Adelfo Cerame - Road to The Wheelchair Nationals '12: The 5x5 of (Re-)Programming Your Workout Routine to Make Continuous Progress.

Image 1: The "roadmap" on Adelfo's back (left) may not yet be as detailed as the one of Phil Heath (right). The one in his head, however is probably as, if not more elaborate than the one of the reigning Mr. Olympia.

As a (hopefully) regular reader of the SuppVersity, I assume that going to the gym for you has become more than a annoying duty - more than something you are doing just because you fear that otherwise you would start looking like the 68.3% majority of Americans you are either overweight or obese (data according to CDC)... as I pointed out in the "Programing Success" part of the Intermittent Thoughts a, if not the major determinant of your dietary (and training) success is that "healthy eating" (and I am not talking about the "whole grains approach" here ;-) and smart, not excessive, training becomes a part of your lifestyle, an appreciated cornerstone of your daily routine. For Adelfo, "our man" at the 2012 Wheelchair Nationals in Florida, physical culture has become even more: It is his passion and his #1 priority and though this is what has brought him to where he is now,  he is well aware that getting too passionate, or let's say, letting your emotions gain the upper hand, can become counterproductive...

Sometimes, keeping on track means holding back

I just checked my calendar… And I have exactly 17 more days left until I reach the12-week mark when I will be halfway through my contest prep. And though I am currently working towards my short term goal of copying, better outperforming Duong's amazing transformation by Christmas, I must keep in mind that the latter is nothing but a "test run" to practice for the real event - the 2012 Wheelchair Nationals. So as much as I want to look incredibly shredded on Chistmas day, I mustn't rush myself by drastically slashing calories (stick to 1600kcal) or overdoing HIIT cardio. So I keep telling myself that I have to stay disciplined, stick to my assigned cheat days and stay on course, knowing that this way I should, no, I will hit my mark.

Image 2: Picture on the left hand side 149.5 lbs. Picture on the right hand side 141 lbs. Lets hope I can maintain the lean muscle mass in the latter part of my prep ;-)

To assure that I won't miss that, I have been weighing myself again: 141 pounds. Maybe you do remember - my previous weight was 149.5 pounds in September. That means that I have lost 9 pounds since I have started my prep back on October, 1st. It took me 2 months to drop 9 pounds, which means that I lost about a pound a week. Compared to what some biggest losers may drop within a week this appears to be quite slow, but as Dr. Andro pointed out in his Intermittent Thoughts on Healthy Weight Loss, the rate by which you will lose weight necessarily slows down, once your body has reached "healthy" body fat levels and it becomes really slow, when you are approaching the unnaturally low body fat percentages you will need to compete on stage. That being said, it should raise the red flag, when you are already decently lean an still lose more than 1-2lbs per week - chances are, that anything beyond that is pure muscle mass and that is something I certainly want to avoid.

Back to a regular exercise split

As those of you who have been following all my blogposts, here at the SuppVersity (thanks for that, by the way!) will be aware of, I really enjoyed training according to the escalating density principle. I got stronger, lost body fat and felt incredible tight... but as I have been hinting at in one of the previous installments, training at such a pace and trying to outperform your personal best every time you hit the gym burns you out pretty fast (specially if you are dieting down for a show). Therefore, and simply to change things up (remember: change and thusly novel stimuli are the prerequisite for adaptation), I decided to "go back" to a more traditional bodybuilding split this month.

Recipe of the week: Spartan Steak.

In line with this week's "traditional" training approach, the recipe of the week is a very "traditional" meal, simple yet delicious and particularly appropriate for a rest day of all of you m@tha-“IF”-ers out there!

