Are You Still Wasting Money on Amino Acid Blends, When Plain Whey Protein Pumps More Protein Into the Muscle & Turns Endurance into Strength Type Fibers?

The indoctrination machine of the supplement industry is pretty efficient. At least that's what I gather from the "bro-talk" in my own gym - I guess you know what I mean, right?

If there is something free form amino acids products can do that plain whey cannot do, it's increasing the revenue of their producers. No wonder that they are touted as "almost as potent as illegal gear" and sold for prices that make me roll with the eyes. Dozens of patented "optimal" BCAA - leucine : valine : isoleucine - ratios and "superior anabolic blends" ... come on, you are beyond believing every lie you are dished up, aren't you?

You never gave in to the temptation? Right you were! A recent study from Japan confirms once more: It's complete proteins trigger complete growth effects, their individual amino acids, which were used in the control arm of a recent (unfortunately) rodent study from the Meiji Company Limited, the Graduate School of Agricultural and Life Sciences and the Kanagawa Academy of Science and Technology in Japan, on the other hand, have comparably weak effects on the post-exercise gene expression profile.

You can learn more about protein intake at the SuppVersity

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Blends over Isolates!

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5x More Than FDA Allows

But, one thing after the other, as you have already gathered from the information in the introduction, the scientists were building on their own results as well as the findings of Rowlands et al. have published in Physiological Genomics in 2011 (Rowlands. 2012). In said study, the researchers had been able to show...

"[...]that post-exercise ingestion of whey protein differentially alters the portion of the transcriptome that is involved in tissue structure and remodelling,  including production of the extracellular matrix, cytoskeleton and contractile proteins." (Kanda. 2014)

In contrast to their previous study, which was the basis of the discussion in an article I wrote last year (" Don't Judge a Protein by Its Amino Acid Content: 17% Higher Protein Synthesis With Whey vs. Free Form Amino Acids" | read previous article) and where their focus was on mTOR and the fractional protein synthesis (see Figure 1), the study at hand focused focused less on the net effect and more on the underlying (genomic) which explains the fact that free form amino acids suck and whey hydrolysate rules.

Figure 1: Fractional protein synthesis (left), AA, glucose & insulin conc. in the blood and expression of mTOR, 4E-BP1 and S6K1 in sk. muscle in response to CHO, whey protein hydrosylate or identical free form amino acids (AA; Kanda. 2013)

To this ends, the researchers fed rodent diets containing either CHO + Whey or carbohydrates (CHO) that were mixed with an iso-energetic amino acid formula which had an amino acid profile that was identical to the one of the whey proteins to investigate the global effect of WPH on gene expression in skeletal muscle in comparison with an identical amino acid mixture (AAM).

Figure 2: Fractional protein synthesis and insulin levels after the ingestion of the free form Amino Acid (identical profile as whey hydro) + CHO or Whey Hydolysate + CHO formulas after the workouts (Kanda. 2014)

Their findings (Figure 2) are, at least for you as a SuppVersity reader, unsurprising. Aside from the increase in insulin, a hormone lean individuals don't have to fear and probably the most potent natural anti-catabolic agent, the scientists were able to identify a dozen of other gene-factors (Table 1) that may be responsible for the 16% increased fractional protein synthesis Kanda et al. observed in their latest study.

Table 1:Significantly enriched Gene Ontology (GO) terms (P,0·01) found in the top 161 up-regulated genes in the whey protein hydrolysate (WPH) group (Kanda. 2014)

Figure 3: Venn and Euler diagrams represent the association of up-regulated genes with multiple GO terms caused by WPH (Kanda. 2014)

• lmmune response
• Regulation of RNA metabolic process
• Positive regulation of RNA metabolic process 
• Positive regulation of transcription, DNA-dependent
• Positive regulation of transcription from RNA
• polymerase II promoter
• Regulation of transcr. from RNA polymerase II promo
• Regulation of transcription, DNA-dependent
• Positive regulation of gene expression
• Regulation of nervous system development
• Regulation of neuron differentiation
• Negative regulation of neuron differentiation
• Response to organic substance
• Response to mechanical stimulus
• Muscle tissue development
• Striated muscle tissue development
• Negative regulation of cytokine production
• Response to wounding

The above list (cf. Table 1) leaves no doubt that the changes the researchers observed a potentially hypertrophy- and health-relevant. Not all of them, were whey exclusive, but the eight specific GO terms that were significantly enriched in the set of up-regulated genes included, as the scientists point out in the discussion of their results "some key elements such as Cd24, Ccl2, Ccl7 and Cxcl1 involved in post-exercise muscle repair" (Kanda. 2014).

Take some time off and reset your protein anabolic response. learn more about detraining and the difference to tapering @ the SuppVersity!

Bottom line: The logical conclusion Kanda et al. draw and I support is that their newest findings "indicate that WPH induces more rapid muscle recovery after exercise than does the AAM" (Kanda. 2014). Moreover, other specific gene changes relate to important transcription factors in skeletal muscle, which are also involved in the activation of the basal muscle anabolic protein Akt and a gene network these interacts with some glucoregulatory enzymes, such as hexokinase, pyruvate kinase and phosphofructokinase, which could explain why whey is a significantly better promoter of increases in muscle glycogen content than free form amino acids.

In conjunction with the donwregulation of genes that are encoded by type II fibers, and the up-regulation of a key transcription factor, Six1, which can reprogram adult muscle from the slow-twitch phenotype into the fast-twitch phenotype. Whey will, unlike free form amino acids eventually turn you into a fast twitch fiber powered sprint and weight lifting monster... well, almost ;-) It will obviously rather promote the development of a higher glycolytic fiber count which in turn will enable you to sprint and lift - And let's be honest, isn't that actually what you want?

