Ecdysterone Beats Popular Anabolics!? Plus 75% Muscle Size in 21 Days in Rats - More Than DHT, IGF-1, Dianabol...

Ecdysterone Beats Popular Anabolics!? Plus 75% Muscle Size in 21 Days in Rats - More Than DHT, IGF-1, Dianabol...

anabolic anabolics build muscle DHT doping ecdysteroids ecdysterone estrogen receptor hypertrophy protein synthesis WADA

Parr et al. suggest that ecdysterone should be added to the WADA list.

Actually, I didn't plan to write a SuppVersity article about an agent of which everybody says that it's a waste of money, but I have to admit that the conclusion that "ecdysterone exhibited a strong hypertrophic effect on the fiber size of rat soleus muscle that was found even stronger compared to the test compounds metandienone (dianabol), estradienedione (trenbolox), and SARM S 1, all administered in the same dose (5 mg/kg body weight, for 21 days)" (Parr. 2015) in the abstract of a recent non-sponsored (no conflict of interest, either) study from the Freie Universität Berlin intrigued me.

In the corresponding study, Parr and colleagues had tested the effects of ecdysterones on the fiber sizes of the soleus muscle (that's mainly slow twitch muscle fibers) of rodents in vivo and in vitro.

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In the less relevant in vitro study, the researchers incubated C2C12 derived myotubes with the test compounds and determination of diameters of 47 myotubes per group (mean of measurements every 10–20 µm along the myotube) by fixing the cells and using photographs of the stained cells to determine the myotube diameters of 50 myotubes every 10–20 µm along the length of the myotube (further details see Parr. 2014). As the authors point out, incubation with ecdysterone showed "sign. increased myotube diameters compared to vehicle treated control cells" (Parr. 2015 | see Figure 1).

Figure 1: Myotube diameter in the in vitro study after incubation with DHT, IGF-1 or Ecdysterone (Parr. 2015).

If you compare the effects of the Ecdy treatment with those of the endogenous anabolic androgenic steroid dihydrotestosterone at the same concentration and those of the anabolic growth factor IGF-1 (concentration for comparison was 1.3 nM) it is quite impressive to see that there was an (albeit non significant) advantage for an active phytoecdysteroid the Russians have supposedly used as early as in the 1980s for doping purposes.

How does ecdysterone work? Previous studies already confirmed the beneficial effects of ecdysterone on skeletal muscle protein synthesis. As early as in the year 2000, V.N. Syrov published a paper in the Pharmeceutical Chemistry Journal in which the beneficial effects ecdysterone and related agents on rodent muscles were documented. Later on, Gorelick-Feldman et al. proposed direct or indirect stimulation of the PI3K/Akt signaling pathway as mechanism for this increased protein synthesis (Gorelick-Feldman. 2008 & 2010). In the study at hand, Parr et al conducted molecular modeling experiments which appear to confirm that the effects of ecydesterone are mediated by estrogen-receptor-β (ERβ) binding, rather than via the androgen receptor which is the target of the many of the other drugs used. 

Obviously, the effects of bathing individual cells in concentrated ecdysterone cannot serve as a reliable litmus test for the anabolic prowess of an agent bodybuilders take as an oral supplement in dosages of usually no more than 1g per day. In this respect, the concomitantly conducted experiment with intact rodents is of much greater interest. In this part of study, the authors fed male Wistar rats (n = 42, Janvier, Le-Genest St-Isle, France) either 5 mg/kg body weight of ecdysterone, metandienone, estradienedione, or the selective androgen receptor modulatar (SARM) S-1, each diluted in a solution of 20% DMSO and 80% peanut oil daily. In that, it is unfortunately not 100% quite clear if the scientists used intraperitoneal or intra-muscular injections, but the composition of the "supplement" and the fact that a previous study (Syrov. 2000) used the same dosage orally, appear to suggest that Parr et al. refer to about IP injections, which mimic oral supplementation, but have the advantage of giving rodents no chance to regurgitate the drug, when they write that the rodents "received injections". What is pretty clear, though, is that the scientists used changes in muscle fiber size of the soleus muscle of male Wistar rats as measure of the anabolic potency of their test substances.

