Update on GAINZ: More Muscle & Strength W/ Exercises You Like | Deadlifting Unshoed NO Power Booster | 50% Sugar NOT Anti-Anabolic | Cryotherapy NO Recovery Boost

No, bro - Losing your shoes won't allow you to magically lift thrice your BW when your current 1-RM is only twice your BW.

Who would have thought that? If trained subjects are allowed to chose their 'favorite' exercises (or those they deem most productive) they gain 63% more lean mass in a realistic 9-week study (difference short of sign., though). I guess compared to this result from a recent study from the University of Tampa, the realizations that deadlifting unshoed doesn't seem to provide a systematic benefit, that sugar does not - if protein intake is adequate - negatively affect anabolism, and that local cryotherapy doesn't just threaten the adaptational processes that occur after your workouts are rather expected results... results that were IMHO still worth summarizing in this October 2017 Suppversity "Update on GAINZ" ;-)

If you want to update YOUR gains, try creatine-monohydrate - safe and proven!

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• Deadlifting unshod changes rate of force development and the medio-lateral center of pressure - albeit with unclear effects on deadlift performance (Hammer 2017).
  
  "While the unshod condition may have produced changes in RFD and ML-COP compared with the shod condition, there is only limited evidence in the current study to support this lifting technique for the conventional deadlift," that's the unfortunately very unspecific conclusion of a recent study in the Journal of Strength and Conditioning Research. Before I am going to tell you that the authors are right, though, "[f]urther investigation is required to clarify any possible implications of this result and its benefit to lifters", let's at least check out what Mark E. Hammer et al. did, observed, and concluded.
  
  For their study, the scientists recruited 10 strong male participants (mean ± SD, age = 27.0 ± 5.8 years; weight = 78.7 ± 11.5 kg; deadlift = 155.8 ± 25.8 kg) with a minimum training history of 2 years. A counterbalanced, crossover experimental design was used with different loads (60% and 80% 1RM). Four sets of four repetitions were prescribed per session with two sets per shoe and with each shoe condition involving one set per load.

  

  Figure 1: Overview of the study results; all values expressed relative to 60% 1RM shoed; statistically significant effects of wearing / not wearing shoes were observed only where %-ages given (Hammer 2017).

  Peak vertical force (PF), rate of force development (RFD), time to peak force (TPF), anterior posterior (COP-AP) and medio-lateral (COP-ML) center of pressure excursion, and barbell peak power (PP) data were recorded during all repetitions. Except for RFD (F = 6.389; p = 0.045; ƞp2 = 0.516) and ML-COP (F = 6.696; p = 0.041; ƞp2 = 0.527), there were no other significant main effects of shoe.
  
  What did matter, obviously, was the load; with significant main effects for PF (p < 0.05), COP-AP (p = 0.011), TPF (p = 0.018) and COP AP (p = 0.011), but there was no interaction between session, shoe and load (p range from 0.944 to 0.086).
  
  So what's the verdict, then? Eventually, we do thus arrive at the previously cited conclusion that "[f]urther investigation is required to clarify any possible implications of this result and its benefit to lifters." That's bad? Well, not really. If you personally like deadlifting without shoes, the study at hand does at least tell you that it doesn't mess with your power... you don't get why one would do that? Well as Hammer et al. point out, it's an "observed practice within the strength and conditioning field" to lose your shoes, because people expect that being unshod during the deadlift exercise can significantly improve your deadlifting performance... for the average experienced deadlifters, this is probably not the case; with the inter-personal differences Hammer et al. observed, though, it may work for you, personally, though.

• No ill effects of sugar-overfeeding w/ amounts equivalent to 50% of the daily energy requirements on protein anabolism in (young healthy) men and women if protein intake is adequate (Jegatheesan 2017).
  
  The dreaded reduction in IGF-1 and leucine and protein synthesis from sugar overfeeding, here an extra 50% of the subjects (12 healthy young male and female volunteers ) daily requirements (this means if you need 2000kcal, you got to eat 1000kcal extra... from 125g of pure sugar).
  
  French and Swiss scientists observed the "low protein" phenomenon, when they supplemented compared diets that were already high in carbohydrates (45% starch) with tons of sugar (delivering a 50% kcal surplus) and either 37.5% lipid and 7.5% protein (HSLP) or 15% lipid and 30% protein (HSHP) for 7-days and analyzed and compared fasting and postprandial plasma insulin, glucagon, and IGF1 concentrations were assessed before and after each intervention, and fasting plasma AAs level.

  "The increase in Ala elicited by sucrose overfeeding was blunted with HSHP (249 ± 18 vs 386 ± 11 μM, p < 0.001) compared to HSLP (251 ± 20 vs 464 ± 33 μM). Leu concentration decreased (130 ± 4 vs 116 ± 5 μM) after HSLP, but not after HSHP (139 ± 6 vs 140 ± 7 μM). Compared to HSLP, plasma BCAA, Phe, Tyr, and Pro were significantly higher with HSHP than HSLP. Fasting IGF1 concentration increased (174 ± 18 vs 208 ± 15 μg/dl) after HSHP and decreased (212 ± 13 vs 173 ± 12 μg/dl) after HSLP (p = 0.04)" (Jegatheesan 2017).

  So what's the verdict, then? As previously highlighted, the results clearly indicate that "sucrose overfeeding decreases IGF1 and Leu level [only] when associated with a LP [low protein] intake" (Jegatheesan 2017). No reason to go overboard on sugar, but at least an 'all-clear' for the occasional CHO refeed.

• Local cryotherapy is ineffective in accelerating recovery from exercise-induced muscle damage on biceps brachii (Lima 2017)
  
  From previous articles at the SuppVersity, you know that cryotherapy can impair the long-time size and strength gains of athletes. Against that background, it is all the more problematic that cryotherapy does not, as most people assume, accelerate recovery from every form of exercise-induced muscle damage ... no matter what.
  
  The reality of a recent study in nineteen untrained women proves this assumption wrong. After having performed an eccentric protocol of damage induction (2 sets of 10 repetitions) in both arms, the cryotherapy was applied for 20 min, twice per day, for 4 days following the eccentric exercise. Randomly, one of the subject’s arms was assigned as intervention and received cryotherapy, the opposite arm served as control. As muscle damage indirect markers, we collected muscle thickness, and echo intensity, delayed onset muscle soreness, and peak torque at baseline (PRE), and at 24, 48, 72, and 96 h.
  