References:

• Kanda, Atsushi, et al. "Post-exercise whey protein hydrolysate supplementation induces a greater increase in muscle protein synthesis than its constituent amino acid content." British Journal of Nutrition 110.06 (2013): 981-987.
• Kanda, Atsushi, et al. "Post-exercise impact of ingested whey protein hydrolysate on gene expression profiles in rat skeletal muscle: activation of extracellular signal-regulated kinase 1/2 and hypoxia-inducible factor-1α." British Journal of Nutrition (2014): 1-12.
• Rowlands, David S., et al. "Transcriptome and translational signaling following endurance exercise in trained skeletal muscle: impact of dietary protein." Physiological genomics 43.17 (2011): 1004-1020.

High Intensity Training + Mesterolone Yield Muscle- and Fiber-Type Specific Size Gains Of Up To 100% & More

Want to learn more about fiber types? ➫ review past SuppVersity articles

I am not telling you a secret, when I say that testosterone alone - in the absence of training - will lead to significant increases in skeletal muscle mass (if you think that sounds like a secret you must have missed my previous article from the "Intermittent Thoughts on Building Muscle" series | read more). To a certain extend, the same is true for DHT (learn more), and - as a recent 6-week rodent study by Karina Fontana, Gerson E. R. Campos, Robert S. Staron and Maria Alice da Cruz-Höfling shows even by the structurally similar, orally bioavailable derivative Mesterolone (aka Proviron), which produces pretty drastic, fiber-type specific increases in muscle size, when it is administered in super-physiological doses for 6 weeks (Fontana. 2013).

AAS +/- HIT = ?

Basically the question the researchers from the universities of Campinas (Brazil) and Ohio had in mind, when they came up with their study protocol was: Do anabolic steroids exert direct effects on the fiber type composition and cross-sectional area of skeletal muscle fibers of sedentary and high-intensity, aerobically-exercised transgenic mice.

DHT & T ⇔ fat & muscle Comp | more

Why did the researchers select 1 alpha-methyl-17 beta-hydroxy-5 alpha-androstan-3-on (Mesterolone), not testosterone? At first sight it may seem stupid not to go for straight testosterone, but Fontana et al. deliberately chose "DHT", for two reasons: (1) oral bioavailability and (2) no hepatoxicity ➫ no injection induced wound-formation or liver damage that would skew the results.

As the scientists point out, the aim of the study was thus "to investigate the role of mesterolone in a supposed catabolic environment" (Fontana. 2013) and answer the following detail questions:

• Does the interaction of anabolic hormone treatment and high-intensity aerobic exercise produce an increase in muscle mass and redistribution of skeletal muscle fiber types? 
• Are muscles with distinct metabolic and contractile properties (i.e., fast/glycolytic vs. slow/oxidative) differently modulated by the anabolic androgenic steroid treatment combined with a high-intensity, endurance-type training program? 
• As such, three skeletal muscles were studied under these experimental conditions: soleus (SOL), tibialis anterior (TA) and gastrocnemius (GAS). 

To be able to do so, assigned their transgenic mice (these mice have been "modified" so that they have a lipid metabolism that's closer to the one of human beings) to four different groups, i.e.

Table 1: Overview of the incremental exercise program the rodents in the "EX-" (=exercise) groups performed on a treadmill 5x per week

• Sed-C - sedentary control
• Sed-M - sedentary + 3x2mg/kg* Mesterolone per week
• Ex-C -5x/week HIT exercise + gum arabic placebo
• Ex-M - 5x/week HIT exercise + 3x2mg/kg* M per week

*Note: The scientists claim to administer "supraphysiological" against that background we must assume that we are talking about 2mg/kg for a human (if that was the rodent dose, the human equivalent) would be 12-15mg and that's clearly not "supra-physiological" - 3 doses of 150-200mg of Mesterolone which comes in 25mg pills, on the other hand, would be "supra-phyiological".

After 6 weeks, the animals were sacrificed, their muscles harvested and an analysis of the entire range of pure and hybrid fiber types was conducted.

Mesterolone is not DHT: Anonymous was kind enough to remind me that the original version of this article did not make a clear distinction between DHT and 1-alpha-methyl-DHT aka Mesterolone (or Proviron). He did however mix his facts up, because contrary to A.'s claim Mesterolone has a 3x higher binding affinity for the androgen receptor in skeletal muscle than "regular" DHT (Saartok. 1984). With a 4x higher affinity for SHBG, it is however difficult to predict the real-world differences. This is particularly true in view of the fact that the growth response could be triggered by non-receptor mediated mechanisms, as well.

Just in case you don't remember all the details you've learned about the different fiber types in previous SuppVersity articles, keep in mind that type I fibers are mainly oxidative, they use fat as a "preferred" substrate and will get you from A to B when you walk or jog. The type II fibers, on the other hand are "glycolytic", this means, that they rely heavily on glucose. Their prerogative are explosive / fast contractions and they carry the lions share of the weight you through around at the gym.

Figure 1: Muscle weight and body weight (in g) at the end of the study (Fontana. 2013)

Against that background it's quite telling that the tibialis, the muscle with the largest amount of Type IIA and Type II AD fibers, fast twitch fibers that can use both, glucose and fat as fuel, is the only muscle where we don't see the following relation between the muscle weight: EX-M > EX-C > SED-M > SED-C.

Figure 2: Detailed analysis of the changes in fiber type composition of soleus, tibialis and gastrocnemius muscle; all data expressed relative to sedentary control (Fontana. 2013)

If you take a closer look at the detailed fiber type analysis the researchers conducted (Figure 2), you will see that a similar trend can be observed in the "intermediate" muscle, the gastrocnemius (see grey arrow). The effects the DHT clone had on the "oxidative" soleus, on the other hand, were in no instance more pronounced than those of the 20-60min treadmill running regimen (see Table 1, for details).