• 7oz RAW grass-fed NY Steak (seasoned w/sea salt & pepper)
• 4 oz mangoes
• 3 oz cantaloupe
• 5 baby carrots

Macronutrients: 42g protein/ 26g CHO/ 18g fat

Tip: Add 1 tbs. coconut oil to the meal for your fat (grass fed beef is naturally lean so you may want to add more fat such as coconut oil or raw butter to add to your fats)

Last month I have been toying around with alternate workouts - doing EDT every other week - but noticed that my body still felt worn down by the fast paced heavy lifts. Especially my wrists did not recover properly, which, for me, is even more of a problem than it would be for most of you, guys, because I depend a lot more on my upper body during my everyday-life: The joints in my shoulders, elbows and wrist take a constant beating, anyway. So that even now that I have cut back on the "beating the crap out of myself"-style of heavy lifting, I am wearing wrist wraps, for the heavy lifts, which are, of course, still an essential part of my current 5x5 split routine.

Figure 1: Adelfo's current 5x5 training split; this is a screenshot I (Dr. Andro) sneaked out from his "secret" training log... let's hope he does not sue me for "breach of secrecy", now ;-)

I will be sticking to this split for the month of December.  For the first 3 weeks of December, I will still keep the intensity high and tension (weight) heavy. On the second to the last week of December, I will do a de-load week, before I do another famine/detox phase during the last week of December. And while I will talk more about sense and purpose of this technique, about which I have learned in Rob Regish's Blueprint, those of you who missed my previous experience with this low protein low calorie + heavy lifting regimen can read up on that in my previous blogpost.

"Deload week? What's that? Ain't that for pussys?"

Image 3: If you think deloading is for pussys, only, chances are you got more brawns than brains.

For those of you that don’t know what a deload is, it’s basically taking a week (or maybe more) off from lifting heavy and intense. In other words, you are taking a short break of that kind of extreme training that is highly productive in the short, yet potentially detrimental in the long run. You can either take the whole week off completely (away from the gym), or just basically play around with the weights. It all depends on how deep the whole was that you have been digging for yourself and how fast your body recuperates... and believe me, the benefits are manifold! Most notably, deloading...

• ... gives central nervous system a rest
• ... gives body & mind a rest
• ... can prevent overtraining & injury
• ... sets you up for new / accelerated progress
• ... refreshes & keeps you motivated

My current plan is to deload for about a week to give my body, especially my joints a rest before I start another famine/detox phase and start the second half of my contest prep. And since I am in contest prep mode, I wont take the full week off and stay away from the gym completely. Instead, I will ease up on the training, lift very light so that I get a little pump going, rack the weights again and head home.  

The beneficial novelty of the tried and proven

In the mean time, I will enjoy the astonishing benefits, I am currently seeing from a 5x5 routine, many of you may (rigthly so) call "old fashioned" or even boring. But I mean, who cares if it works? My strength has increased significantly in my bench press, and I give most of the credit to the techniques and tricks I have adapted from Rob Regish’s Blueprint. If I keep progressing like that, I do foresee myself bench-pressing three 45 plates on each side for 5 reps before the end of my contest prep (I’ll try to shoot a video for you guys next week on my progress with my bench).

Image 4: By incorporating techniques from the Blueprint Adelfo is making constant progress.

As for my back exercises, my strength may have come to a halt. This is specifically the case with any type of high rows or high pulls, and I think this is mostly due to my weight dropping from 149.5 to 141 pounds. So I didn’t necessarily lose strength but I can’t increase the weight in my lifts as much as I want to, because of the weight distribution. I only weigh 141 pounds now, and I’m lifting weight twice my body weight (250+ lbs). Also keep in mind that I don’t have the function in my legs to plant and keep me grounded, so my body can only withstand so much weight until I am lifting myself off the seat.

That being said, my energy and the intensity in the gym are still very high. Part of this could be because you can focus more on the individual lifts during a 5x5 training split vs. the fast paced as escalating density training

And now that we are already talking about training at a fast pace, Dr. Andro asked my opinion on the discussion that has been revolving around his recent blogpost on time under tension and lifting slow vs. fast:  I’ve never been a fan of lifting lightweight slowly… "What am I!? Some sissy just wanting to tone up, because I’m scared to put on too much muscle!?" Lol, just kiddin'… But seriously? Isn’t this the training myth women fall usually fall for, because they are afraid of getting too buff or bulky? So they lift light weights slowly and for high reps, believing that this will "tone" their muscles? I mean, from what the studies and the research in the “TUT” article shows, this would be the exact opposite of what these women should avoid because it increases protein synthesis right?