Figure 2: Anabolic effect of ecdysterone (Ecdy) expressed as fiber size of soleus muscle in intact rats (Parr. 2015).

The results of the comparison of ecdysterone to the anabolic androgenic steroids metandienone (dianabol) and estradienedione (trenbolox) as well as the selective androgen receptor modulator S-1 are plotted in Figure 2. Quite impressive , no? And this is not an outlier study. As Parr et al point out, their study is not the first to show that "ecdysterone induces hypertrophy of muscles with a comparable or even higher potency as shown for anabolic androgenic steroids, SARMs or IGF-1", as analogous findings have been reported in the previously cited study by Syrov back in 2000. Human data, as well as data that would confirm similar effects on muscles that are predominantly fast-twitch (the soleus which was examined in the study at hand is mostly slow twitch) are yet missing. The latter is of particular interest, because estrogen treatment appears to favor a more oxidative (=more slow vs. fast twitch) fiber muscle fiber composition (Suzuki. 1985).

Hormonal Response to Exercise, Revisited: A Consequence, not a Determinant of Your Mood, Effort & Performance | learn more

Bottom line: In spite of the fact that the study provides quite convincing evidence in favor of the unexpected potency of Ecdysterone, there is a problem with dosing. While the scientists say they used 5mg/kg body weight in order "mimic the situation in athletes", the correct rodent equivalent of the aforementioned dosages of up to 1g per day would be roughly 50-75mg/kg per day and thus far more than the meager 5mg/kg the researchers used.

In other words, if they didn't accidentally give us the human equivalen dose instead of the actual rodent dose, those 1g/day some bodybuilders may be taking should be way more than you'd need to see significant increases in muscle gains and that is a problem.

Why? Well, not because I'd believe that dosages as high may have toxic side effects, but rather in view of the fact that you can hardly imagine that a drug as effective as that wouldn't be all over the place in the discussions on pertinent bulletin boards. A 2006 study by Wilborn et al. even fuels the doubts, because it found no performance or hypertrophy effects in the 15 out of 45 subject of their 8-week training study who consumed 30 mg of 20-hydroxyecdysone per day from an allegedly standardized (but not tested) extract from Suma root. An even older study by Simakin et al. (1988), however, appears to confirm the existence of potent anabolic effects of ecdysterone in humans with significant increases in lean (6-7%) and reductions in fat mass (10%) in a 3-week study on 78 highly-trained male and female subjects. In view of the conflicting evidence, I am still very skeptical whether (a) the results translate to human beings, whether (b) the growth promoting effect is maybe restricted to slow twitch fibers and thus of little use to bodybuilders and whether (c) the supplements that are already being sold actually contain ecdysterones | Comment!

References:

• Gorelick-Feldman, Jonathan, et al. "Phytoecdysteroids increase protein synthesis in skeletal muscle cells." Journal of agricultural and food chemistry 56.10 (2008): 3532-3537.
• Gorelick-Feldman, Jonathan, Wendie Cohick, and Ilya Raskin. "Ecdysteroids elicit a rapid Ca 2+ flux leading to Akt activation and increased protein synthesis in skeletal muscle cells." Steroids 75.10 (2010): 632-637.
• Parr, Maria Kristina, et al. "Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone." Molecular nutrition & food research 58.9 (2014): 1861-1872.
• Parr, M. K., et al. "Ecdysteroids: A novel class of anabolic agents?." Biology of sport 32.2 (2015): 169.
• Simakin, S. Yu. "The Combined Use of Ecdisten and the Product'Bodrost'during Training in Cyclical Types of Sport." Scientific Sports Bulletin 2 (1988).
• Suzuki, S., and T. Yamamuro. "Long-term effects of estrogen on rat skeletal muscle." Experimental neurology 87.2 (1985): 291-299.
• Syrov, V. N. "Comparative experimental investigation of the anabolic activity of phytoecdysteroids and steranabols." Pharmaceutical Chemistry Journal 34.4 (2000): 193-197.
• Wilborn, Colin D., et al. "Effects of methoxyisoflavone, ecdysterone, and sulfo-polysaccharide supplementation on training adaptations in resistance-trained males." Journal of the International Society of Sports Nutrition 3.2 (2006): 19-27.