Suggested: "Serum & Intramuscular Testosterone, DHT and Androgen Receptor Response to High vs. Low Volume Training" | more

So what can we learn from this study? (1) Contrary to the common believe that muscle building was a prerogative of testosterone, Mesterolone (Proviron, DHT) can obviously build muscle, as well - at least, when it is administered at supra-physiological doses (see comment above; plus: don't do that at home ;-). (2) Despite the fact that the orally bioavailable DHT derivative does build muscle, even in the absence of physical activity, the changes are really pronounced only, when it is combined with intensive exercise. (3) Astonishingly, even running, i.e. a simple endurance exercise has significant anabolic effects on both oxidative (this is what you would expect) and glycolytic (this is actually surprising) muscle fibers. (4) This effect is highly amplified by Mesterolone - particularly in the Type IIA + IIAD fibers of the gastrocnemius, which has a particularly high content of "glycolytic only" Type IIB fibers (>50% in the exercise groups).  

This fourth and point, is actually the most interesting one. It does after all confirm what I mentioned only casually in previous articles about DHT, the true androgen, which is rapidly deactivated in the muscle and does still appear to play an important role in the structural changes your musculature undergoes, when you exercise. Speaking of changes, I guess you will already have realized that the highly pronounced increase in muscle fiber size of the type II fibers stands in line with the often-touted "strength building" effects of designer steroids with structural resemblance to DHT. The overall mass gains - and this is something you may have heard about said AAS, as well, on the other hand, are rather mediocre (see Figure 1).

References:

• Fontana, Karina, et al. "Effects of Anabolic Steroids and High-Intensity Aerobic Exercise on Skeletal Muscle of Transgenic Mice." PloS one 8.11 (2013): e80909. 
• Itil, Turan M., et al. "Male hormones in the treatment of depression: effects of mesterolone." Progress In Neuro-Psychopharmacology 2.4 (1978): 457-467. 
• Ly, Lam P., et al. "A double-blind, placebo-controlled, randomized clinical trial of transdermal dihydrotestosterone gel on muscular strength, mobility, and quality of life in older men with partial androgen deficiency." Journal of Clinical Endocrinology & Metabolism 86.9 (2001): 4078-4088. 
• Saartok, Tönu, Erik Dahlberg, And Jan-Åke Gustafsson. "Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin." Endocrinology 114.6 (1984): 2100-2106.
• Singh, Keerti, Asha Singh, and A. K. Sarada. "Assessment of mesterolone therapy in oligospermic males." www.ijpsi.org Volume 2 Issue 3 March 2013.

Classic Beats Super Slow; Single 198 Second Sprint More Time Efficient Than Work-Matched HIIT; Exercise Better Than THC; Metformin + Cardio + Lifting = Anti-Obesity Triplet; Self-Efficiacy & Training Adherence - Plus: More!

This is just a random selection of the unlimited movement patterns your body has been designed to execute - don't make the mistake and rely on only one of them!

The amount of really interesting, let alone revolutionary new studies on the effects of different exercise modalities is not exactly high, to say the least. I am not quite sure, what the reasons are, but as I have stated before, part of it certainly is that you cannot monetize on the results by producing patentable drugs based on your findings and will thus have a hard time to find sponsors / get funding. It is therefore no wonder that many published papers are spin-offs of small scale trials that have been conducted as part of dissertations. Others simply use rodent models, which may provide relatively reliable data, when it comes to the effects of running on a treadmill, but are not exactly what I would want to see, when it comes to weight lifting or any other of the myriad complex movement patterns our bodies can, but these days way too often don't do.

I have nevertheless been able to compile another potpourri of studies of which I would hope that one or the other will enlighten or at least entertain you. That being said, let's get started with this weeks installment of the Exercise Science Special of "On Short Notice", here at the SuppVersity...

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HIT it short, hit it hard, hit the glucose and be smart! Yo, this awesome rhyme would be my advice to the very busy chubby manager-types with compromised insulin sensitivity out there and it's based on the results of a very recent study by scientists from the Institute of Cardiovascular and Medical Sciences at the College of Medical, Veterinary and Life Sciences of the University of Glasgow in the UK (Whyte. 2012)

Figure 1: Power, workload (top) and metabolic effects of SIT and ES regimen (vs. control; bottom)

When Laura J. Whyte and her colleagues compared the effects of the single bout of very high-intensity exercise (SIT: 4x 30-s maximal sprints w/ 4.5min recovery between each) to a single maximal extended sprint (ES) matched with SIT for work done, they found that the immediate advantage of higher insulin sensitivity (measured via oral glucose tolerance test) in the work-matched continuous sprint the shorter duration 190s (TOTAL!) as well as almost identical...

• decreases is RER and carbohydrate oxitation, and
• increases in fatty acid oxidation

on the day after the exercise bout, in the presence of statistically significant reductions in insulin sensitivity only after the ES trial.

In other words: A single all out sprint on a braked cycle ergometer (as fast as you can; with obviously decreasing power in the course o the sprint) elicits greater metabolic effects within a 85% shorter timespan (198s vs. 1360s!), than work-matched classic HIIT training, with allegedly very long periods of active recovery.

That being said, I strongly caution against taking the results of this study as an incentive to perform the classic "go as fast as you can, for as long as you can" HIT sessions on exercise bikes, treadmills or ellipticals - those SUCK! *full stop* Be smart and either perform that one 3min sprint (if you really have no more time), or modify your HIIT training to incorporate longer high intensity phases (45-90s) at a work to active recovery ratio of 1:3 - 1:2, so that a resulting workout could look like that 4x 60s sprints, interspersed by 120s of active recovery. I would bet money that this protocol outperforms a work-matched continuous sprint in terms of its immediate and long-term metabolic effects.

