effects of the common gut bug Akkermansia muciniphila in a rodent model of diet-induced obesity (Everard. 2013).

Figure 3: The AM count is reduced in response to the dietary enviroment, the environment - not the lack of bacteria - is the root cause of the negative effects on fasting glucose, fat mass gain and thickness of the intestinal mucus lining all of which can be partly (the latter even fully) restored to normal with supplementation (Everard. 2013)

If we take a look at the data in figure 3 it is undebatable that the provision of exogenous live (this does not work at all with dead bacteria) Akkermansia muciniphila (AM) can significantly reduce the weight and fat gain in the rodents receiving a species inappropriate high fat diet. As the data on the AM content of the gut microbiome of the obese mice on the right hand side of figure 3 reveals this effect is yet a simple result of the restoration of the "original" microbial composition in the intestinal tract of the rodents.

Siberian tigers on corn fields!? Does this really make sense?

Since the term "original" refers only to the amount of the bacteria Dr Antoon Akkermans identified as one of the many bacteria the count of which is decreased / changed in obese rodents (and humans), it is yet not surprising that we are seeing nothing but ameliorative effects.

Glutamine may offer another way to accelerate gut healing and improve amino acid absorption or rather avoid the "abuse" of BCAAs, arginine etc. for other metabolic purposes (learn more)

Within our cognitive framework of "ecosystems" and "adaptations", the chronic administration of living bacteria to counter a specific aspect of the diet induced detrimental effects on the gut microbiome has may be compared to the laughable efforts of biologists to save certain animals from extinction by breeding them in a Zoo and releasing them into an environment, where deforestation, pollution and all the other nasty things, we, the crown of evolution, enjoy about as much as the average Westerner likes to wash down his super-sized fast food menu with a "refreshing" *rofl* 2L XXL pot of coke (drinking plenty is healthy for you, ain't it? ;-), will have them die before their time unable to reproduce in time to contribute to the species' natural survival.

Once you understand that, you will have to realize that you are wasting your time and money on false promises if you don't change the environment, i.e. the way you live and the foods you eat first before you even think of using probiotic supplements as an adjunct to accelerate the normalization process, which should - just like the detoriation - take place irrespective of the supplementation as a mere results of the dietary modulation of your gut microbiome, anyways.

With these insights, I am going to release you into the weekend... and who knows, maybe you'll notice the effects the environment you expose yourselves to in the coming days has all sorts of beneficial or detrimental influences on your physical and mental health. Listening to even more non-science-based Angelina Jolie news on the television and radio, for example, is probably not going to have beneficial effects on your psyche ;-)

References:

• Ball MF, el-Khodary AZ, Canary JJ. Growth hormone response in the thinned obese. J Clin Endocrinol Metab. 1972 Mar;34(3):498-511.
• Everard A, Belzer C, Geurts L, Ouwerkerk JP, Druart C, Bindels LB, Guiot Y, Derrien M, Muccioli GG, Delzenne NM, de Vos WM, Cani PD. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci U S A. 2013 May 13.
• Van Dyke JM, Bain JL, Riley DA. Stretch activated signaling is modulated by stretch magnitude and contraction. Muscle Nerve. 2013 Apr 26.
• Vestergaard ET, Krag MB, Poulsen MM, Pedersen SB, Moller N, Jørgensen JOL, Jessen N. Ghrelin and growth hormone induced insulin resistance: no association with retinol-binding protein-4 Endocr Connect EC-13-0019; published ahead of print May 7, 2013, doi:10.1530/EC-13-0019