"HIIT-ing it After Arm Workouts Will Ruin Your Gains", Study Says and Confuses Statistical and Practical Significance

"HIIT-ing it After Arm Workouts Will Ruin Your Gains", Study Says and Confuses Statistical and Practical Significance

arms build muscle build strength cardio concurrent concurrent training exercise order HIIT strength training

Does this look as if sprinting would impair muscular development of arms or any other muscle? I mean, come on - look at the average sprinter: Many gymrats dream of the arms and overall muscular physique they have; no wonder that the data from the full-text shows a different picture than the abstract would suggest.

I have repeatedly written about combining strength and classic endurance training. With endurance first, endurance last and even endurance in-between the studies yielded often very different results in terms of what would be the optimal way to combine both. With a few exceptions in which resistance training was combined with crazy endurance training sessions, however, I've yet never written about nor seen compelling evidence for the often-heard claim that "cardio ruins your gains".

For HIIT, i.e. high-intensity interval training, a recent study from the Nippon Sport Science University does now claim, though, that my that combining HIIT and weight training may be a very bad idea, ... an idea that may in fact, just as the broscientific nightmare suggests "ruin your gains, bro!" Upon closer scrutiny, however, things appear less unambiguous than the abstract would have it...

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The purpose of the study was to examine whether or not lower limb sprint interval training following arm resistance training influences training response of arm muscle strength and hypertrophy. Or in short: Will doing HIIT sprints immediately after an arm workout ruin the strength and strength gains you've primed before? 

Figure 1: According to the study, you better don't do HIIT sprint training after an intense arm workout if you don't want to ruin the strength and size gains you "primed" with curls and co (photo from Kikuchi. 2015)

The subjects, twenty previously only lightly trained men, were divided into resistance a training group (RT, n=6) and concurrent training group (CT, n=6).

• The RT program was designed to induce muscular hypertrophy (3 sets x 10 repetitions (reps) at 80% 1 repetition maximum [1RM] of arm curl exercise), and was performed in an 8-week training schedule carried out 3 times per week on nonconsecutive days. 
• Subjects assigned to the CT group performed identical protocols as strength training (ST) and modified sprint interval training (4 sets of 30-s maximal effort, separated in 4m 30-s rest intervals) on the same day. 

The relevant study outcomes the researchers evaluated were the changes in maximal oxygen consumption (VO2max), muscle cross-sectional area (CSA), and 1RM that were measured before and after the 6-week study.

Figure 1: Relative changes in VO2max (conditioning), muscle size (CSA) and strength (1-RM) over 6 wks (Kikuchi. 2015).

As the data in Figure 1 reveals, significant increases in VO2max from pre- to post-test were observed only in the CT group (p=0.010, ES=1.84), but not in the RT group (p= 0.559, ES= 0.35). The rest of the results in Figure 1, however should be kind of surprising to anyone who has read the researchers conclusion that "our data indicate that concurrent lower limb sprint interval training interfere with arm muscle hypertrophy and strength" (Kikuchi. 2015).

No, you are not mistaken. The average muscle size and strength gain in the combined training group was larger. The reason the scientist still claim that their study would show that HIIT impedes strength adaptation is a statistical one. While the changes in the CT group had p-values p > 0.05 and were thus not statistically significant. The (albeit smaller) mean increase in the RT group was significant. Accordingly, the corresponding "effect size" in the RT group is larger than the one in the CT group and thus HIIT training must be bad, right? Well,... I don't think so.

If you take a closer look at the individual muscle  size and strength development, you should notice that being afraid that sprints would ruin your arm development is unwarranted and the statistical significance and effect sizes of the changes practically irrelevant.

Beware of bling faith in abstracts! If you look at my plot of the individual data the scientists luckily published with their full-text, it is yet obvious that this study does not prove and if we are honest, not even really suggest that there practically relevant negative effects of doing HIIT in this workout. If you just read the conclusion to the abstract, which reads "our data indicate that con-current lower limb sprint interval training interfere with arm muscle hypertrophy and strength" (Kiku-chi. 2015), you may be inclined to make unne-cessary changes to your workout that are neither necessary or productive. After all, the objective result of the study is that in some individuals it is possible that the addition of HIIT to an arm workout may have a minor impact on their gains.