  

  Figure 2: Neither the most important (=strength/torque) nor the auxiliary marker DOMs improved (Lima 2017).

  The muscle soreness markers increased in both, the experimental and the control arms, significantly compared to the PRE value at 24, 48, and 72 h. In a similar vein, the peak Torque of both experimental and control arm was significantly reduced and the scientists didn't find changes in any of the indirect markers of muscle damage between arms at any moment (p > 0.05).
  
  So what's the verdict, then? While they do risk a long(er) term reduction in gains in strength and size. Rookies will not be able to control their muscle soreness or improve their exercise recovery with local cryotherapy.

• More than 60% increase in average lean mass gains when experienced trainees are allowed to auto-regulate (=self-select) exercises (Rauch 2017).
  
  In contrast to previous studies on auto-regulation of training parameters, the study at hand did not allow its subjects, N=32 strength-trained volunteers, who were able to squat and bench 1.75 and 1.3 times their body mass, did not primarily address quantitative resistance training variables (e.g., volume, intensity, rest interval), but allowed the subjects to modify their exercise selection - a qualitative variable about which there is, according to Rauch et al. "a paucity of data" (Rauch 2017).
  
  Dietary intake was monitored using MyFitnessPal, subjects consumed used a pre-workout (Dymatize M.Pact) and 25g of whey (Dymatize Elite Whey Protein, 4g leucine) before and after workouts, respectively. Total protein intake was required to be >1.5g/kg per day if any subject’s protein intake fell short of this goal, they were given additional nutritional guidance from a certified sports nutritionist. Body composition was assessed using DXA.
  
  The workout the subjects had to follow was a full body-training regimen (3d per week, 9 weeks total). Each workout consisted of six different exercises. A 90-120 second rest interval was allowed between sets while two minutes were respected between exercises.
  

  "A daily undulating periodization model was implemented for both groups as follows: Day 1: 6-8RM, Day 2: 12- 14RM and Day 3: 18-20RM. The training regimen was divided into three mesocycles, the number of sets progressed in each mesocycle; Mesocycle 1: four sets per exercise, Mesocycle 2: five sets per exercise, and Mesocycle 3: six sets per compound exercise and five sets per accessory exercise. [...] Four certified strength and conditioning specialist were present for every training session, providing verbal encouragement and ensuring the proper amount of sets and repetitions were being performed" (Rauch 2017).

  The only difference between conditions was the exercises performed. The fixed exercise selection group (FES) group was handed a workout sheet with seven predetermined exercises.

  

  Table 1: Overview of the fixed exercise order and selection in the FES group (Rauch 2017).

  The auto-regulatory exercise selection (AES) group, on the other hand, was handed a workout sheet in which they had to select one exercise per muscle group... a small change that made a significant differences you can see in Figure 3  (note: with 15 dropouts, the scientists had to resort to a 95% confidence analysis to establish potential inter-group differences, though):
  

  

  Figure 3: Workout volume(s) and strength parameters in the 17 out of initially 32 trained subjects (>3y experience) who made it through the 9-week study without falling off the wagon (Rauch 2017)

  With the total volume load being significantly higher during mesocycle 2 and 3 when the subjects were allowed to auto-select their exercises (AES: 573,288kg ± 67,505, FES: 464,600 ± 95,595, p=0.0240), it is also not exactly completely surprising that the intra-group confidence interval analysis (95%CIdiff | analysis for conducted only within groups, because the inter-group difference was too small) Rauch et al. conducted suggests that only AES significantly increased LBM (AES: 2.47%, ES: 0.35, 95% CIdiff [0.030kg: 3.197kg], FES: 1.37 %, ES: 0.21, 95% CIdiff [-0.500kg: 2.475kg]) - the relative difference in changes in lean mass between treatments was 63% (1.6 kg vs. 0.98 kg), practically relevant, but statistically not significant (probably at least also because 15 subjects dropped out for unknown reasons).

  

  Figure 4: The changes in lean mass show a clear advantage for the AES group - in particularly in view of the fact that only one subject in the AES group (vs. 4 in FES) lost lean mass over the 9-wk period (Rauch 2017).

  We are, after all, talking about already trained individuals who are not going to pack on slabs of muscles within 8 weeks and for whom Figueiredo et al. (2017) have only recently pointed out that 'more helps more' - with the currently available evidence not suggesting a high likelihood of overtraining and reduced gains w/ increasing volume.
  
  Significant effects on bench-press strength (95% confidence analysis) were likewise observed only for the AES group (AES: 6.48%, ES: 0.50, 95% CIdiff [0.312kg: 11.42kg; FES: 5.14%, ES: 0.43 95%CIdiff [-0.311kg: 11.42kg]) while for back squats the 1RM responses were similar between groups, (AES: 9.55%, ES: 0.76 95% CIdiff [0.04kg: 28.37kg], FES: 11.54%, ES: 0.80, 95%CIdiff [1.8kg: 28.5kg]).
  
  So what's the verdict, then? It remains to be seen if the significant increase in training volume was a physiological or psychological effect. What seems to be certain, however, is that it's the mechanism which eventually drove the increase in lean mass and bench press gains in the AES group... a result that clearly refutes the over-generalized notion that the "exercises you tend to avoid will build the most muscle" (broscience).
  
  In that it may be worth mentioning and important to point out that (a) the effect on training volume occurred only in the 2nd and 3rd mesocycle, i.e. when the subjects' volume was already high, and that (b) the average lean mass increase of 1.6kg (see Figure 4) may not seem like much, but you should keep in mind that the guys in the study have been busting their a%% on the grind for years. So you cannot expect newbie gains of 2lbs per week. Plus: Only one subject in the AES group, but four subjects in the FES group actually lost muscle mass over the course of the 9-wk study period... makes you wonder if the inter-group difference had achieved significance if all N=32 subjects had made it from week one to week nine (15 dropped out and thus reduced the statistical power of the study significantly).

Even if done 5x/wk "weights" won't trigger the female athlete triad - that's your beloved "cardio", ladies.