Lift heavy and intense, but with good form and a focus on constant progression


For me the fundamental denominator of every successful training protocol is that you lift heavy and intense, use a good form and keep an eye on "progress", i.e. increasing the tension you apply to your muscles... that's all it takes to grow! ... well, I guess it goes without saying that eating smart is a necessary prerequisite without which even the best exercise protocol is pointless.

Image 5: Don't train like Phil Heath, unless you are Phil Heath.
(Flex Magazine cover from July '08)

Moreover, it is important to realize that "increasing tension" is a very complex process, which can be achieved by slow negatives (which I am a big fan of by the way), exaggerated stretches (overhead pulls), static holds, modifications in set and rep ranges, reduced rest, increased TUT, etc. etc. It should thus be obvious that there is no such thing as a one size-fits-it-all solution to constant progress. As Dr. Andro said, it comes down to the individual’s preference and what works for you as an individual at a given point in your "career". What may be an optimal set and rep range for one person may be counterproductive for another. And as my own example shows, while EDT may be the best way to train for weeks A-D, in week E your progress may stall and another regimen will be the "best way" for you to train. If that was not the case, everyone who wanted to look like Phil Heath would just follow his training regimen from Flex Magazine and SHAZAAM! He would look like Mr. O!

You have to find what work for you (no matter what it is) and build on it.

Personally, I enjoy lifting heavy the majority of the time whether it is in the 4-6 rep range, using a 5x5 routine or during EDT-esque workout routines - all of these are part of my training arsenal, an arsenal I am constantly expanding and revising and where higher rep ranges are just another tool I use whenever I feel that switching things up training with higher reps and more volume could benefit me... it's a matter of knowing what works for you, and for me that mostly is using low(er) reps and high(er) weights. What is it for you, guys? Use the comments on the bottom of the page and let me know!

3.2g of Beta Alanine Reduce Rate of Perceived Exertion, Increase Time to Exhaustion and Ventilatory Threshold. Vegetarians, Older People and Diabetics May Benefit Most.

Image 1: If you are into running, ladies, beta alanine is for you ;-)

Those of you who make sure that they are getting their highly educative daily dose of the SuppVersity *rofl* will be aware that today's blogpost is, once again, dealing with beta alanine. Contrary to yesterday's post, which dealt with its pharmacokinetics, we are today going to have another look at what kind of real world performance outcomes the average (female!) physical culturist can expect from taking at least 3.2g of the beta amino acid per day - a dosage that has been shown in previous studies to increase intra-muscular carnosine levels by 27–39% in fast- and slow-twitch muscle fibers, respectively (Baguet. 2009). And though I do not want to spoil things, I can already tell you that the results make it quite clear why beta alanine is not the next creatine.

Somehow ergogenic, yet not really antioxidant

For the study that was conducted at the Applied Physiology Laboratory at the University of North Carolina, study that was conducted by A.E. Smith recruited 24 "recreationally active" women, of which the authors state that they "engag[ed] in 3–7 days per week of aerobic, resistance or recreational activities, but were not highly trained competitive athletes". With a mean age of 21.8 years, a height of 165cm and a body weight of 61.5kg the subjects are thusly representative of the average young woman who goes to the gym to either get or keep in shape. I am specifically emphasizing this, because - at least in the early days - beta alanine was heavily marketed as "the creatine for women" who fear the water retention people still claim was an inevitable side effect of creatine supplementation.

Image 2: If you retain water, this is not due to creatine monohydrate. Either you are taking to much (creatine loading is a thing of the past) or you have bought a product with shitloads of carbs in it - in that case, chances are its not only water you are gaining ;-)

Does creatine supplementation inevitably lead to water retention and weight gain? Just because this myth is still perpetuated, especially among female figure competitors, I thought it may be worth addressing this again: Pure creatine monohydrate without the sugar and the other bullshit you will find in many creatine supplements does not necessarily lead to increases in either total body or water weight. A study by Rawson et al. showed only recently that the consumption of 0.03g/kg creatine for six weeks did not result in statistically significant changes in body weight or water in men or women, despite significantly increased plasma creatine concentration and enhanced resistance to fatigue during repeated bouts of high-intensity contractions (Rawson. 2011).