In view of the facts that there's (a) one person with a roughly ~41% increase in sleeve sizes in each group and that (b) the average increase in sleeve size would be 23% in the CT and only 21% in the RT group if the two outlayers who lost muscle (one in each group) were excluded, though, I would suggest you ignore this possibility unless you realize that you're making no gains at all with concurrent training. This doesn't falsify the scientists' conclusion, which is based on scientific standard procedure, i.e. look for statistical significant results, use those to make your conclusion, but I felt I needed to write this article to put the theoretically correct interpretation of results of an unquestionably under-powered study into perspective | Comment!

References:

• Kikuchi et al. "The effect of high-intensity interval cycling sprints subsequent to arm-carl exercise on muscle strength and hypertrophy in untrained men: A pilot study." Journal of Strength and Conditioning Research Publish (2015): Ahead of Print | DOI: 10.1519/JSC.0000000000001315

2909 IU of Vitamin D3 per Day - That's What Mr. Average Needs | What Do You Need? 3094, 4450, or 7248 IU/day?

2909 IU of Vitamin D3 per Day - That's What Mr. Average Needs | What Do You Need? 3094, 4450, or 7248 IU/day?

25-(OH) D3 25(OH)2D 25(OH)D 25OHD D3 health RDA vitamin D vitamin d deficiency vitamin D3 vitamin deficiency vitamin requirements

Your BMI or rather the associated level of inflammation and bodyfatness determines your D3 requirements.

I know that I have previously written about estimated vitamin D requirements, but in contrast to previous articles that were based only on 1-3 studies, today's article about the purported vitamin D requirements of the average Westerner, however, is based on the same previous 108 published estimates and new calculations based on the vitamin D status of 13,987 individuals in various studies Veugelers, Pham and Ekwaru used as the observational database for what is a of now probably the most tangible vitamin D recommendation in their recently published study in Nutrients (Veugelers. 2015).

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Now, as the headline already tells you, their analysis of said data lead the researchers to conclude that "2909 IU of vitamin D per day is needed to achieve serum 25‐hydroxyvitamin D (25(OH)D) concentrations of 50 nmol/L or more in 97.5% of healthy individuals" (Veugelers. 2015). To get to this value, the researchers from the University of Alberta used quantile regressions to

"model the effect of vitamin D supplementation on the 2.5th percentile, the median and the 97.5% percentile of serum 25(OH)D concentrations [and an] exponential model [and] logistic regression [for the estimates and] to estimate the probability of having serum levels above a lower and below an upper serum 25(OH)D concentration, [respectively]" (Veugelers. 2015). 

In that it is important to know that in this model the limit of the 'normal' vitamin D concentrations (58-171 nmol 5(OH)D/L) was defined in accordance with the values Luxwolda et al observed in traditionally living populations in East Africa who have mean serum 25‐hydroxyvitamin D concentration of 115 nmol/l or more (Luxwolda. 2012). So, we are not talking about absolute minimum levels, but rather about levels many researchers would call "optimal".

Figure 1: Plot of the results of the model calculations (left) and my visualization (right) of the calculated vitamin D requirements in IU/day for normal-weight, overweight and obese individuals (Veugelers. 2015).

As a SuppVersity reader you will be aware that normal-, overweight and obese subjects will need different amounts of supplemental vitamin D3 to achieve these "optimal" levels. To accomdate for these differences and to provide adequate estimates for normal weight, overweight and obese participants, Veugelers et al conducted separate analysis and used suitable logistic regression models to identify the log term of supplementation that provides the best fit. Needless to say that this sub-analysis was conducted based only on those studies that either included exclusively normal-, overweight or obese subjects or distinguished between the three of them yielded. It is thus only logical that this analysis yielded different results of which the 3094 IU/day, which is the suggested daily amount of vitamin D3 to maintain optimal vitamin D levels for normal-weight individuals, is yet pretty much identical to the previously cited "optimum" for Mr. Average Joe.