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Opioid-like effects of exercise depend on intensity I guess you will be familiar with the term "runner's high"? Now, while the latter is usually ascribed to the exercise induced release of serotonin, the improved affect, the sense of well-being, the anxiety lowering and calming effects of exercise are probably mediated by the release of endocannaboids, of which scientists from the University of Arizona, the University of Texas Health Science Center and the Eckert College in St. Petersburg, Florida, have recently shown that the levels of these endogenous THC-like compounds depends on the intensity of the workout (Raichlen. 2012).

Liar, liar, THC junkie on fire ;-) You don't need to smoke weed before a workout if you get the intensity right! But could exercise also help people who recover from major depression to battle their tendency to obsess with negative thoughts and feelings?

At least in the 10 healthy regular runners who participated in the study, the results of which have been published in the Journal of Applied Physiology the endocannaboid exercise induced increase in circulating anandamide was most pronounced (~2x), when the subjects exercised at ~72% of their maximal heart rate (the workout consisted of 30min of treadmill walking, jogging, running at 45, 72, 83, and 92% of their maximal heart rate). Moreover, the post hoc analysis of the blood samples that had been immediately before and after the workout revealed that exercising at both the lowest and highest intensities had the exact opposite effect, although the reductions in serum anandamide were - when considered in isolation - were not statistically significant.

In conjunction with the results of another recent study that has been conducted at the Stanford University, it becomes evident that these results could actually be more than just "scientific masturbation", so to say. The Stanford researchers compared the reactions of 41 female patients who had recovered from major depressive disorder (MDD) and those of 40 healthy control, both of whom had been randomly assigned to either exercise for 15 minutes or quiet rest, to two sad mood inductions (once before and once after exercise or rest) and found that

"[while r]ecovered depressed participants who had not exercised exhibited higher NA [neagtive affect] after the second sad mood induction [...], both recovered depressed participants who had engaged in acute exercise and healthy control participants showed no increase in NA in response to the repeated sad mood induction." (Hogan .2012)

A reaction that goes against the so-called sensitization effect, which describes the tendency of depressed people (or people with a propensity to develop depression) to react with an increased level of negative effect to a repeated negative stimulus (Eisenstein. 2001) and would thus predict an increase in negative affect in response to the second stimulus as it was observed in the non-exercise group (figure 2, red box).

Figure 2: Negative and positive affect after 1st and second sad mood induction (left) and before and after exercise (right), respectively, in 41 female patients who had recovered from major depressive disorder (data from Hogan. 2012)

Moreover, the 15 minutes of exercise at an intensity the participant felt comfortable with led to an increase in positive affect participants in the exercise groups after the exercise bout, but failed to produce the same beneficial effect on the positive affect in the subsequent double-exposure to the filmic sad mood stimuli:

"However, in contrast to our hypothesis, we did not find any interaction between exercise condition and diagnostic group in level of reported PA following the repeated sad mood inductions that would be consistent with the notion of sensitization or habituation." (Hogan. 2012)

And who knows, if the exercise intensity had been higher, so that there had been more anandamide and other endocannaboids floating around in the brains of the study participants, this could even have changed the positive affect trajectory from the first to the second filmic sad mood induction? "Yo, that's so sad... hahaha" ;-)

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Image 1: Otsuka Long-Evans Tokushima fatty rats (OLETF, right) have a  genetic disposition to develop type II diabetes.

When metformin is good for the obese (pre-)diabetic and exercise is good, as well, metformin + exercise cannot be bad, right? At least in OLETF rats, one of the common rodent models of the metabolic syndrome, this assumption appears to apply (Jenkins. 2012).

According to the recently published paper by Nathan T. Jenkins and his colleagues, metformin and exercise do in fact work synergistically - at least as far as the obesity induced inflammation is concerned. While metformin decreased the pro-inflammatory overexpression of leptin, the rodents that have been exposed to an endurance type exercise regimen exhibited higher levels of the anti-inflammatory cytokine IL-10, which limit and ultimately terminate inflammatory responses (Moore. 2001).

Not just in view of the fact that IL-10 has also been implicated in the prevention and even treatment of auto-immune diseases, such as lupus erythematosus and multiple sclerosis (Beebe. 2002), I would always choose exercise over metformin - this is all the more true, if you are not morbidly obese in the first place!

And if you want to go even one step further, you simply add couple of interval sprints to the equation as those have been shown - in the same rodent model, by the way - to elicit greater improvements in HbA1c, the long-term marker of glucose management that "classic" steady state endurance exercise (Martin. 2012). Since the latter were mediated via differential microvascular changes than those Martin et al. observed in endurance trained OLETF rats, it is furthermore almost certain that they will add up. Probably not 1+1, but 1.5 and even 1.1 would still be better than 1.0, wouldn't it?

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The lack of the feeling of  self-efficacy is one of the best predictors of not sticking to a workout routine. And you know what? Oftentimes it's not your your, Joe or Jane who is to blame, but simply their cookie-cutter trainer or unqualified cousin who's dragging them to the gym. Now, think about that... could it be that you are a cousin / trainer like that!? No way, right?

A feeling of accomplishment is one of the main determinants of exercise compliance Have you ever wanted why you really enjoy going to the gym, while your obese cousin will only drag his ass over there if you kick him into the latter? Well, according to the latest study from the Johns Hopkins University School of Nursing and Division of Cardiology at the The Johns Hopkins University School of Medicine in Baltimore, Maryland, it may in fact be you and not Joe or whatever his name is, who is to blame. Probably you are just having him copy what you do, with either way too much weight, or so little weigh that he does not just feel bad about it, but cannot make real progress either (Nam. 2012).

The scientists call that which Joe is lacking a feeling of "self-effiacy", when he is going to the gym training next to his 75lbs lighter cousin, lifting sissy weights and looking like a fat balloon.