You still want more? Well, what about this one, then: Ikezoe, et al. (2017) report in their latest paper in the Journal of Strength and Conditioning Research (once again) that low load high rep training will produce the same gains as high load low rep training - this time, albeit even if the subjects didn't go to failure... cool? Well, not really: the subjects were, after all, untrained. Just like most subjects in studies like these. Schoenfeld et al.'s 2016 meta-analysis highlighted that and a "trend [...] for superiority of heavy loading" in their latest meta-analysis (2016): " | Comment on Facebook!

References:

• Figueiredo, V. C., de Salles, B. F., & Trajano, G. S. (2017). Volume for Muscle Hypertrophy and Health Outcomes: The Most Effective Variable in Resistance Training. Sports Medicine, 1-7.
• Hammer, M. E., Meir, R., Whitting, J., & Crowley-McHatten, Z. (2017). Shod versus barefoot effects on force and power development during a conventional deadlift. Footwear Science, 9(suppl. 1), 99.
• Ikezoe, T., Kobayashi, T., Nakamura, M., & Ichihashi, N. (2017). Effects of low-load, higher-repetition versus high-load, lower-repetition resistance training not performed to failure on muscle strength, mass, and echo intensity in healthy young men: a time-course study. The Journal of Strength & Conditioning Research.
• Jegatheesan, P., Surowska, A., Campos, V., Cros, J., Stefanoni, N., Rey, V., ... & Tappy, L. (2017). MON-P291: Dietary Protein Content Modulates the Amino-Acid and IGF1 Responses to Sucrose Overfeeding in Humans. Clinical Nutrition, 36, S285-S286.
• Lima, et al. (2017) "Local cryotherapy is ineffective in accelerating recovery from exercise-induced muscle damage on biceps brachii." Sport Sciences for Health. August, Volume 13, Issue 2, pp 287–293
• Rauch, J. T., Ugrinowitsch, C., Barakat, C. I., Alvarez, M. R., Brummert, D. L., Aube, D. W., ... & De Souza, E. O. (2017). Auto-regulated exercise selection training regimen produces small increases in lean body mass and maximal strength adaptations in strength-trained individuals. The Journal of Strength & Conditioning Research.
• Schoenfeld, B. J., Wilson, J. M., Lowery, R. P., & Krieger, J. W. (2016). Muscular adaptations in low-versus high-load resistance training: A meta-analysis. European journal of sport science, 16(1), 1-10.

Native Whey, a Superior Muscle Builder? Recently Observed Impressive Absorption Rates Tell You Nothing About 'Gains'

Do you have to replace your whey protein concentrate with "native whey" product to avoid missing out on massive gains? The study to answer this question has not yet been, done, but the study at hand certainly does not warrant this conclusion.

You will probably have seen the results of the latest study from a recent paper by scientists from the Norwegian School of Sport Sciences (Hamarsland. 2017). The one, where 20g of native whey protein showed significantly faster amino acid absorption than 20 g of whey protein concentrate 80 (WPC80), hydrolyzed whey (WPH), microparticulated whey (MWP), and milk proteins (Milk) after being administered to thirteen healthy male subjects (age: 26.6 ± 7.4 years, height: 180.8 ± 6.3 cm, weight: 80.8 ± 6.3 kg) in a single-blinded, randomized, five-way crossover, controlled study - a study, of which I am pretty sure that various snake oil vendors are already (ab-)using it to sell expensive "native", i.e. unprocessed whey protein as "superior" anabolic".

High-protein diets are much safer than some 'experts' say, but there are things to consider...

Practical Protein Oxidation 101

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More Protein ≠ More Satiety

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Protein Timing DOES Matter!

High Protein not a Health Threat

Fortunately (for your wallet), Hamarsland's study does not provide evidence that the accelerated amino acid absorption would translate into real-world muscle gains in a long-term study.

Figure 1: Graphical illustration of the events on the five testing days (Hamarsland. 2017).

As you can see in the graphical illustration of the events on the five testing days in Figure 1, the Norwegian scientists had their subjects meet at the lab at 07:00 am on each of the five study days that were separated by at least 14 days fasted. When the subjects arrived at the lab, ...

"[t]hey received a standardized breakfast consisting of oatmeal and a glass of orange juice (1855 kJ: 9.2 g fat, 69.3 g carbohydrates and 16.6 g protein). [...] Two hours after breakfast, the participants performed the standardized resistance exercise session in 40 min and consumed one of the five protein supplements within 6 min after the end of the session. Blood serum and plasma samples were collected at 0, 30, 45, 60, 90, and 120 min after ingestion of the protein supplement. Additional blood samples were collected at 22 and 30 h on the study days when milk and native whey were ingested. During the study days with milk and native whey, recovery of muscle function was measured as changes in maximal isometric voluntary contraction knee extensions (MVC), counter movement jump (CMJ) 30 min prior to, and 0, 6, 22 and 30 h after the exercise session. The 0 h time point was immediately after the workout and about 20 min after the last set of leg exercise" (Hamarsland. 2017).

Unlike some of you would probably have expected before reading (about) the paper, hydro whey, which is often advertised as the "fastest whey protein your money can buy", did not rank first in the authors' analysis of the blood samples (see Figure 2).

Figure 2: Blood concentrations of total amino acids (a), essential amino acids (b), BCAAs (c) and leucine (d) before and after a bout of strength training and intake of 20 g of protein from milk, microparticulated whey (MWP), whey protein hydrolysate (WPH), whey protein concentrate 80 (WPC-80) or native whey (NW) in young men (Hamarsland. 2017).

Rather than that, the rarely studied "native whey", which is eventually nothing than cross-flow micro-filtrated (CFMF) raw milk produced the highest amino acid levels - and that despite the fact that WPC, which is usually produced by ultra-filtration of the "cheese whey", a byproduct of cheese manufacturing and was thus exposed to enzymatic processes and (optionally) pasteurization, and "native whey" have virtually identical amino acid profiles.

Previous acute response studies say: speed doesn't determine protein synthesis

If we rely on the often-heard claim that faster protein absorption would translate into increased gains, this would imply that the fractionate protein synthetic response to native whey should be higher than that we'd see in response to any other of the five tested proteins. Now, unfortunately, this response was not measured in the study at hand.

