Understanding Muscle Hypertrophy - Study Sheds More Light on Process of Satellite Cell Recruitement: SRF, IL-6, STAT3, COX2, IL4 + More Funky Acronyms With Important Roles in the Structural Component of Muscle Growth.

No pain inflammation, no gain? In the long(er) run this could in fact be true.

All of you who followed my advice to "like" the SuppVersity Facebook page and are thus keeping up with the numerous additional news I am posting there, should actually have seen the news item on the non-significance of the exercise-induced interleukin-6 (IL6) response for the exercise induced improvements in glucose metabolism (read more). The mere fact that the glucose metabolism of IL6(-) mice, which are mice who simply cannot express IL6, is still improved by "working out" does yet by no means preclude that the demonized cytokine does play a fundamental role in the exercise-induced systemic and local benefits. In fact, an even more recent rodent study would suggest that a certain degree of inflammation and the respective increase in IL6 immediately after a workout is even essential for persistent skeletal muscle hypertrophy.

As you may remember from the Intermittent Thoughts on Building Muscle Series there is more to skeletal muscle hypertrophy than the simple messages such as "increases protein synthesis by X%" that are printed in shiny letters on the boxes of hundreds of the currently available "natural muscle builders" on the real and digital shelves of the supplement vendors. One of these "mores" is the recruitement of satellite cells, muscle stem cells that are incorporated into the musculature to replace damaged myonuclei or increase the myonuclear density to allow for greater protein accretion (learn more).

Decreasing domain sizes = better function + higher growth propensity

"Hold on those are rodents and rodent studies are not relevant!" While it is a good thing to critically assess whether the results of a certain study can be species specific. The contemporary practice to question all rodent studies which are not part of your own cherry picked arsenal is getting onto my nerves. So, please check out the pretty analogues (short term unfortunately) human study by McCay from 2009 (McCay. 2009), before you stop reading after spotting the word "rat" in this article.

It is this process of satellite cell activation and incorporation of which Gwenaelle Begue and her colleagues from the University of Montpelier have now confirmed that it depends on the activation of the IL-6/STAT1/STAT3 signaling pathway in a prolonged 10 weeks resistance training scenario. In the course of the latter,  36 male Wistar rats were randomly assigned to one out of the following six groups:

• CTL2, CTL4, CTL10 (CTL = non-training controls, n = 6 in each group) and 
• TR2, TR4 and TR10, which were rats trained for 2, 4 and 10 weeks. 

The rodents in the TR-X groups were supposed to climb an apparatus with initially 50% later up to 210% of their body weight strapped to their back, five times a week. The load was increased every two days, if the rodents still managed to do "10 reps" = climb 10 steps and reached quite impressive levels of 120% of the body weight after two, 150% of the body weight after four and 210% after ten weeks of training.

Where is the rodent squat machine?

No rodent squat in the study at hand, but the "stair climbing" is a better full-body workout, anyways.

Now, this may not be as "realistic" a program as the rodent squat Aguiar et al. used in their 2013 study, but is is - and this is interesting - very similar to a test that has been done by many researchers with myostatin negative mice. As you will remember from the Intermittent Thoughts on Building Muscle Series (click here to read the pertinent part) those heavily muscled mice are unable to lift their own bodyweight, mainly because of the fact that the myonuclear domains within their muscle grew beyond a threshold where they absence of an adequate number of myonuclei per volume unit enders the muscle useless.

"Healthy" muscle growth does therefore require both, protein synthesis (increase in volume), as well as structural adaptations, so that the domain size does remain constant - at least!

"10 weeks of resistance training did not affect the myonuclear domain"

Against that background the last subheading, which is in fact a direct citation from the full text of the Begue paper is - contrary to what a non-SuppVersity reader could believe - good news. Very good news, to be precise:

Figure 1: Changes in fiber type ratios (left), cross sectional diameter according to fiber type (middle) and  fiber area per myonucleus (right; Begue. 2013)

As you can see in figure 1 (right hand side), there was even a small, yet statistically non-significant decrease in the fiber area each myonucleus had to control and that despite quite impressive increases of 77%, 92% and 100% in the cross-section of the type-I, type-IIa and type-IIx fibers of the animals (figure 1, middle).

Satellite cell recruitment, necessary of optional if you want to get big?