No wonder he is falling off the wagon! Specifically, if you also take into consideration that in addition to the missing feeling of accomplishment, which increases his chance of non-compliancy by 19%, Joe also exhibits most of the other features Nam et al. have found to increase the chance of dropping out, specifically,

• low fitness - 26% increased chance of dropout and
• higher insulin resistance - 17% increased chance of dropout,

in the course of their experiment with 140 overweight, sedentary individuals with type II diabetes, who were randomly allocated to a 6-month, 3 times per week exercise intervention or a non-exercise control. And while bodyfatness, i.e. a higher total and subcutaneous abdominal fat percentage appeared to be indicators of higher compliance, when the scientists just looked at the raw data, these positive effects vanished, when they plied a multiple logical regression analysis.

So what's the take home message, here? Cousin or not, people won't do well on cookie cutter plans that won't allow them to make, see and feel progress.

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Isn't it astonishing how versatile and important these stem cells from the bone marrow are (image NIH. 2001)

1h of exercise thrice a week increases hematopoietic stem cell (HSC) count in the bone marrow With the almost magic effects of stem cell therapy being on everybody's lips, these days. You will probably be intrigued to hear that researcher from the McMaster University have recently established that a very reasonable amount of 3x 1h of exercise per week increased the quantity of hematopoietic stem cells in the bone marrow of exercised mice by +20% compared to their sedentary peers (de Lisio).

With it's likewise statistically significant effect on the proportion of whole BM cells in G(2)/M phase of cell cycle (p<0.05 and an increase in the number of spleen colonies (+48%, p<0.05) in those "model patients" who received transplants from the exercised compared to transplants from sedentary mice, it is thus likely that people who exercise regularly will benefit from both the quantitative increase, as as well as the qualitative improvements these multipotent stem cells, which  give rise to all the blood cell types from the myeloid (monocytes and macrophages, neutrophils, basophils, eosinophils, erythrocytes, megakaryocytes/platelets, dendritic cells), and lymphoid lineages (T-cells, B-cells, NK-cells), undergo in response to a moderate amount of exercise.

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Finally acknowledged: "[C]ombination exercise g[ives] greater benefits for weight loss, fat loss and cardio-respiratory fitness than aerobic and resistance training modalities", alone! And this is only the first part of the conclusion of a recently published paper by Suleen S Ho, Satvinder S Dhaliwal, Andrew P Hills and Sebely Pal, who explicitly suggest that

"Therefore, combination exercise training should be recommended for overweight and obese adults in National Physical Activity Guideline" (Ho. 2012)

How the scientists came to that conclusion? Well they could simply have read the SuppVersity news, but instead they conducted a 12-week trial, in the course of which 97 overweight or obese men (n = 16) and women (n = 81) (BMI >25 kg/m² or waist circumference >80 cm for women and 90 cm for men), aged 40 to 66 years, were randomly assigned to a either aerobic, resistance or combined training regimen (n=16 for each) or a sedentary control group (n=15). The results, spoke for themselves.

Figure 3: Changes in body fat (%; top) and VO2Max (bottom) in the course of the 12-week trial (based on Ho. 2012)

In the absence of statistically significant reduction in energy intake, or macronutient composition, the combination subjects in the combination group were the only ones to lose statistically significant amounts of

• body weight (-1.6kg),
• body fat (-1.9kg or 1% body fat), 
• android (=visceral) fat (-1.3kg),

had the most pronounced reduction in waist circumference (-2.6% vs. -2.5% in RT and -2.0 in AT) and were the only ones with statistically significant improvements in VO2Max, a marker of general cardiovascular fitness.

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Is there maybe more room in your training regimen for slow reps, than you may have thought? If you go by the statement "Slow speed-resistance training induced a greater adaptive response compared to training with a similar resistance at 'normal' speed" from a paper by Mark D. Schuenke and his colleagues from the University of New England, the Rocky Vista University, the College of Health Sciences and Profession and the Ohio-University that was published in the October Issue of the Journal of Applied Physiology (Schuenke. 2012), it would seem so.

If you do however take a closer look at the actual results you realize how important the adjoining qualificatory remark "However, training with a higher intensity at 'normal' speed resulted in the greatest overall muscle fiber response in each of the variables assessed" really is. After all, the "intensity" is per definitionem 20-45% higher in a classic strength training regimen compared to the often laughed at slow-speed resistance training (SS), which was - at least in the study at hand - defined as follows:

• SS: 6-10 reps, super-slow (10s) concentric (no typo!) and slow (4s) eccentric TUT, 40-60% of the individual 1-RM

Both the traditional strength training (TS) as well as the strength endurance regimen (TE) to which this protocol was compared used a TUT of 1-2s on the concentric and eccentric phase, but differed in terms of the weight and rep-numbers, which were

• TS: 6-10 reps at 80-85% 1-RM
• TE: 20-30 reps at 40-60% 1-RM

So, based on the qualificatory remark and a short glimpse on figure 4 you already know that the TS regimen yielded the best results during this 6-week resistance-training program that targeted the quadriceps femoris muscle group, in a total of 17 training sessions (only 2 in the first week), which were supervised to ensure that the 34 young, untrained female participants went to positive failure within the targeted repetition range on all three sets of the three exercises (leg press, squats, and knee extension) they performed after brief warm-up with ~2 min rest between sets and exercises.

Figure 4: Changes in body composition (left) and changes in muscle fiber cross-sectional area (all expressed relative to group baseline; data calculated based on Schuenke. 2012)

What's still missing though is the effect on overall body composition, where the super slow regimen did in fact produce almost identical results, while the "pump" workout ... ah, I mean the "strength endurance workout" sucked here just as it did as far as its effect on the increase in growth the number of hypertrophy-prone type II fibers is concerned.

So what's the take home message here? If you want some diversity, you can incorporate super slow sets into your regimen... but do you have to? At least based on the results of the study at hand, which was unfortunately conducted with untrained young women (who by the way love this alternative training styles) and is therefore not exactly representative for the average advanced trainee, the answer is "rather not, no!"