Figure 3: The faster absorption and increased aminoacidemia of whey vs. milk protein in Mitchell et al. (2015) did not translate to (A) significantly increased acute (A) and aggregate (B) myofibrillar protein synthesis.

From previous studies, we do know, however, that an increase in aminoacidemia as it was also observed in Mitchell's 2015 comparison of whey and milk protein concentrate does not translate to an increase in skeletal muscle protein synthesis (see Figure 3).

Previous "real world" (=longitudinal) studies say: speed doesn't build extra muscle

Now, the acute protein synthetic response can be misleading. A similar, but longitudinal, comparison of the effects of whey protein concentrate and hydrolysate supplementation on lean mass gains in 56 resistance-trained men by Lockwood et al. (2016) found no increase in the skeletal muscle hypertrophy response to 8 weeks of resistance training either.

Figure 4: Total lean mass (kg) before and after 8 weeks of standardized resistance training and supplementation with whey protein concentrate (WPC), WPC + lactoferrin and whey protein hydrolysate (WPH) in Lockwood et al. (2016).

In conjunction with the lack of effect the 4 sets of 10RM repetitions of leg press and knee extensions, and 3 sets of 10RM repetitions of bench press and seated rowing had on the subjects' countermovement jump (CMJ) performance in the study at hand, the existing evidence does, therefore, refute the conclusion that the results of the study at hand would imply that native whey protein is a better muscle builder (or a more effective recovery promoter) than any of the other dairy proteins Hamarsland, et al. tested.

Previous research suggests that faster amino acid absorption don't translate to increased gains and the observed increase fat loss w/ hydro whey is probably a result of its bio-active peptides | learn more  

So what does all that mean? While it may appear as if you'd have to get rid of your beloved whey protein concentrate, isolate or hydrolysate brand, the one you chose, as I have previously suggested, based on taste, price, and credibility, and buy some "native whey". There are two reasons why I believe this would be a mistake,

Reason #1 can be found in the study itself. After all, the authors readily admit that "[they] were not able to show any differences in recovery of muscle function after consumption of native whey compared to milk after a bout of heavy load strength training" (Hamarsland. 2017) - practically relevant effects on your workouts do thus not exist.

Reason #2 can be found in the literature, which shows consistently that there's no relevant increase in protein synthesis (and long-term gains) with so-called "fast(er)" proteins (Mitchell. 2015). Now, this doesn't mean that you can be sure a long-term study would not reveal other differences, such as the increased fat loss Lockwood et al. (2016 | reviewed here) observed when they compared regularly to faster absorbing hydrolyzed whey - this effect, however, has nothing to do with accelerated amino acid absorption and all with the different concentration of bioactive peptides (learn more), which could be present in "native whey", as well. After all, it is subjected to less processing steps than regular whey proteins | Comment on the SuppVersity Facebook Page!

References:

• Hamarsland, Håvard, et al. "Native whey induces higher and faster leucinemia than other whey protein supplements and milk: a randomized controlled trial." BMC Nutrition 3.1 (2017): 10.
• Lockwood, Christopher M., et al. "Effects of Hydrolyzed Whey versus Other Whey Protein Supplements on the Physiological Response to 8 Weeks of Resistance Exercise in College-Aged Males." Journal of the American College of Nutrition (2016): 1-12.
• Mitchell, Cameron J., et al. "Consumption of milk protein or whey protein results in a similar increase in muscle protein synthesis in middle aged men." Nutrients 7.10 (2015): 8685-8699.

40 vs. 70g of Food Protein per Meal? No Ceiling Effect for Improvement(s) in Net Protein Balance (+65% w/ 70 vs. 40g)

This study does almost everything right and yet, it still needs a follow-up study to address the question whether the results would be the same for fast(er) digesting proteins such as whey protein where 'more', i.e. ever-increasing boluses of protein, could actually increase the amount of protein that is being fed into gluconeogenesis, bros.

You've read it here, you've read it elsewhere: Simply doubling your protein intake ain't going to double your gains. That's true and the latest data from the Center for Translational Research in Aging and Longevity at the University of Arkansas for Medical Sciences ain't going to change that.

The questionable, if not incorrect overemphasis on postprandial (meaning right after you ingested a protein shake) and/or post-exercise and -prandial (meaning after the protein shake you consumed right after a resistance training workout) skeletal muscle protein synthesis of the vast majority of studies that investigate the effects of different doses of protein on acute protein kinetics has, however, given rise to the intrinsically flawed idea that any extra protein (in excess of 20-40g of high EAA protein, depending on the study you look at | the younger the subjects, the less appears necessary) would be wasted.

High-protein diets are much safer than pseudo-experts say, but there are things to consider...

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Satiety: Casein > Whey? Wrong!

Protein Timing DOES Matter!

High Protein not a Health Threat

In the experiment for their latest paper, Kim, Schutzler, Schrader, Spencer, Azhar, Ferrando and Wolfe went one step further. In a previous study in older subjects (discussed at the SuppVersity News a year ago | read it), the authors have already proven the ...

Read my article about the previous study.

"potential importance of suppression of protein breakdown in response to dietary [meaning intake from food] intake of meals containing two levels of protein totaling either 0.8 or 1.5 g protein/kg/day...

[More specifically, they] found that at both levels of dietary protein [i.e. 0.8 or 1.5 g protein/kg/day from food] whole body net protein balance became positive in the fed state compared with the fasted state, mainly due to reductions in protein breakdown" (Kim. 2015) 

This novel focus on the response to (a) food proteins and (b) the important net protein balance differentiates the study at hand, as well as the previously quoted preceding study from the rest of the pack which focused entirely on the response of muscle (often to various forms of protein supplements, instead of foods) and may thus (a) underestimate the total anabolic response to feeding and (b) give the false impression that it takes protein supplements to maximize the postprandial/postworkout protein anabolic response... to cut a long story short, Kim et al. are completely right to say that it is thus only...