In this context, Begue et al. speficially point out that the "recruitment of additional nuclei derived from SC incorporated into muscle fibers" occurs parallel to the better known "resistance training induced enhancement of protein synthesis" that occurs "after the training session and last[s] up to 24–48 h in humans" (Bengue.2013). 

"Indeed, several works in humans have evidenced an increase in the number of myonuclei per fiber when fiber size increases approximately more than 25% (Kadi. 2004; Petrella. 2008). Thus, the myonuclear domain (i.e. the theoretical amount of cytoplasm supported by a single myonucleus in a muscle fiber) remained constant although a large increase in fiber CSA via the addition of SC-derived nuclei occurs." (Begue. 2013)

Since estrogen plays an important role in the regeneration of the satellite cell pool, it's pretty likely that you can literally "SERM your growth potential away" (learn more)

Notwithstanding the heavily quoted results of the 2011 study by McCarthy et al. in which the reasearchers were able to demonstrate that rodent muscle can grow even when it is satellite cell depleted, my personal conviction is that the latter process, i.e. the incorporation of new (not just even the replacement of damaged myonuclei is an obligatory prerequisite for persistent gains.

With +40% increased domain sizes, after only two weeks, it would have been interested to see how things would have developed in the subsequent weeks. I bet(!), the normal mice would have kept growing while their satellite cell depleted peers would have hit a plateau, where their own body woul have pulled the emergency brake aka myostatin (in this context, it's also interesting to remark that myostatin stops the proliferation of satellite cells and does thus indirectly divert the existing ones towards differentiation and incorporation into the muscle, cf. figure 2)

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Bottom line: The study at hand delivers further evidence for the intimate connection between "inflammation" or rather the expression of the still demonized inflammatory cytokine interleukin-6 and the incorporation of "fresh" satellite cells into the muscle. With the latter being a necessary prerequisite to keep the domain sizes within functionally optimal limits while the cross section of the fibers is expanding (the muscle is growing), it is likely an (I want to emphasis that!) not yet disproven that continuous muscle growth requires satellite cell recruitment.

Basically you can think of it like the Army. While it is (or at least has historically been) relatively easy to find any recruits (=increase protein synthesis), people who are qualified to become officers and coordinate the actions of the rank and file are hard to find and without an adequate number of them you will end up with a chaotic mess instead of a powerful army. That's actually pretty much what happens to the myostatin negative mice, who may be able to recruit officers,... ah, I mean to recruit satellite cells, but simply outgrow the maximal pace of satellite cell incorporation.

Figure 2: IL-6 is the first myokine you should remember, it "wakes" the quiescent satellite cells up, he COX-2 activated IL-4 is myokine #2 and initiates the differentiation / incorporation process which will eventually result in the formation of a new nucleus. .

What, oh yes, of course! I had almost forgotten the unfortunately quite complicated connection to IL-6. If you take a parting look at the figure on the right, you will realize that a diagram explains things much better than I could. In fact, the "motor" of the whole growth business is the contraction induced expression of serum responsive factor, of which Guerci et al. have found in 2013 that it is the previously missing link between muscular contractions on the one hand and the expression of myokines, who happen to be the same molecules we know as "inflammatory cytokines" in other contexts. Il-6 and the COX-2 activated IL-4 are then getting things rolling (Guerci. 2013)... what? No, I cannot tell you whether taking antioxidants will block that, but I can promise you that you will learn more about this tie-in within the next 7 days, so stay tuned ;-)

What I can tell you in advance, though, is that strength and size gains of IL-6(-) mice are compromised (Serrano. 2008). So even if I would have to qualify my previous statement that satellite cells are necessary for continuous growth - one thing is sure: Their activation by IL-6 is necessary for optimal growth.

References:

• Begue G, Douillard A, Galbes O, Rossano B, Vernus B, Candau R, Py G. Early Activation of Rat Skeletal Muscle IL-6/STAT1/STAT3 Dependent Gene Expression in Resistance Exercise Linked to Hypertrophy. PLoS One. 2013;8(2):e57141. 
• Guerci A, Lahoute C, Hébrard S, Collard L, Graindorge D, Favier M, Cagnard N, Batonnet-Pichon S, Précigout G, Garcia L, Tuil D, Daegelen D, Sotiropoulos A. Srf-dependent paracrine signals produced by myofibers control satellite cell-mediated skeletal muscle hypertrophy. Cell Metab. 2013 Jan 4;15(1):25-37.
• Kadi F, Schjerling P, Andersen LL, Charifi N, Madsen JL. The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol. 2004; 558: 1005–1012.
• McCarthy JJ, Mula J, Miyazaki M, Erfani R, Garrison K. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle. Development. 2011; 138: 3657–3666
• McKay BR, De Lisio M, Johnston AP, O'Reilly CE, Phillips SM, Tarnopolsky MA, Parise G. Association of interleukin-6 signalling with the muscle stem cell response following muscle-lengthening contractions in humans. PLoS One. 2009 Jun 24;4(6):e6027. doi: 10.1371/journal.pone.0006027.
• Petrella JK, Kim JS, Mayhew DL, Cross JM, Bamman MM. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol. 2008. 104: 1736–1742
• Serrano AL, Baeza-Raja B, Perdiguero E, Jardí M, Muñoz-Cánoves P. Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy. Cell Metab. 2008 Jan;7(1):33-44.

Exercise Science - True of False? Large Muscles First for Growth? Cooling Works Before & After Workouts? Senior Olympians Have Healthy Bones? Hypoxia + HIT = WIN?

I know it's difficult to resist guys, but first things first: Study confirms, you better train the large muscle groups of the upper body first, before you go progress to what many of you probably love the most... no, not what you think now, I am talking about training arms ;-)

I know that you probably think that I had forgotten about the exercise science quickie I announced in Saturday's installment of On Short Notice. Today's SuppVersity article is written proof that this is not the case. With topics that range from the redundancy of hypoxia training and intense workouts and the beneficial effects of training the large muscle groups first in your workout to the usefulness of the internal and external application of cold water and other stuff before and after workouts to elicit performance gains and speed up recovery and the unique benefits only heavy resistance training has to offer to elderly bones, I'd hope that everybody will find at least one item he / she is interested in.

And in the fortunate case that you know all the "right" to the true or false", already, you may want to pick up a couple of recent SuppVersity Facebook news to satisfy your cravings.

Adding hypoxia on top of already intense workout is probably useless

(Holis. 2013) -- No further improvement if intensity is already high!? Yep, that's at least what a recently published study by scientists from the University of Exeter would suggest. The researchers subjected 9 physically-active male participants to three weeks of intensive single-leg knee-extensor exercise training.

Erratum: Other than I initially wrote the study used identical training sessions for both legs with the sole difference being that one was trained under hypoxic and the other under normal oxygen conditions for 25 minutes (no cuffs here, thx David for the heads-up!).

Suggested read: A brief summary of a summary o the current state of the art as far as blood flow restricted (BFR) / Kaatsu training is concerned (read it).

When they evaluated the results, Holis et al. found that neither the most straight forward parameter, namely the time-to-exhaustion during incremental exercise nor the changes in muscle metabolite concentrations during the workout were significantly different between the leg that was trained under normal and that which was trained under hypoxic conditions. Now this does not necessarily mean that there may not be minimal or other benefits you could derive in the long run (I am thinking about mitochondrial biogenesis) by making an already intense routine even more intense by training under hypoxic conditions. However, if there was such an effect, it is  probably going to be minuscule and certainly not something anyone, but an Olympic athlete would benefit from.

Large muscle groups first! Common BB-wisdom confirmed once again

(Simã. 2013) -- You've certainly heard about the "growth promoting effects" of squats, deadlifts etc., right? Of course you have! And as a diligent student of the SuppVersity you will also be aware that this growth promoting effect is supposed to be the result of the workout induced endocrine response.

Want another Exercise Science Quickie? What about news on light training with high TUTs, the HIIT vs. Liss Formula for more T, DHT & cortisol and the effects your left leg has on your right one (learn about all).
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"The results indicate that the GH concentration increased after both sessions, but the increase was significantly greater (p < 0.05) after the sequence in which larger muscle-group exercises were performed prior to the smaller muscle-group exercises. No differences were observed between sessions for TT [total testosterone], FT [free testosterone], SHBG [sex hormone binding globulin], C [cortisol], or the T/C [testosterone / cortisol] ratio at baseline or immediately after resistance exercise. These results indicate that performing larger muscle-group exercises first in an upper-body resistance-exercise session leads to a significantly greater GH response." (Simã. 2013)

Don't worry I am not going to discuss for the 1003rd time, whether the absence of any hormonal difference outside of the increased growth hormone response is good or bad for your gain. I just want your to memorize that the GH response corresponds with the workout volume, which was significantly higher, when the 20 male subjects trained the large muscle groups of the upper body before the smaller ones. So even if it was only a question of workout economy, the longstanding rule of thumb to train large muscle groups first would obviously still have its place in today's in parts sometimes ueber-scientificated workout planning.