Against that background, it is yet all the more important to note that the average overweight or obese Westerner will yet need significantly more vitamin D3, 4450 IU/day and 7248 IU/day, to be precise, to keep his / her labels stable. Based on what you should remember from the role of 25OHD as an anti-inflammatory acute phase reactant (Waldron. 2014), though, this is not really surprising.

So what's the verdict, then? While the study at hand certainly provides the hitherto best estimate of our individual vitamin D3 requirements, I still wouldn't put blind faith into the results of Veugelers' model calculation. To be sure you're not too extra-ordinary to be average, I would suggest you test your 25OHD levels after 6 months on the suggested dosage. If you're "in the zone", everything is fine. If not, adjust appropriately.

Fat loss will trigger decent increases in vitamin D, but vitamin D will not trigger significant fat loss | more

Apropos adjusting, as the authors point out, the previously discussed figures may not even be the most practically relevant result of the study. Rather than that, it is the "large extent of variability in 25(OH)D concentrations" of which the authors rightly say that it "makes a RDA for vitamin D neither desirable nor feasible" (Veugelers. 2015) that's the most relevant results of the study.

And yes, you've read that right. The 400, 600 and 1000 IU/day RDA you will find in different countries all over the world is total bogus, not just because it is too low, but because stating a recommended daily allowance based only on the age, not the weight, or rather inflammatory status of an individual, is absolute bogus | Comment on Facebook!

References:

• Luxwolda, Martine F., et al. "Traditionally living populations in East Africa have a mean serum 25-hydroxyvitamin D concentration of 115 nmol/l." British Journal of Nutrition 108.09 (2012): 1557-1561.
• Veugelers, Paul J., Truong-Minh Pham, and John Paul Ekwaru. "Optimal Vitamin D Supplementation Doses that Minimize the Risk for Both Low and High Serum 25-Hydroxyvitamin D Concentrations in the General Population." Nutrients 7.12 (2015): 10189-10208.
• Waldron, Jenna Louise, et al. "Vitamin D: a negative acute phase reactant." Journal of clinical pathology (2013): jclinpath-2012.

Hormonal Response to Exercise, Revisited: A Consequence, not a Determinant of Your Mood, Effort & Performance

Hormonal Response to Exercise, Revisited: A Consequence, not a Determinant of Your Mood, Effort & Performance

build muscle DHT female GH growth hormone HIIT hormones performance resistance training testosterone women women strength

Studies in men suggest no effect of the hormonal response on training outcome - What about women? A news study provides insights that may be relevant for both female and male gymrats.

It has been a few years that I last wrote about the "hormonal ghost". Back in the day, Stuart M. Phillips published an excellent paper that debunked the myth of a mechanistic link of post-exercise increases in testosterone, growth hormone, IGF-1 and co., on the one hand, and exercise-induced strength and size gains, on the other hand. And for those for whom Phillip's review of the literature was not convincing enough, Daniel WD West's 2012, which showed none of the expected associations between exercise-induced hormone profiles (first and foremost higher post-workout testosterone levels) and the rate or significance of muscle strength and size gains in a large cohort of young men after weight training, should have been evidence enough to stop believing in "hormonal ghosts", but alas... you will probably know that "training for testosterone increases" is still en vogue.

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That's stupid stubbornness, nothing else, right? Well, even though I don't believe in ghosts, I have to admit that a closer look at West's data will have you reject the hypothesis that the post-workout testosterone response would augment size gains, it does yet also show other hormonal changes do correlate with the changes in the study's subjects' lean mass (Figure 1, left) as well as type I (middle) and type II fiber size increases (Figure 1, middle & right).

Figure 1: Sign. associations between PWO hormone levels and lean mass, as well as fiber size increases (West. 2012).

As you can see in Figure 1, this was the case for the cortisol response and the lean mass gains and the growth hormone (GH) response and the increases in type I ('endurance') and type II ('strength') fiber size. Even though I don't believe that more than 1% of the gymrats world-wide who still believe that maximizing the post-workout "anabolic response" would help them to maximize their gains even know about these results, you could argue that these correlations fuel their beliefs - even if that's paradoxical, because - in bro-scientific terms - you'd have to maximize the catabolic response, i.e. the increase in cortisol (which could by the way simply be a measure of training intensity) in order to maximize the overall gains in muscle size, but alas...