"[...] reasonable to examine whole body effects of exercise in the context of quantifying the anabolic response to different levels of dietary protein [as they did it in their latest study in which they] have quantified protein kinetics (protein synthesis (PS), breakdown (PB), and net balance (NB)) at the whole body level before and throughout the response to two levels of protein intake in mixed meals with or without prior resistance exercise in healthy young adults, [hypothesizing] that 1) the whole body net anabolic response (NB) would be greater with intake of 70 g protein, compared with 40 g protein in mixed meals; and 2) the whole body net anabolic response to either level of dietary protein in mixed meals would be greater following resistance exercise" (Kim. 2016).

To test this hypothesis, the scientists recruited twenty-three healthy subjects [18–40 yr] who didn't suffer from diabetes, or any other active malignancy within the past 6 mo, didn't have gastrointestinal bypass surgery, a chronic inflammatory disease, low hematocrit or hemoglobin concentration, low platelets, concomitant use of corticosteroids, any unstable medical conditions, and who already performed resistance exercise more than once per week.

Table 1: Subject characteristic (before the experiment | Kim. 2016)

We are thus dealing with previously trained, albeit not exactly jacked young subjects (see Table 1 for detailes subject characteristics) who may be considered representative of 'the average gymgoer' who were randomly assigned to the resistance exercise group (X) or the resting group (R).

"The resistance exercise bout consisted of 3 sets of 10 repetitions of bench press, lateralis pull-down, leg press, and leg extension each at 80% of 1 repetition maximum (1 RM, the maximum weight that can be lifted for 1 repetition). Each set was completed within 30 s. The rest interval between sets was <2 min, and the entire exercise bout was completed in ∼45–50 min" (note: the subjects trained only on day 4 | my emphasis in Kim. 2016).

To standardize the subject's dietary intake(s) the meals for both, the medium and high protein groups were provided for both, the 3-day run-in period (intended to be dietary normalization period) before the metabolic study and the metabolic study on day 4.

This is not the end of the 30g of protein per meal rule: Why's that? Well, first of all the scientists measured total body protein turnover. It is thus not possible to say how much of the 65% decrease in protein breakdown was muscle specific (some people will argue the answer is zero). In addition to that, the study at hand provides evidence only for the acute effects of a single large high protein meal. The chronic effect could be different or less pronounced - especially if this meal is consumed as part of a diet that is already high in protein.

The protein source of choice was, just as in the previously cited study in older individuals (Kim. 2015) 85% lean ground beef from a local grocery that was formed into patties weighing 113.4 g (4 oz) or 283.5 g (10 oz) of the beef (pre-cooked/raw).

Table 2: Macronutrients of 3-day run-in on day 1–3 and metabolic infusion study on day 4; Values are expressed as means SE. Each subject consumed his or her respective interventional foods based on their sex; n number of subjects. X, exercise group; R, resting group; MP, low protein; HP, higher protein; M, male; F, female; CHO, carbohydrate (Kim. 2016)

Subjects were asked to record time of meal consumption and percentage of meal consumption and to photograph the meal before and after consumption, as well as to return all unused or empty meal/supplement packaging on the morning of the fourth day when they reported to the lab for the metabolic study (only subjects who achieved a minimum compliance of 80% consumption of meals progressed to the metabolic study).

Timing may matter albeit only for trained individuals, it seem.

Remember: For trained individuals timing may matter - While the evidence for nutrient and protein timing may be skinny (Kerksick. 2008; Aragon 2013; Schoenfeld. 2013), it's not as if there was no data suggesting that you want to put a special emphasis on consuming adequate amounts of high quality [=high essential amino acid (EAA)] protein such as whey (or dairy in general), meat, eggs, fish, soy or pea protein in the vicinity of your workouts.

Needless to say that this does not imply that you "wasted" your time whenever you fail to get your protein shake or high protein meal in within X minutes after your workout! 

By the means of phenylalanine as a tracer amino acids, the subjects' individual whole body protein kinetics were calculated based on the determinations of the rate of appearance (Ra) into the plasma of phenylalanine and tyrosine and the fractional Ra of endogenous tyrosine converted from phenylalanine as in the previous study (18). The analysis of this data yielded the following results (Kim. 2016): (a) Exercise did not significantly affect protein kinetics and blood chemistry, the feeding, however, (b) resulted in a positive net protein balance (NB) at both levels of protein intake, but...

• 

  Figure 1: Changes in rates of whole body protein net balance (NB), synthesis (PS), and breakdown (PB) from the fasted state in response to meal containing 40 g (MP) or 70 g (HP) of dietary protein with prior resistance exercise (X) or time-matched resting (R | Kim. 2016).

  the net protein balance (NB) was  65% greater in response to the meal containing HP vs. MP (i.e. 40g vs. 70g of protein; P < 0.00001) - irrespective of exercise, 
• the greater NB with HP was achieved primarily through a 66% greater reduction in protein breakdown (PB) and to a lesser extent stimulation of protein synthesis (for all, P < 0.0001), and 
• the HP resulted in greater plasma essential amino acid responses (P < 0.01) vs. MP, with no differences in insulin and glucose responses - likewise without sign. differences in the exercise (X-MP and X-HP) vs .the resting (R-MP and R-HP, respectively, in Figure 1) condition. 

As the scientists point out in the conclusion of their study, the ingestion of an increased amount of protein in form of a whole protein (in this case lean beef) will thus significantly improve the whole body net protein balance in the rested and trained state in healthy, young male and female subjects - mostly due to a previously often overlooked reduction in protein breakdown.

Bottom line: The study addresses an important question that had been left open in the previously discussed study in older subjects, i.e. 'Is the beneficial effect of increased protein intakes an age-specific phenomenon?' - with the answer being 'no, it isn't' and the study providing further evidence of the benefit of extra protein in both a sedentary and resistance training context, the study at hand provides further incentive to 'super-size" your average per meal protein intake to achieve total protein intakes way beyond the USDA recommendation of only 0.8g/kg body weight.

Latest Study Shows that a 3.3 g/kg High-Protein Diet is Safe -- And Yes, This Means it Doesn't Hurt Your Kidney or Liver | more

What the study does not do, however, is to address the question whether that's the same for fast-absorbing (more anabolic) whey protein, where both, the protein anabolic response (i.e. acute postprandial protein synthesis) as well as the postprandial protein breakdown could still show a ceiling effect in both, young and older individuals. Until this interaction with protein quality / the type of protein will not have been investigated, it still appears to make sense to aim for a higher per meal (and thus total) protein intake - after all, Antonio et al. (2016) have only recently shown that the often-cited potential detrimental effects on your health simply don't exist | Comment on Facebook!