Competitive sports is not a good means to protect your bone mineral density

(McCory. 2013) -- According to the latest study from the University of Pittsburgh Clinical and Translational Research Center old the mere participation in regular (intense), bot not strength specific physical activity alone does not offer any protective effect against age induced bone loss.

"Our results imply that participation in highly competitive senior athletics does not have a protective effect on BMD, perhaps because of a lower bodyweight or other confounding factors." (McCory. 2013)

Among the parameters which did apparently figure were (you guessed it) bodyweight, and calcium and vitamin D intake. The higher those three parameters were the better the bone mineral density.  Plus: The knee extension peak torque explained another 3.4% of the variance, but only in the hips.

Taking calcium supplement has been associated w/ prostate cancer and CVD in some, but not all studies (Baron. 2005; Spence 2013) With up to 14x elevated lead levels in some OTC calcium supplements the differences may well depend on whether you pick the wrong one (learn more).

That being said I personally believe we'd have seen very different study outcomes if the researchers had not made the common mistake of confusing "sports" with endurance exercise and would thus not have narrow-mindedly focused on those participants of the "Senior Olympics", who competed in running events longer than 400 m (n = 44; 28 males, 16 females), cycling events longer than 5K (n = 17; 11 males and 6 females), and any swimming event (n = 43; 25 males and 18 females). After all, a very recent study from the Catholic University of San Antonio did just confirm that high resistance circuit training (HRC) and heavy strength training can improve the bone mineral density in an elderly population (Romero. 2013).  And what's more, the high resistance had the added benefit of inducing significant improvements in body composition in the thirty-seven healthy men and women (61.6±5.3years) who participated in the randomized trial.

Is cooling a useful tool for performance recovery?

(Poppendieck. 2013) -- According to the latest review by scientists from the University of Saarbrücken, Germany, "the average effects of cooling on recovery of trained athletes were rather small (2.4%, g=0.28)" (Poppendieck. 2013) With a peak in performance increase roughly 4-days after the initially exercise bout and the greatest benefit being observed with endurance athletes, it does also look as if there were particular subgroups of athletes who'd benefit most: Those expose their bodies to several high intensity stimuli within a relatively short timespan, namely.

What about pre-cooling, then? With average performance increases of +8.6%, +6.0% and +4.2% endurance athletes performing open-end tests, graded exercise tests and time trials are the ones who benefit most. Similar effect was observed for intermittent sprints (+3.3%, g = 0.43), whereas performance changes were smaller during short-term, high-intensity sprints (−0.5%, g = 0.03). Across all sports included in the most recent review of the literature (Wegman. 2013), cooling the musculature before a training session will have a larger effect on performance in hot (+6.6%, g=0.62) than in moderate temperatures (+1.4%, g = 0.004).

The most promising cooling methods were cold drinks (+15.0%, g= 1.68), cooling packs (+5.6%, g = 0.70) and a cooled room (+10.7%, g = 0.49), whereas a cooling vest (+4.8%, g = 0.31) and water application (+1.2%, g = 0.21) showed only small effects. Regardless of the method, the best trained subjects (highest VO2Max) saw the greatest benefits.

For those who want to try it and don't have access to a cryotherapy chamber (effect +3.8%), I'd recommend to go "hard core" and do - irrespective of which muscle group you may have been training - a full-body water immersion. The latter has been shown to be 70% more effective than water immersion of individual body parts. The use of icepacks, on the other hand, will rather compromise than promote recovery (-1.4%).

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Two bad, one good news: The first bad news is that this was it for today - at least if you don't count the facebook news that are already available, e.g.

• Black cohosh for breast cancer prevention? The jury is still out there (learn more)
• Adiponektin does not work in women? With a low type II fiber count and correspondingly lower receptor density it is at least not as effective as in men (learn more)
• Whole grains taste like sh*t? That's at least what the participants of a recent epidemiological study thing and probably also the reason they won't eat them (learn more)

as well as as those I am still going to post within what probably would count as "today" at least for some of you.