Figure 2: Changes in anabolic and catabolic hormones in response to AM and PM HIIT and RT training (Toon. 2015).

In a series of experiments Rebecca Toone conducted for her thesis, she re-addressed the issue of the acute hormonal effects on performance with female study participants (yes, a long-term study was not part of her thesis, but I promise, the results are still noteworthy).

Higher sprint cadence (RPM) during HIIT, higher increase in DHT in the female study participants (Toon. 2015).

DHT another acute phase reactant? Even though the overall results of the study suggest that increased pre- vs. post workout changes in DHT as Toone observed the with higher RPM-numbers during HIIT sprints are not the reason, but rather the consequences of training at higher intensities, it is worth mentioning that this is the first study to observe the existence of an association between DHT and HIIT performance in women and that the results are in line with the results of previous research suggesting that DHT, not its precursor, testosterone, has a direct influence on skeletal muscle force production in vitro. 

After some preliminary testing, Toone began with another of the infamous "AM vs. PM" workout studies in which she unsurprisingly confirmed that...

"[...] it could be beneficial to perform resistance training in the afternoon preceded by interval exercise in the morning in order to stimulate a hormonal milieu that may be more conducive to stimulating muscle protein turnover" (Toon. 2015). 

If you scrutinize the data in Figure 2, you can see that this hypothesis is warranted, because of the differential response of the anabolic hormones, testosterone and IGF-1, and the stress / catabolic hormones, cortisol and prolactin, she observed in her young female subjects. Against that background it is quite interesting that Toone's last and most important experiment, in which she investigating the potential acute effects of hormones on performance, failed to demonstrate a direct correlation between changes in testosterone or other "anabolic" hormones and her subjects' performance.

"The trial consisted of a 20 min effort at a target power of 80% of the average power obtained during the maximal 20 min TT, followed by a 5 min break, before completion of a bout of repeated sprint interval cycle exercise consisting of 10 x 30 s sprinting, with 90 s recovery. The session was self-paced with real-time numerical feedback provided on elapsed time, cadence and power. Participants were given verbal encouragement at specific time-points throughout the trial. The same protocol was repeated for the second main trial one week later. Participants were permitted to drink water ad libitum throughout the trials. Trials were completed in a group setting as a group of six and a group of eight. A trial timeline schematic is displayed [in Figure 3]" (Toon. 2015).

Instead, the results of the previously described exercise test point towards affective variables, i.e. mood and effort, as the factors that mediate any link between hormonal changes and performance markers during an acute bout of high intensity cycling.

Figure 3: Design of the last and most important experiment of the study (Toone. 2015).

And guess what, the effort Toone's subjects invested into their workouts was not just a predictor of their performance, it was also positively associated with the percent change in testosterone concentration from post-sprint 4 to post-exercise (r = 0.449; P < 0.01).

Note: We are till talking about associations and correlations. That one of these, e.g. the one between the effort we put into our workouts and the preformance and hormonal response exists because of a causal link is thus in view of the results of the study at hand logical, but still hypothetical. As I am about to point out in the bottom line, future studies will have to investigate that - even though I have to admit that it will be difficult to develop an effective design for these studies.

In conjunction with the subjects' affect, which was inversely correlated with the rate of perceived exertion, which in turn showed positive correlations with cortisol, the results highlight a previously overlooked role of effort and affect when it comes to both, exercise performance and its effect on certain hormones.

Figure 4: The hormonal response is rather the consequence than the trigger of acute performance.

Or as Toone has it in her interpretation of these somewhat surprising results: The acute short-term effects of hormone concentrations on performance may be more related to mood and behaviour" than the actual type / time of exercise in the context of her study.

What does that mean? Practically speaking this would confirm what I have said about the initially cited West study in several previous SuppVersity articles. In said study, cortisol probably has no mechanistic effect on muscle size. Rather than that, the increase in cortisol could serve as a measure of how much effort the subjects put into their workouts; and this, in turn, determined their muscle gains (more effort = bigger growth stimulus = greater gains).