What neither the advanced nor the rookie who is striving to improve his or her body composition should do, however, is to train in the hilarious strength endurance range of 20-30 reps per set. If you want to build muscular endurance you either go out sprinting, beat the punching bag or do plyometrics.

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As I know you, you still want more, hah? Well, too much volume is not good for you and in case you cannot wait until next week, there will be some intriguing exercise news in the days to come, probably more on the SuppVersity Science Round-Up with Carl Lanore, on the Super Human Radio Network on Thursday, this week and obviously every day on the SuppVersity Facebook Wall @ www.facebook.com/SuppVersity - like it and always be the first to now!


References:

• Beebe AM, Cua DJ, de Waal Malefyt R. The role of interleukin-10 in autoimmune disease: systemic lupus erythematosus (SLE) and multiple sclerosis (MS). Cytokine Growth Factor Rev. 2002 Aug-Oct;13(4-5):403-12. 
• Eisenstein, E. M., Eisenstein, D., & Smith, J. C. The evolutionary significance of habituation and sensitization across phylogeny: A behavioral homeostasis model. Integrative Physiological & Behavioral Science. 2001; 36, 251–265.
• Ho SS, Dhaliwal SS, Hills AP, Pal S. The effect of 12 weeks of aerobic, resistance or combination exercise training on cardiovascular risk factors in the overweight and obese in a randomized trial. BMC Public Health. 2012 Aug 28;12(1):704.
• Jenkins NT, Padilla J, Arce-Esquivel AA, Bayless DS, Martin JS, Leidy HJ, Booth FW, Rector RS, Laughlin MH. Effects of Endurance Exercise Training, Metformin, and their Combination on Adipose Tissue Leptin and IL-10 Secretion in OLETF Rats. J Appl Physiol. 2012 Sep 27. 
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"80-85% 1RM, 6-10 Reps"? Changes in Muscle Fiber-Type in Response to Classic, Super Slow and Light Training Confirm "Old School Training" Rules and Will Always Prevail!

Image 1: If you don't want to be strong and look good naked, you better not train like "old school" like Arnold, Franco Columbu (img), Dave Draper, Frank Zane & Co.

Although, I do assume that you just dropped everything, went home from work early, or simply did not leave the house at all to be able to listen to my appearance on Carl Lanore's Super Human Radio, yesterday, I know that sometimes more important things (whatever that may be) get into one's way and will thusly give you a second chance, today (click here to download the podcast)... well, so far for the humorous part of this post. Assuming that by now, you did listen to the podcast you should remember that I promised to have something about exercise and strength training in the news, today. And as Carl will probably assert, Super Humans usually stick to their promises, although - and I did mention that yesterday, as well - the number of significant studies, i.e. studies that do not involve frail elderly or morbidly obese people, is relatively scarce.

Bro, you know the revolutionary new "GHRWZAR-642421 training principle"?

Image 2: If you are looking for a collection of proven routines, instead of bunch of old hats with funky new names, the Blueprint would be a good choice.

Beside the fact that our interest in improving our health and the way we look by diet and nutrition is not getting all too much love in the major scientific publications, another factor, which in all fairness should not be forgotten is that we do actually know what works, don't we? Sleep, eat, train... with the "common wisdom" with respect to "what is the best diet" being in constant flux, I guess, we are simply expecting to see similarly paradigm changes in the realms of exercise physiology, but aside from the occasional letter salad people are trying to sell you as the latest and greatest new training technique, which then turns out to be the 1001 iteration of what the fathers of physical culture have been doing for ... I guess, centuries, would be correct... the basics, which are to pick up a heavy weight move it through time and space for about 6-10 reps and rack it, never change - for a good reason as the pretty detailed results of a freshly published (actually still ahead of print) study from Mark D. Schuenke and his colleagues just confirmed anew (Schuenke. 2012). 

Lifting heavy objects makes women ... dunno, but not bulky, to say the least ;-)

I guess, I better mention it right away in order to avoid that you get all to psyched out and are disappointed in the end: The study participants were 34 untrained young women (21.1 § 2.7 years). And just to make sure there are no misunderstandings, here - the downside for physical culturists is that these women were untrained not that they were women! The latter, is, as the scientists point out, actually an advantage, because "in pre-vious studies, it has been easy to find eager, untrained female subjects with excellent compliance to protocols", which by the way is another thing, Carl and I talked about in yesterday's installment of Super Human Radio ;-)

The reason that the subjects training status ("untrained") is somewhat of a downside, is yet that the early adaption which occur once you first pick up the weights, are fundamentally different from the painfully slow gains of an advanced trainee or elite athlete. In the end, the latter is yet also part of the reason that scientists don't recruit athletes for studies like this, after all the gains" (both strength- as well as muscle-wise) these subjects would have made over the course of the 6-week study period, in which the ladies in this study performed a total of 17 training sessions (two in the first week, three per week in the subsequent 5 weeks), would have been hardly "significant" - and in this case we are talking about both, statistical, as well as real-world significance.

Figure 1: Graphical illustration of the three experimental conditions / training regimen in the study.

Figure 1 should give you the general idea of the three different training regimen the women were randomly assigned to. With the first one being heavy + fast (TUT was in fact 1-2s for both concentric and eccentric part of the movement; verbal count was provided to make sure the tempo was correct) representing what has worked pretty well for generations of strength athletes, the second one being a variety of the Super Slow principle and the third one representing the "I don't want to build muscle"-approach to weight lifting that is unfortunately still very popular among women, we have the whole spectrum from tried and proven to tried and worthless in here ;-) I guess, it should be mentioned that the number of sets (3 sets, to failure) and the exercises, which were leg presses, squats and knee extensions (I suppose the latter is identical to "leg extensions", but I thought I rather stick to what Schuenke et al. wrote) were identical so that the effective parameters which influenced the study outcome were time-under-tension (TUT + reps) and intensity (% of 1RM) - or to make a long story short: Lift heavy and fast, give yourself a hard time by lifting slow or just pump away with lousy weights to "shape your body" (I hope you see the irony wrt to the last point).