These pics are more than 2 weeks old and I can tell you that Adelfo's "anatomy chart" physique has kept improving ;-)

The 2nd bad news is that there won't be a SuppVersity Science Round-Up tomorrow. I had hoped that my voice would recover, but since it failed me several times in the cause of the day, I heavily doubt that you would understand anything I would be grunting into the phone, anyway.

But don't worry, there is also good news. Tomorrow is one of those "every other week" Thursday's where Adelfo Cerame is "in the house" and will (at least that was the pan last week) fill you in on the differences between the current and previous content preps... and I can assure you that's going to be a post even those who are not planning to compete will probably find very useful (I hope you read this Adelfo, 'cause I am just rising the bar, here ;-)

References:

• Baron JA, Beach M, Wallace K, Grau MV, Sandler RS, Mandel JS, Heber D, Greenberg ER. Risk of prostate cancer in a randomized clinical trial of calcium supplementation. Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):586-9.
• Holliss BA, Fulford J, Vanhatalo A, Pedlar CR, Jones AM. Influence of intermittent hypoxic training on muscle energetics and exercise tolerance. J Appl Physiol. 2013 Jan 10. 
• McCrory JL, Salacinski AJ, Hunt Sellhorst SE, Greenspan SL. Competitive Athletic Participation, Thigh Muscle Strength, And Bone Density In Elite Senior Athletes And Controls. J Strength Cond Res. 2013 Feb 25. 
• Poppendieck W, Faude O, Wegmann M, Meyer T. Cooling and Performance Recovery of Trained Athletes - a Meta-Analytical Review. Int J Sports Physiol Perform. 2013 Feb 02.
• Romero-Arenas S, Blazevich AJ, Martínez-Pascual M, Pérez-Gómez J, Luque AJ, López-Román FJ, Alcaraz PE. Effects of high-resistance circuit training in an elderly population. Exp Gerontol. 2013 Mar;48(3):334-40.
• Simão R, Leite RD, Speretta GF, Maior AS, de Salles BF, de Souza Junior TP, Vingren JL, Willardson JM. Influence of upper-body exercise order on hormonal responses in trained men. Appl Physiol Nutr Metab. 2013 Feb;38(2):177-81.
• Spence LA, Weaver CM. Calcium intake, vascular calcification, and vascular disease. Nutr Rev. 2013 Jan;71(1):15-22.
• Wegmann M, Faude O, Poppendieck W, Hecksteden A, Fröhlich M, Meyer T. Pre-cooling and sports performance: a meta-analytical review. Sports Med. 2013 Jul 1;42(7):545-64.

Farmer's Walk or Squat, Tire Flip or Bench Press, Stone Lift or Seated Row - Is Strongmen Training as "Anabolic" as Classic Hypertrophy Training and Which is "Best"?

Is he (or she?) going to be muscular when he grows up, or is this kind of exercise just making him strong?

I guess we all know that the most muscular guys are not necessarily also the strongest men in the gym - but why is that the case? And moreover, how does this fit in with the notion that you'd have to use heavy weights to induce skeletal muscle hypertrophy? Yeah, I know. Many scientists believe that's nothing but "broscience" (cf. Burd. 2013) and if you look at the muscle fiber composition of a bodybuilder in this previously published article, you will see that it is by no means type II and thus "strength-specific". And let's be hones does not the advent of blood flow restricted training signify that we are about to witness a "paradigm change"? With the classic approach (heavy weight and 8-10 reps) being on the upper end of a "optimal growth continuum"?

Notwithstanding this contemporary trend towards "making light weights heavier" (let's be honest, BFR for example does exactly that), a group of researchers from the Health and Human Performance Laboratory at the Hofstra University and the Gridiron Training Facility in Hempstead, New York, did actually dare to "waste" their time on research on the opposite extreme of the heavy vs. light lifting divide.

Don't forget: The paradigm determines the research design

Before we delve further in to the methodological issues, let me briefly get one thing straight. Ghigiarelli and his colleagues firmly believe in the significance of the immediate and early endocrine response to a workout. They specifically cite the work from Stuart Phillips lab, I have been referring to numerous times times, but (and this is science, guys!) politely disagree with the conclusion that the relationship between elevated endogenous testosterone levels and hypertrophy function was non-existent or at least irrelevant, stating that...