The women were advised to simply stick to their usual routine and to refrain from taking any supplements and medications except from their 2x800mg beta alanine tablets. The latter were to be taken 3x a day... so according to Cocker, they should have consumed 2x0.8g x3/day = 4.8g/day and not, as the scientists state "3.2 g daily". Now, according to Smith et al. this was the "required dosage" all participants met. I can however not say, whether this means that the third dose was optional... and this is not the only oddity in this study, where it is well worth to look beyond the assessments and conclusions of the authors.

At the beginning and the end of the 28-day supplementation period, the women had to perform a graded oxygen consumption test (VO2max) to evaluate VO2max, time to exhaustion, ventilatory threshold and establish peak velocity (PV), as well as a "non-damaging treadmill run (oxidative stress run) for 40 min at 70% PV [peak velocity]". Before, immediately after and in the 2-6h post running window total antioxidant capacity (TAC), superoxide dismutase (SOD), 8-isoprostane (8ISO) and reduced glutathione (GSH) were measured. In addition to that, heart rate and ratings of perceived exertion were recorded during the 40 min run. The two main metrics of the study were thusly the potential anti-oxidant effects (TAC, SOD, 8ISO, GSH) and the anticipated immediate ergogenic effects (VO2Max, time to exhaustion, heart rate and perceived exertion) of beta alanine supplementation.

Figure 1: Effect of 28 days of beta alanine supplementation on maximal oxygen consumption (VO2max), time to exhaustion during a graded exercise test (VO2TTE) and ventilatory threshold (VT) and qualitative practical significance (data and caption adapted from Smith. 2011)

If you now have a look at the my graphical rehash of the scientists own evaluation of the effect beta alanine supplementation had on VO2Max, the time to exhaustion (VO2TTE) and the ventilatory threshold (VT), you will have to concede that mean improvements of 0.28%, 6.6% and 3.7%, respectively, as well as the large discrepancies among the subjects (from beneficial over negligible to harmful) do not actually speak for beta alanine.

Figure 2: Effect of beta alanine supplementation on oxidative stress markers measured as total
antioxidant capacity (TAC) and glutathione (GSH) and the qualitative practical significance
for women (data and caption adapted from Smith. 2011)

Things get even more confusing when we take a look at the antioxidant effects of beta alanine. Not only were the levels of superoxide dismutase (SOD) and 8-isoprostane (8ISO) not different between groups, and the effect of beta alanine on the total antioxidant capacity (TOC) of the subjects negligible, the scientists' summary of the effects does even suggest that, after an initial amelioration of the negative effect of treadmill running on GSH, there was some sort of a "likely harmful" rebound 6h after the 40 min exercise bout. Before you do now flush your beta alanine stores down the toilette, I suggest you first take a look at the actual (absolute) effects beta alanine supplementation had on the exercise induced changes in GSH levels:

Figure 3: Absolute GSH levels (in µM) immediately before (pre), post, 2h and 4h after treadmill running in the placebo and beta alanine supplemented women before (pre) and after (post) the 28-day supplementation period (compiled based on data from Smith. 2011)

As you can see in figure 3, there was an (unexplained) increase in GSH in the course of the 28-day supplementation period in both groups. With 2%, the latter was statistically non-significantly greater in the beta alanine group, and the "likely harmful" effect of beta alanine supplementation 6h after the end of the treadmill-run is simply the result of a smaller increase in GSH, when you compare the pre- to post-supplementation levels at the 6h mark - and I guess, you would agree that a +27% increase in GSH is not exactly something that deserves to be called "likely harmful", wouldn't you?