References:

• Antonio J, Ellerbroek A, Silver T, et al. A high protein diet has no harmful effects: a one-year crossover study in resistance-trained males. J Nutr Metab. 2016.
• Aragon, Alan Albert, and Brad Jon Schoenfeld. "Nutrient timing revisited: is there a post-exercise anabolic window?." Journal of the international society of sports nutrition 10.1 (2013): 1.
• Kerksick, Chad, et al. "International Society of Sports Nutrition position stand: nutrient timing." Journal of the International Society of Sports Nutrition 5.1 (2008): 1.
• Kim, Il-Young, et al. "Quantity of dietary protein intake, but not pattern of intake, affects net protein balance primarily through differences in protein synthesis in older adults." American Journal of Physiology-Endocrinology and Metabolism 308.1 (2015): E21-E28.
• Kim, Il-Young, et al. "The anabolic response to a meal containing different amounts of protein is not limited by the maximal stimulation of protein synthesis in healthy young adults." American Journal of Physiology-Endocrinology and Metabolism 310.1 (2016): E73-E80.
• Schoenfeld, Brad Jon, Alan Albert Aragon, and James W. Krieger. "The effect of protein timing on muscle strength and hypertrophy: a meta-analysis." Journal of the International Society of Sports Nutrition 10.1 (2013): 1.

Revisiting Caffeine + Lactate - In Combination They May be Powerful Muscle Builders Which Boost Satellite Cell Activity + Anabolic Signalling And Trigger Muscle Hypertrophy

High intensity training builds muscle and maximizes lactate build up. Caffeine helps you to train at maximal intensities. Correct, but there appears to be a more direct link between lactate accumulation, caffeine supplementation and skeletal muscle hypertrophy.

No, you are not mistaken: The headline says and means that caffeine and lactate are powerful agents that may promote skeletal muscle hypertrophy by boosting satellite cell activity and anabolic signalling in favor of muscle hypertrophy.

After a thorough review of the existing literature discussing the individual effects of caffeine and lactate on skeletal muscle metabolism and anabolism, Yoshimi Oishi and colleagues from the Ritsumeikan University hypothesized that "a lactate-based supplement containing caffeine, an activator of intracellular calcium signals, could elicit proliferation and differentiation of satellite cells, activate anabolic signals in skeletal muscle, and thereby increase muscle mass when combined with low-intensity exercise training."

Are you looking for other muscle building tips?

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Study Indicates Cut the Volume Make the Gains!

Well, you already know that they were able to proof their hypothesis, right? Let's still take a look at how they did that - at least briefly:

"To assess this hypothesis, we initially examined whether lactate and/or lactate-caffeine treatment could elicit proliferation and differentiation of satellite cells or activate anabolic signals in C2C12 skeletal muscle cells. Furthermore, we examined whether the administration of a mixed lactate and caffeine compound (LC compound), concomitant with endurance exercise training, could effectively increase muscle mass via activated satellite cells and/or anabolic signals in rat skeletal muscle" (Oishi. 2015)

I know, the human study is missing, but if you think about the intensity dependent increase in lactate production it appears logical to assume that increasing lactate levels which as previously been shown to...

• upregulate the expression of MCT1 and genes coding for other components of the mitochondrial reticulum in skeletal muscle (Brooks. 2009)
• increase myogenin (the satellite cell activator) mRNA in skeletal muscle cells in the petri dish (Hashimoto. 2007)

Now, this raises the question how calcium comes into play. According to Oishi et al. its beneficial effects are related the ability of caffeine supplements to increase the amount of intracellular calcium (Lu. 2007), which activates calcineurin, which will in turn induce slow and fast fiber hypertrophy (Talmadge. 2008) - unfortunately, this effect appears to favor type I (=endurance fiber) over type II hypetrophy, but this may well depend on the trigger that's used, i.e. endurance training as it was the case in a rodent study by Talmadge et al. or your strength workouts.

Figure 1: Graphical illustration of the mechanism by which caffeine and lactate may increase your gains.

Too complicated? Well, check out my graphical summary in Figure 1. I guess this should explain the basic mechanism: Lactate up = increase satellite cell proliferation = hotbed for muscle hypertrophy + calcium up = increased calcineurin = trigger for increased hypertrophy.

Bicarbonate supplementation buffers the decline in muscle pH and allows for 15% greater increases in lactate levels while still increasing training performance on a high volume, high intensity leg workout | read more

High intensity = high lactate, high intensity + bicarbonate = even higher lactate: The study at hand used lactate + caffeine supplementation and low intensity exercise. With high intensity exercise the increase the usefulness of additional lactate supplements may be significantly reduced, because higher intensity equals higher lactate accumulation anyway. As a previously discussed study on high intensity high volume leg training indicates, this effect can be augmented by sodium bicarbonate supplementation which allows for increased lactate levels in the absence of the debilitating effects of skeletal muscle acidosis (read more).

In the study at hand, the researchers quantified the effects on skeletal muscle hypertrophy by weighing the gastrocnemius and tibialis muscle of the rodents after 4 weeks of treadmill training and the effects on muscle restructuring via incorporation of new muscle nuclei (learn more) by measuring the increase in DNA content from exercise training alone and exercise training in conjunction with lactate + caffeine supplementation.

Figure 2: Exercise and exercise + supplementation induced changes in muscle weight and DNA content of skeletal muscle in mice exposed to four weeks of low intensity treadmill running (Oishi. 2015).

As the data in Figure 2 indicates, both muscle hypertrophy and the exercise induced increase in satellite cell activity were further augmented by the addition of lactate and caffeine in dosages of 1g/kg sodium-lactate and 36mg/kg caffeine.

In conjunction with the likewise observed increases in myogenin and follistatin expression of the fast twitch (that's what you use for lifting weights) gastrocnemius muscle relative to the exercise alone, the results of the study at hand clearly warrant the scientists conclusion that the administration of sodium lactate and caffeine "can effectively increase muscle mass concomitant with elevated numbers of myonuclei, even with low-intensity exercise training, via activated satellite cells and anabolicsignals" (Oishi. 2015).