Everyone who believes in "shaping your body with high reps and light weights" raise your hand!

I guess, for most of you it won't  come as a surprise, when I am telling you that there were no changes in total body mass in the course of this 6-week training intervention, but what I guess will be surprising is that the body composition of the women did not change either (cf. figure 2)!

Figure 2: Fat mass (in kg) and fat free mass (in kg) before and after 6 weeks with a total 17 leg training sessions (data adapted from Schuenke. 2012)

If you scrutinize the data in figure 2 you could make a point that there was a 0.1% increase here and a 0.025% decrease there, but I guess, even if you have no clue how those p-values, which indicate if the change in a measured parameter could be mere coincidence are calculated, it is quite obvious that none of these changes reached statistical, let alone real-world significance.

If we take a closer look at what happened "inside" the vastus lateralis muscle from which the scientists took muscle biopsies before and at the end of the study period, it does yet become obvious that our "conventional exercise wisdom" is in fact much more reliable than its nutritional counterpart.

Figure 3: Changes in relative fiber composition in vastus lateralis muscle in response to 6 weeks of leg training with different loading / TUT / rep schemes (data adapted from Schuenke. 2012)

As you would expect, the muscle fiber-types shifted according to the load and the TUT / reps that were used with a generally more pronounced increase in the still highly glycolytic type IIA and type IIAX fibers in the classic standard RT group and a shift towards a more oxidative type II fiber type (type IIC) in the super slow group. As those of you who have read the Intermittent Thoughts on Building Muscle will know, the former precipitates both strength and size gains, while the latter would be something a "strength-oriented endurance athlete", as maybe a rower, could be interested in. What all three training regimen have in common though, is the decrease in the exclusively glycolytic type IIX fibers, of which those of you who have followed the aforementioned series will know that they are quasi-nonexistent in elite bodybuilders.

Training light does work, but does not really do the job

What is also noteworthy, is that the light, yet fast training with high reps, induced what you may call a "transition status", with initial changes in the type IIX fibers (becoming type IIAX), but without the a complete switch from the "unflexible" glucose guzzling type IIX fibers to the cornerstones of strong and big muscles - the type IIA fibers. In view of the fact that the scientists did not quantify the strength gains and that the "higher growth propensity" of type IIA fibers is somewhat of an urban myth, the study outcome with the greatest real-world significance is unquestionable the increase in fiber size, which, as the data in figure 4 goes to show was maximal in all three major fiber types in response to the classic training protocol.

Figure 4: Changes in cross sectional area of the different fiber types (data adapted from Schuenke. 2012)

If that is not enough to convince at least the male part in the audience that there is good reason that the good old "6-10 reps in the 80-85% 1RM range" is still around, I guess they must be beyond help... and as far as the ladies are concerned: I know you don't "wanna get big", but let me tell you this - "strong is the better sexy", and as Carl Lenore would probably add "muscle is metabolic currency". So, if you want to stay mobile into your old days, do your joints and bones a favor by strengthening them in time. Moreover, with the mitochondrial powerhouses in full-gear, a few fixes to your diet should suffice to make those "problem areas" not magically, but gradually disappear.

Apropos diet, while the subjects did not have to log their calorie let alone macronutrient intake, I would bet that with a simple protein shake after their training and some general tweaks to their diets, those favorable changes in body composition, i.e. decreases in fat and increases in lean mass, which are at the heart of "looking good naked" would have come about... with the "I love my pasta and red-meat gives you cancer"-diet from the latest cosmopolitan, on the other hand, you better stick to baggy jeans and huge sweaters instead of bikinis and speedos, ladies and gentlemen ;-)

Ripped & Buffed vs. Skinny and Sinewy: Training Velocity, not Load, Appears to be Sole Determinant of Exercise Induced Shifts from Slow- to Fast-Twitch Muscle Fibers.

Image 1: Who would you like to be?
And how do you train to achieve
his physique?

Sprinter or marathon runner? Ripped and buffed or skinny and sinewy? Although this is, after all, a question of muscle vs. fat, bone and tissue mass, it is upon closer examination as much a qualitative question, as it is a quantitative one - a question that may well be influenced by the way you train!

Unlike our adipose tissue which has almost unlimited capacity to grow, the size of our muscles appears to limited by a number of factors, among which the individual fiber-make-up, i.e. the ratio of slow-oxidative endurance-type fibers (type I) to fast-twitch type IIA (fast-oxidative glycolytic), and fast twitch IIX (fast glycolytic) seems to play an important role, when it comes to getting big and buffed or skinny and sinewy.

Figure 1: Slow- and fast-twitch faber composition in athletes and non-athletes (data based on Carrol. 1998; Widrick. 2002)

As the data in figure 1 goes to show, athletes, unlike untrained individuals, who have about the same amount of fast and slow-twitch fibers, exhibit discipline specific adaptations in muscle fiber composition, with sprinters having the lowest and middle distance runners the highest ratio of slow to fast twitch muscle fibers. According to data from Aagard and Andersen, Bergh et al. and Fry et al. (Berg. 1978; Aaagard. 1998; Fry. 2003), the range of slow to fast twitch fiber ratios extends from ultra-endurance runners with a 90:10 slow to fast twitch ratio down to weight lifters and sprinters with a minimum of 20:80 slow to fast twitch fiber ratio.

Muscle fiber type and weight loss: Contrary to what you may have guessed, or read elsewhere, obese patients with a higher amount of oxidative slow-twitch fibers have been shown to lose weight easier than their "heavier muscled" peers. In a 2002 study Tanner et al. report (Tanner. 2002):

With weight loss intervention, there was a positive relationship (r = 0.72,P < 0.005) between the percentage of excess weight loss and the percentage of type I fibers in morbidly obese patients. These findings indicate that there is a relationship between muscle fiber type and obesity.