Suggested read "Anabolic Workouts Revisited"

"[...] a much larger body of evidence supports the integral role that the acute hormonal response to RE [resistance exercise] has on muscle hypertrophy (Schoenfeld. 2010; Vingren. 2010) and its role in strength training adaptation (Hansen, 2001;Kvorning. 2006). Those in support of an endogenous testosterone response stand by the belief that RE causes an initial downregulation on AR content in the target tissue (i.e., skeletal muscle) followed by a subsequent upregulation during the recovery period, thus increasing free testosterone uptake facilitating protein synthesis." (Ghigiarelli. 2013)

It is therefore not a design flaw, when the scientists take the acute testosterone response to the workout as a measure of it anabolic potential and speculate that a strongmen-esque workout, which engages much more muscle fibers than even a compound based bodybuilding workout does, would elicit a stronger hormonal response than a "classic" hypertrophy training (additional read => the Saturdaily installment of On Short Notice) .

Real trainees, real workouts, real (?) results?

To probe their hypothesis the scientists recurited trained athletes from various athlete backgrounds. The mean age of the

• tan recreational strength trainees (>4 training sessions per week, >2 years of training),
• one wrestler and one football player, 
• two competitive bodybuilders, 
• one competitive powerlifter and one competitive o-lifter

was 24 years, whose mean 3-RMs , i.e. the weight the participants can maximally perform for 3 reps, were 161kg for the squat and 126kg for the bench press.

Main result: Not superior, but "similar"testosterone responses

I guess, when you read the word "similar" (which is a real quotation from the full text) in the above subheading and take a loot at the actual data in figure 1 some of you may not without good reason complain that Ghigiarelli et al. use the word "similar" pretty generously.

Figure 1: Salivary testosterone response to immediately after (post) and 30 min after work-matched classic hypertrophy,  strongmen and mixed routines (Ghigiarelli. 2013)

If you look at the raw data on the left, it does after all look as if the classic hypertrophy workout with its squats, the leg presses, bench presses and seated rows was way more "anabolic" than

• its strongmen counterpart that consisted of tire flips, chain drags, farmers walks, keg carries and stone lifts, 

• the mixed protocol which was build around tire flips, squats, chain drags, bench presses and stone lifts 

when all exercises were performed for 3 sets x 10 reps with 75% of the weight the subjects could lift... and what should I say? You are right!

"Hold on! I don't see any 'similar' response!?"

What the average data in figure 1 (left) does yet not convey, are the large inter-individual differences. If you take those into account and use some statistical shenanigan to compensate for differences in the workout duration and the individual exercise intensity (whatever that may be, see Steele's recent paper on the absence of a clearcut definition of "intensity"), the superiority does turn into "a nonsignificant trend of greater testosterone release after the H protocol" (Ghigiarelli. 2013) - a trend, the researchers ascribe to the "abnormal response" they observed in response to the hypertrophy training (abnormal as compared to other studies, where the reponse hypertrophy training is usually in the 70% range, as well), which in turn would be attributable to 6 high responders with extreme spikes testosterone spikes of 165-493%.

Does true mastery of the exercise determine skeletal muscle anabolism?

Usually outliers like that are a problem, but sometimes there are cases where the exception from the rule has the greatest explanatory value and in this case, the latter may well be the case. How come? Well, the two hypothesis Ghigiarelli et al. come up with to explain the differences is simply too attractive to discard it as being irrelevant. Firstly, the scientists believe that it would be plausible that the anxiety level due to the unfamiliarity of strongman lifts may have reduced the testosterone spike.

You have no goals or don't track your results? Huge mistake (learn why)!

"This possibility is supported by previous literature examining the hormonal responses to different RE protocols in seasoned trainers (Beaven. 2008). Beaven et al. suggested that the novelty and stress of the situation are likely to be perceived based on experience. Thus, the stressors of the ST and XST sessions and the lack of familiarity of the exercises can suppress the actual physical nature of the stimulus. This psychological nature of the hormonal response in our subject pool may have caused a different response to protocols with which they were unfamiliar with or disliked." (Ghigiarelli. 2013)

Now, if you go one step further and expand on this idea by involving my mantra that training is not about moving weights from point A to point B and rephrase all that using a term Nicolas Burd et al. mentioned in their recent review in Applied Phyisology and Nutrition, in which they advance the idea that it does not really matter on which extreme of the low vs. heavy weight continuum you train, as long as your protocol elicits "high intensity contractions" (Burd. 2013), you could also argue that the subjects may have moved the weight for 3 sets of 10 when they did the farmer's walk etc., but did not to so using "high intensity contractions".