The meager and transient increase in testosterone after your workouts has none of the muscle building and fat shedding effects of exogenous testosterone. The latter however, can turn back the time and an aging pouch into a true best-ager | learn more.

In the study at hand, the situation appears to be similar. Mood and effort determine performance and hormonal response of the female study participants. Accordingly, there may be associations between exercise performance and certain hormones, but those are of corollary, not causative nature. In the absence of an additional experiment that would investigate the correlations and associations between mood, effort, RPE, hormones and the exercise-induced adaptation in the long run, we can still only speculate that making the workouts more fun and stimulating maximal effort would promote both, the adaptive response and the hormonal response and thus confirm that mood and effort are in fact the most relevant determinants of the outcome of your workouts | Comment!

References:

• Phillips, Stuart M. "Strength and hypertrophy with resistance training: chasing a hormonal ghost." European journal of applied physiology 112.5 (2012): 1981-1983.
• Toone, Rebecca. Assessing the Hormone Response to High Intensity Exercise and Identifying Associations with Performance. Diss. University of Bath, 2015.
• West, Daniel WD, and Stuart M. Phillips. "Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training." European journal of applied physiology 112.7 (2012): 2693-2702.

Mix Things Up ⇨ Up Your Gains: Altering Loading Schemes in Every Session Accelerates the Strength Gains in 6-Week Study Involving 200 Experienced (5 Years+) Trainees

Mix Things Up ⇨ Up Your Gains: Altering Loading Schemes in Every Session Accelerates the Strength Gains in 6-Week Study Involving 200 Experienced (5 Years+) Trainees

experienced trainees gain strength performance periodization training experience undulating periodization veterans workout routines workouts

Looking for a new routine for your new-years gym resolution? This SuppVersity article offers suggestions that will pay off in form of strength gains. 

For the rookie, everything works. If you have more than five years of series training experience under your belt, however, you will be progressing much slower - often frustratingly slow(er)... This is why the results of a a soon-to-be-published study in the Journal of Strength and Conditioning Research are particularly interesting. In contrast to your average resistance training study, the subjects of this study belonged to previously described group of experienced trainees. With a mean training experience of more than 5 years, the initially more than 300 volunteers were thus significantly more representative of the average SuppVersity reader than the "recreationally trained" subject who goes for a jog once a month.

The method used int he study is an alternative to classic periodization schemes.

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What was likewise remarkable about the study at hand is the number of participants. Ok, after 67 dropouts, there were only 200 subjects left when the author, Christoph Eifler from the Department of Applied Training Science at the German University of Applied Sciences for Prevention and Health Management (DHfPG) in Saarbrücken, Germany, kicked out another 33 subjects to get identical sample sizes and a homogenous gender distribution in all study groups. N=200, however, is still far from what the average resistance training study has to offer.

Table 1: Study design: constant and variable loading parameters (Eifler. 2015).

Overall, this means we have N=50 participants in each of the 4 samples in which the subjects trained as shown in Table 1:

• CL - constant load and constant volume of repetitions over 6 weeks.
• IL - increases in load and decreasing volume of repetitions made every 2 weeks.
• DL - decreases in load and increasing volume of repetitions made every 2 weeks.
• DCL - daily changing load and volume of repetitions.

The total number of repetitions were identical between samples. In addition, both within- and between-set rest was standardized between samples, to isolate the variables of interest (i.e. intensity and volume).

What's the mechanism? While we cannot tell for sure what triggered the increased strength gains in the study at hand, the author's suggestion that "[i]t is possible, that the ongoing alteration between training intensity and training volume prevents habituation effects, at least in short-term resistance training periods" (Eifler. 2015) constitutes a very convincing hypothesis, also in view of the fact that we may assume that "this loading scheme [DCL] places greater stress on the neuromuscular system, so greater strength gains are the result" (ibid.). Supporting evidence for this hypothesis comes from Rhea et al. (2002) who reported as early as in 2002 that DCL-like loading periodization-schemes support a greater adaption of the neuromuscular system.