So, what does this mean in practice? Assuming the same effects would occur in human beings the effective dosages of sodium lactate and caffeine would be 81mg/kg and 2.9mg/kg, respectively. Practically speaking you would have to take ~6.5g of sodium lactate and 232mg of caffeine.

Remember? Study suggests, significant increases in mitochondrial builder PGC1-a with HIIT + sodium bicarbonate | read more

That's quite a reasonable amount and should not have nasty side effects. Whether the sodium lactate offers additional benefits to trainees who work out far beyond the lactate threshold (remember: the rodents did only "light exercise"), remains questionable. The same goes for the question whether the addition of sodium bicarbonate would elicit similar beneficial effects on the lactate induced increase in satellite activity. In view of the fact that previous studies show that it does potentiate the beneficial effects on another albeit not directly related marker of mitochondrial changes in muscle structure, namely PGC-alpha (see previous SuppVersity article), I personally believe this would be worth investigating | Comment on Facebook!

References:

• Brooks, George A. "Cell–cell and intracellular lactate shuttles." The Journal of physiology 587.23 (2009): 5591-5600.
• Hashimoto, Takeshi, et al. "Lactate sensitive transcription factor network in L6 cells: activation of MCT1 and mitochondrial biogenesis." The FASEB Journal 21.10 (2007): 2602-2612.
• Lu, Ying-Mei, et al. "Imbalance between CaM kinase II and calcineurin activities impairs caffeine-induced calcium release in hypertrophic cardiomyocytes." Biochemical pharmacology 74.12 (2007): 1727-1737. 
• Oishi, Yoshimi, et al. "Mixed lactate and caffeine compound increases satellite cell activity and anabolic signals for muscle hypertrophy." Journal of Applied Physiology (2015): jap-00054.
• Talmadge, Robert J., et al. "Calcineurin activation influences muscle phenotype in a muscle-specific fashion." BMC cell biology 5.1 (2004): 28.

Carnitine as Repartitioning Agent? IGF-1, p-AKT & mTOR Up, Catabolic Proteins Down + 7% Improvement in Lean- to Total Mass Ratio W/ HED of 1-1.5 of Carnitine/Day

It won't spare you the sweat, but carnitine could make it even more worthwhile by ramping up the anabolic and shutting down the catabolic signals.

Until 2006 l-carnitine has been known as a fat-burner, an in-effective fat-burner and an expensive and pretty useless supplement (depending on whom you were asking). Then, in July 2006, Kraemer et al. published a paper (a human study, above all!) in the journal Medicine & Science in Sports and Exercise a consequential paper so to say; a paper in which the authors report that l-carnitine l-tartrate supplementation at a dosage of 2.933g/day (this amount of LCLT contains 2g of pure carnitine) led to a statistically significant increase in androgen receptors in the vastus lateralis after a heavy resistance training protocol in previously strength trained male subjects (Kraemer. 2006).

Still, the evidence has always been inconclusive to say the least

Despite the fact that the concomitantly elevated post-workout luteinizing hormone levels (+19%) Kreamer et al. observed would tell you that the testosterone that would have been necessary to activate those receptors was already on its way, I have never considered this study as convincing evidence of the anabolic prowess of l-carnitine. Plus, let's be honest, differences in whatever serum markers in response to an acute bout of resistance training have failed us way too often, not to look at studies like these with appropriate skepticism.

Do you remember the Ratames study from 2005? The one that showed that high volume training lowers the no. of androgen receptors on the trained muscles? This certainly makes l-carnitine sound like the perfect addition to high volume routines, right? (learn more)

That the same principle of "calm down and don't get too excited over the results of a single trial" does all the more apply to rodent studies should be self-evident and still, science is all about taking each and every experimental result into account to form a theory that can explain all of them, or, alternatively, is able to bust short-comings in previous studies that don't comply with the predictions of the respective theory.

Now, the soon-to-be-published paper by Janine Keller and her colleagues from the University of Giessen (Germany) certainly qualifies as part of the evidence we simply cannot ignore, when we are looking for evidence in support of the theory that l-carnitine could be an overlooked muscle builder or repartitioning agent.

After all, their observation of decreased levels of the proteolytic (=catabolic) MuRF1 protein, as well as the ubiquitin-protein conjugates, which are increased in catabolic states such as starvation and atrophy denervation (cf. Wing. 1995) , alone, would signify that l-carnitine could make a valuable addition to everybody's supplementation regimen.

Lower catabolism + increased anabolism = ???

There is more, however, the addition of 1250 mg L-carnitine/kg to a basally "low carnitine" vegetarian diet also led to significant increases in systemic IGF-1 concentrations in plasma and a local increase in the activity of the PI3K/Akt/FoXO-1 signalling pathway (see figure 1)

Figure 1: IGF-1 mRNA and serum levels, as well as the muscle specific expression and phosphorylation (ph) Akt, mTOR & co after four weeks on the low or high carnitine diets (Keller. 2013)

These results do yet not stand in isolation as the ones by Kraemer et al. still do. Other recent studies by the same research group in Giessen, as well as colleagues from the University of Barcelona have already confirmed the anti-catabolic effects of l-carnitine in piglets and a cancer cachexia model in rodents, respectively (Keller. 2012; Busquets. 2012).

"And you are telling me that works in humans, as well? "

What's the best form of carnitine to take to elicit these effects: I knew you would ask this, so I react to two facebook questions by adding this red box willingly admitting that I just cannot tell you what the best form of carnitine is. There simply is no study that would compare e.g. acetyl-l-carnitine (ALCAR) and l-carnitine l-tartrate (LCLT) in a scenario that would be relevant to the above question. What I can tell you though, is that it appears as if you were better off with LCLT than with ALCAR, if your goal is to top off your intra-muscular carnitine levels. That being said, even normal creatine can do that - you will just have to take more of it. If you are looking for more information you can check out the part of the Amino Acids for Super Humans Series that's dealing with "the carnitines", here.

In this context it does yet also have to be mentioned that the effects of l-carnitine are at least in part species specific. How we know that? Well, in contrast to the said study by Basquets et al. the provision of an carnitine to piglets (Keller. 2012) did not only reduce the MuRF-1 expression, but also the level of its likewise catabolic E3 ligase cousin atrogin-1.