Image 2: For someone who already got morbidly obese, a higher ratio of type II fibers may well be counter-productive if his/her overall goal is weight loss.

Another result of the same study, which could easily be misinterpreted as politically incorrect is the genetically determined higher raio of type II muscle fibers within the African American part of the female study population, which made it increasingly harder for these women to burn the fat. And just in case, you still wonder why a type I fiber, something obviously only skinny people have in excess would help with losing fat, just think about the term "oxidative muscle fiber" for a moment, then add to that the experimental observation that type I fibers have greater mitochondria volume densities than type II fibers (Sullivan. 1978) and you will realize that a highly oxidative muscle fiber is more valuable when it comes to burning fat than a glycolitic one, reagardless of whether or not the latter may "look" better ;-)

In a recent review of the literature Wilson et al. provide the following biological explanation for the differences that exist between endurance and strength athletes (Wilson. 2011):

[...], type I fibers have been observed to have both greater mitochondria volume densities as well as capillary-fiber contact length when compared to type II fibers.  In addition, mitochondria volume density was highly correlated (r = 0.99) with O2 diffusion coefficients across three different muscle groups (retractor, sartorius, soleus) suggesting greater aerobic capacity in type I fibers.

While type I muscle fibers will thus figuratively carry their owners in 80 days around the world, type IIX and IIA fibers exhibit a 10x and 6x greater peak power and a 4x and 3.3x greater contractile velocity than their oxygen-hungry slow twitch cousins.

Figure 2: Relative peak power and contractile velocity of fast twitch fibers vs. slow twitch fibers (data based on Wilson. 2011)

The reason that the two guys from image 1 do not only perform but also look completely differently, lies yet in the greater capacity of type II fibers for exercise-induced hypertrophy (Schoenfeld. 2000). The relative number of type II to type I fibers is thus of paramount importance, if you want to look like a sprinter - not like a marathon runner and if you want to lift heavy weights instead of running cross-country. Fry et al., for example found strong correlations (r = 0.94; almost "causative") between the percentage of type IIA fibers and 1 repetition max snatch performance in national caliber Olympic athletes (Fry. 2003). Now the obvious question is: "How can I influence my individual fiber composition, or is this simply genetically determined?"

It stands to reason that genetics is a major determinant of fiber composition, but, hardgainer or not, with appropriate training and nutrition everyone can - at least to a certain degree - shift his muscle fiber make-up from a slow-twitch oxidative to a fast-twitch glycolytic type, even without the use of clenbuterol and other beta-2 agonists which hav been shown to trigger respective shifts from type I to type II muscle fibers in a rodent model (Zeeman. 1988).

Training for shifts in fiber composition

From Wilson et al.'s review of the literature it becomes quite obvious that standard exercise regimen, like jump squats at either 30% or 80% do not provide satisfactory results for someone looking to increase the number, not the size of his glycolytic muscle fibers (Wilson. 2011). In a study by Liu et al. (Liu. 2008), a 5x3RM bench press protocol, performed 3 times per week for 6 weeks, on the other hand, triggered a shift within the type II fibers. It increased the percentage of type IIA fibers from 44.9% to 66.7%, but decreased the type IIX fibers from 33.4% to 19.5%, thus leaving the percentage of slow twitch type I fibers unchanged. A second group from the same study who used a more versatile routine, with the same 5x3 regimen on Mondays, 10x concentric-repetition bench press throws at 30% of their 1RM on Wednesday and 10 stretch-shortening type push-ups on Friday for 5 sets, each, were able to increase the number of type IIA muscle fibers (from 47.7% to 62.7%) without decreases in the number of type IIX fibers, but a profound -50% reduction of slow-twitch oxidative fibers (from 18.2% to 9.2%). Wilson et al. go on and cite several other studies that were able to show the modulatory (increase in type II, decrease in type I) effects of high-velocity contractions on muscle fiber composition (Wilson. 2011) and corroborate that results with findings from other studies which corroborate these results with ...

[...] findings that the percentage of type I fibers may be increased with various types of aerobic training protocols such as endurance cycle training (+12% Type 1) and long distance running (+17% Type 1), [where, on the other hand] studies indicate that sprint training may facilitate the change of slow twitch fibers to fast twitch fibers.

Interestingly, Hortobagyi et al. were able to show that laziness taken to the extreme, i.e. 3 weeks of knee immobilization, also reduced the amount of type I fibers (-9%) and increased the number of type IIX fibers (+11%) in 48 recreationally active men and women (Hortobagyi. 2000). These results should yet be treated with appropriate caution and I would strongly advice against lying on the couch to increase your propensity for muscle growth by decreasing the number of slow twitch and increasing the number of fast twitch muscle fibers, because "recreational activity", for most people, consists of aerobic type of exercises, playing soccer, tennis or whatever - all sports that by and out of themselves would trigger shifts towards a more oxidative (predominant type I) muscle composition. It is thus not surprising that refraining from such activities for 3 weeks would reverse those changes.

So how should you train, then?

In view of the paramount importance of speed, not load in the few experiments which challenge the hitherto established paradigm that muscle fiber composition was largely determined by genetics and transformation was possible only within type II fibers, i.e. from type IIA to type IIX and vice versa, the incorporation of respective training techniques, e.g. concentric-repetition bench press throws at 30% of your1RM, as they were used in the study by Liu et al. (Liu. 2008), into a more versatile hypertrophy-specific routine which would

1. trigger a hypertrophy response, on "classic" strength training days (like 3x5 or 3x8-10), and
2. increase propensity for growth, on "speed-rep" days with exercises like plyometric push-ups, concentric-repetition bench press throws at 30% 1RM, etc.

would appear to be the most reasonable way to train for anyone out there, who does not belong to the "genetic elite" of born sprinters.