To asses the effect of the different approaches to "periodize" the subjects' workout regimen, the author used a standardized 10-RM- and 1-RM-test that was performed before and at the end of the 6-week intervention:

"Both 10-RM-testing and 1-RM-testing were designed with the following procedure: 5 minute general warm-up with an intensity of 60% of the theoretical maximum heart rate; one warm-up set with 50% of the load in the first test set; performance of 3 at most test sets to quantify RM (trial and error principle) by 3 minutes rest interval between test sets. Pre- and post-testing occurred at the same time of day to eliminate the potential influence circadian rhythm on strength. The documentation of the test results followed standardized test protocols. At each date of testing, all participants were interviewed about their current state of motivation and their form of the day. Moreover, the temporal gap between the last resistance training session and the presence of muscle soreness and muscle stiffness were recorded" (Eifler. 2015).

Familiarization sessions were unnecessary as subjects had recent experience with all exercises, i.e. horizontal leg presses, chest presses, butterfly, lat pulldowns, horizontal rows, dumbbell shoulder press, cable triceps pushdowns, and dumbbell biceps curls, they had to perform in the given order and over the full range of motion (ROM) in each of their workouts.

Figure 1: Effect sizes of the 6-week training intervention with different loading schemes (Eifler. 2015); * denotes significant differences compared to all other groups - in short: only the DCL workout made a significant difference.

Even though using trained and highly motivated subjects obviously has its advantages, the author adds for consideration there may be selection effects caused by voluntary participation or Hawthorne effects (Macefield. 2007). More specifically, the volunteers in the study at hand were probably (just like you ;-) more likely to comply to changes in behavior and to put maximal physical effort in testing and training. In addition, even though the subjects were told to refrain from additional physical activity and to maintain their regular diets, not all confounding variables, such as differences in nutritional intakes, prior sleep, or interferences caused by other fitness club customers, could be eliminated in this field test study.

Figure 2: Relative strength increases in the four study groups (Eifler. 2015); due to the large inter-individual differences, evidenced by the long error bars, the DCL advantage was not statistically significant.

As Eifler rightly points out, though, "the probability of occurrence of these confounding variables, selection effects or Hawthorne effects, is equal in all samples" (Eifler. 2015), which is why they should average out when you compare the inter-group effect sizes and relative strength increases based on the pre vs. post 1-RM and 10-RM strength test (see Figures 1 & 2).

Overall, there's thus little reason to doubt the results of the study at hand. Results that clearly suggest an advantage of the daily changing load regimen when it comes to maximizing strength increases in trained individuals over the course of a six-week period - and that in spite of the fact that Eifler failed to detect statistically significant effects for the relative strength increases due to the large inter-personal differences (see Figure 2).

This is not the first SuppVersity article discussing evidence in favor of "changing up things more frequently". Back in 2012 I already discussed Spinetti's linear vs. undulating periodization studies w/ similar benefits on the subjects' strength gains.

So what's the verdict, then? Just as the author says, while DCL is widely known, the fact that it is rarely practiced may have average and extraordinary gymrats miss out on a "potential for improving resistance training in commercial fitness clubs" (Eifler. 2015). After all, there's little doubt that the data from the study at hand "indicates that resistance training following DCL is more effective for advanced recreational athletes than" (ibid.) more conventional loading patters, i.e. CL, IL, DL.

Whether the benefits are due to a novelty effect that would be lost over long(er) training periods and whether the same or similar benefits could be achieved in untrained subjects will have to be determined in future research, for the time being however, daily changing load (DCL) and volume of repetitions appears to be worth adding to your list of things to try in the gym in 2016 | Comment on Facebook!

References:

• Eifler, Christoph. "Short-term effects of different loading schemes in fitness-related resistance training." The Journal of Strength & Conditioning Research (2015).
• Macefield, Ritch. "Usability studies and the Hawthorne Effect." Journal of Usability Studies 2.3 (2007): 145-154.
• Rhea, Matthew R., et al. "A comparison of linear and daily undulating periodized programs with equated volume and intensity for strength." The Journal of Strength & Conditioning Research 16.2 (2002): 250-255.