"It has been shown that myofibrillar proteins, like myosin light chain proteins are the main targets of MuRF1for ubiquitination. Thus, carnitine might suppress particularly the degradation of myofibrillar proteins, which under physiological conditions comprise around 60% of total muscle proteins. In contrast to MuRF1, atrogin-1 tags primarily proteins for degradation which are important for controlling protein synthesis and myoblast differentiation, like myogenic factor MyoD, myogenin and the eukaryotic initiation factor of protein synthesis eIF3-f." (Keller. 2013)

With pigs usually being a superior model of the human physiology, this would suggest that the anti-catabolic effects l-carnitine could have on humans are probably more, not less pronounced than those that were observed in previous rodent studies.

Whether the same goes for the IGF-1 response cannot be said, but just like the anticatabolic effects, the pro-anabolic increase in IGF-1 has been observed in previous trials, including a human trial by Di Marzio et al. who observed a significant increase in IGF-1 in HIV patients in response to the provision of 3g/day of acetyl-l-carnitine (Di Marzio. 1999). In the absence of the existing evidence from animal studies, these results would yet have little significance for healthy human beings, whose growth hormone and IGF-1 levels are not rock bottom to begin with (Viganò. 2003).

---

Bottom line: Irrespective of the absence of human data on the IGF-1 boosting effects from non-HIV patients - or even better in training scenarios - it would warrant future studies if an adequate amount of carnitine in the diet can exert beneficial effects in non-obese human beings. For the "sedentary", or let's rather say non-exercised rodents in the study at hand, the latter was a mere fat loss effect - despite the elevations in p-AKT, m-TOR, IGF-1 and the overall more "anabolic" state the rodents were in their lean body mass was not increased compared to their peers on the low carnitine diet.

"Just another set!" ... "I don't know man, we've already pumped away 100,000kg today... do you really believe that's productive, I mean, yeah, we are cuttin', but still" ...learn what this dialog is all about and whether and if / when "another set" is / isn't a good idea (read more)

The lean-to-total mass ratio of the rodents, on the other hand was ~7% higher in the rodents in the high carnitine group. If we do however take into consideration that most of you will not be vegetarians and thus not similarly carnitine deprived as the rodents in the control group on the <1mg/kg carnitine diets, it is highly questionable if the addition of the human equivalent of the 1.25g/kg chow, i.e. 15mg/kg body weight (HED) would actually yield any measurable benefit to non-vegetarians - irrespective of whether they train or not. After all, even the average omnivore human being consumes 100-300mg of carnitine per day (Broquist. 1994), so that the difference between your basal carnitine intake and the supplemental equivalent dose of 1050-1500mg/day is more than 100x lower than the exorbitant difference between the low (if not deficient) carnitine diet in Keller's rodent study at hand (remember: the basal diet had less than 1mg/kg chow; the supplemented diet hat 1250mg/kg diet!).

So what's the verdict then? I guess, I will leave the final words to Burke et al. who reviewed the usefulness of carnitine as an ergogenic aid in one of the first installments of the "A-Z Supplement Review" in the British Journal of Sports Medicine and wrote "future work with l-carnitine may also find some useful outcomes" (Burke. 2009) - needless, to say that the SuppVersity is going to be the place, where you will read about it first ;-)


References:

• Broquist HP. Carnitine. In Shils ME, Olson JA, Shike M (eds): "Modern Nutrition in Health and Disease." Malvern, PA: Lea & Febiger, 1994. 459– 465.
• Burke LM, Castell LM, Stear SJ, Rogers PJ, Blomstrand E, Gurr S, Mitchell N, Stephens FB, Greenhaff PL. BJSM reviews: A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance Part 4. Br J Sports Med. 2009 Dec;43(14):1088-90.
• Busquets S, Serpe R, Toledo M, Betancourt A, Marmonti E, Orpí M, Pin F, Capdevila E, Madeddu C, López-Soriano FJ, Mantovani G, Macciò A, Argilés JM:  l-Carnitine: An adequate supplement for a multi-targeted anti-wasting therapy in cancer.  Clin Nutr. 2012;31:889–895.
• Di Marzio L, Moretti S, D'Alò S, Zazzeroni F, Marcellini S, Smacchia C, Alesse E, Cifone MG, De Simone C. Acetyl-L-carnitine administration increases insulin-like growth factor 1 levels in asymptomatic HIV-1-infected subjects: correlation with its suppressive effect on lymphocyte apoptosis and ceramide generation. Clin Immunol. 1999 Jul;92(1):103-10.
• Glass DJ:  Signalling pathways that mediate skeletal muscle hypertrophy and atrophy. Nat Cell Biol. 2003; 5:87–90 .
• Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ, Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exerc. 2006 Jul;38(7):1288-96.
• Keller J, Ringseis R, Koc A, Lukas I, Kluge H, Eder K:  Supplementation with l-carnitine downregulates genes of the ubiquitin proteasome system in the skeletal muscle and liver of piglets. Animal. 2012;6:70–78.  
• Keller J, Couturie A, Haferkamp M, Most E, Eder K. Supplementation of carnitine leads to an activation of the IGF-1/PI3K/Akt signalling pathway and down regulates the E3 ligase MuRF1 in skeletal muscle of rats. Nutrition & Metabolism. 2013; 10:28. 
• Lösel D, Rehfeldt C. Effects of l-carnitine supplementation to suckling piglets on carcass and meat quality at market age. Animal. 2013 Mar 11:1-8.
• Salama AF, Kasem SM, Tousson E, Elsisy MK. Protective role of L-carnitine and vitamin E on the testis of atherosclerotic rats. Toxicol Ind Health. 2013 Feb 13.
• Viganò A, Mora S, Brambilla P, Schneider L, Merlo M, Monti LD, Manzoni P. Impaired growth hormone secretion correlates with visceral adiposity in highly active antiretroviral treated HIV-infected adolescents. AIDS. 2003 Jul 4;17(10):1435-41.
• Wing SS, Haas AL, Goldberg AL. Increase in ubiquitin-protein conjugates concomitant with the increase in proteolysis in rat skeletal muscle during starvation and atrophy denervation. Biochem J. 1995 May 1;307 ( Pt 3):639-45.