The intensity of the contraction determines the gains

Knowing the "101 of Pre Workout Protein Supplementation" can make a difference. Over all the supplement shenanigan many trainees do yet tend to overlook the basics and simply  assume that as long as they move weight from A to B the use of the right powders and popping the right pills at the right times would have the largest impact on their results - big mistake!

In other words, the calculated "intensity" and the real muscular tension, i.e. the intensity of the contraction, were not identical and certainly sub-optimal for those of the trainees who have never flipped tires or carried kegs before. The bodybuilders and certainly also most of the recreational athletes may well have been so focused on the novel exercise that they could not pay any attention to the one thing that's at the bottom of skeletal muscle growth the "high intensity contraction".

Now, it is probably undebatable that the actual work that is done by the muscle and not the physical work, you would calculate by multiplying the weight (respectively the force you would apply to it in an ideal scenario) and the length of the way along which you dragged, carried or flipped it, is the physiologically relevant number here. In this context it would also be irrelevant, if the endocrine response to a workout does actually correlate with the net gains in muscle size or strength, as long as the "intensity of the contraction" did. In the end, it is thus not the weight or the exercise that determines the actual growth stimulus, but rather your ability to use a given weight in a given exercise to induce those damn high intensity contractions.

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Bottom line: For 90% of the trainees out there, the first step to improve their gains would thus to improve their game. To take the true meaning of "training", of which the venerable Oxford English Dictionary says that it is  "the sustained instruction and practice (given or received) in an art, profession, occupation, or procedure, with a view to proficiency in it." (OED Online. 2013). For the majority of trainees I see at the gym, it would thus be much wiser to follow Adelfo Cerame's recent advice and focus on a handful of exercises, instead of hopping from one exercise to the next, whenever a study says: Subjects, X,Y and Z gained 0.5% more mass doing farmer's walks vs. squats.

For others, it may yet be time to move on or to expand their arsenal of exercises with what Ghigiarelli et al. feel are "unique and exciting" exercises which provide "effective alternative to traditional resistance training, but require a lot of training to even master them "manipulate the specific combinations of rest intervals, loading, and volume toward [your] desired training goals" (Ghigiarelli. 2013).

References

• Beaven CM, Gill ND, Cook CJ. Salivary testosterone and cortisol responses in professional rugby players after four resistance exercise protocols. J Strength Cond Res. 2008 Mar;22(2):426-32.
• Burd NA, Mitchell CJ, Churchward-Venne TA, Phillips SM. Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Appl Physiol Nutr Metab. 2013 Jun;37(3):551-4. doi: 10.1139/h2013-022. Epub 2013 Apr 26.
• Ghigiarelli JJ, Sell KM, Raddock JM, Taveras K. Effects of strongman training on salivary testosterone levels in a sample of trained men. J Strength Cond Res. 2013 Mar;27(3):738-47.
• Hansen S, Kvorning T, Kjaer M, Sjøgaard G. The effect of short-term strength training on human skeletal muscle: the importance of physiologically elevated hormone levels. Scand J Med Sci Sports. 2001 Dec;11(6):347-54.
• OED Online. "training, n.". December 2013. Oxford University Press. < http://www.oed.com/view/Entry/204425 >  accessed March 04, 2013.
• Kvorning T, Andersen M, Brixen K, Madsen K. Suppression of endogenous testosterone production attenuates the response to strength training: a randomized, placebo-controlled, and blinded intervention study. Am J Physiol Endocrinol Metab. 2006 Dec;291(6):E1325-32.
• Schoenfeld BJ The mechanisms of muscle hypertrophy and their application to resistance training.J Strength Cond Res. 2010; 24: 2857–2872.
• Steele J. Intensity; in-ten-si-ty; noun. 1. Often used ambiguously within resistance training. 2. Is it time to drop the term altogether? Br J Sports Med. 2013 Feb 12. 
• Vingren JL, Kraemer WJ, Ratamess NA, Anderson JM, Volek JS, Maresh CM. Testosterone physiology in resistance exercise and training: the up-stream regulatory elements. Sports Med. 2010 Dec 1;40(12):1037-53.