All-clear: Beta alanine is not ergolytic ;-)

Now that we have gotten that straight, let's get to the last (and most) significant benefit the women in the beta alanine group had from taking the supplement: a statistically significant reduction in the rate of perceived exertion during treadmill running (cf. figure 4).

Figure 4: Rates of perceived exertion during 40 min treadmill running before (pre) and after (post) 28 days of supplementation with beta alanine or placebo; small graph: relative difference post supplementation in women receiving BA vs. placebo (data calculated based on Smith. 2011)

It goes without saying that being 18% less fatigued is something that could well be worth spending the roughly 7$ for a 28-day supply on (calculation based on a dose of 3.2g per day taken over 28 days and assuming you buy your beta alanine in bulk at one of the major suppliers). This, by the way, could be particularly true if you belong to one of the following groups, who have been found to have low intra-muscular carnosine levels, to begin with:

Image 3: Older people are only one of the three groups who are "at risk" of low carnosine levels and are thusly most likely to benefit from beta alanine supplementation.

1. vegetarians - a 2011 study by Evaraert et al. found that "Vegetarians have a lower carnosine content of 26% in gastrocnemius compared to omnivores" (Everaert. 2011); and according to another recent study, the soleus carnosine content of vegetarians was "non-significantly" reduced by -9% after 5 weeks of sprint training, while the same protocol elicited increases of +11% in omnivores (Baguet. 2011)
2. older people - Evaraert et al. found a linear decline (ca. -10% in 20 years) in carnosine levels with age (correlation r=-0.26; Everaert. 2011); and Stout et al. report a highly significant +29% increase in physical working capacity at the fatigue threshold in twenty-six men (n = 9) and women (n = 17) (age ± SD = 72.8 ± 11.1 yrs) who  had been supplementing with 800 mg three times per day for 90 days (Stout. 2008)
3. type-2 diabetics - according to Gualano et al. type-2 diabetics have "significantly lower carnosine content (−45%) in gastrocnemius muscle", a relative deficiency of which the scientists argue that it "may be partially associated with defective mechanisms against oxidative, glycative and carbonyl stress in muscle." (Gualano. 2011)

After all, it does yet not really matter whether you are a type-2 diabetic, a vegetarian or simply getting older, compared to many (if not most) of the other overpriced ergogenics that are advertised all over the web, beta alanine is certainly not only one of the cheapest, but also one of the most promising candidates for the 3rd place on your list of staples, where (whey) protein and creatine should nevertheless still occupy position 1 and 2, respectively. And the fact that it did not prove to be a potent antioxidant in this study need not really be a disadvantage, after all, we still do not know whether the exercise-induced oxidative "damage" is not what actually triggers the highly desirable adaptive responses (cf. previous posts on "hormesis"), we are all looking for, when we are hitting the gym.

Better Sip Your Beta Alanine: Decreased Urinary Excretion from Time Released Beta-Alanine Formula.

Image 1: Tabbing or cabbing, or just washing it down with some water - what is the best way to take your beta alanine?

If you have been following the supplement scene for quite some time now, you will probably remember headlines such as "Beta Alanine, the next creatine!"... well, the hype which was deliberately fueled by the supp-companies, who realized that the price umbrella on creatine was shriveling, has abated and yet, beta alanine and, of course, creatine are both still there. Compared to the number of studies on creatine monohodrate, which were and still are published on almost a monthly basis, the science on beta alanine and most importantly its mechanism of action is however pretty skinny. I am thus happy to share with you a few interesting findings from two recently published studies - one today, the other tomorrow ;-)

The more it tingles the less it works... !?

Despite the fact that I personally like the awkward feeling you get when you take tons of beta alanine, I have always suspected that the "tingling" sensation - whatever its underlying reasons may be - is a very unsatisfactory indicator of whether the supplement "works" or not. After all, there is no physiological reason why the intended recombination of beta alanine + histidine to carnosine and the storage of the latter inside of your muscle tissues would go hand in hand with a "pins and needles" kind of flush. I was thus not surprised to see that Jacques Décombaz and his collegues from the Nestlé Research Center in Lausanne, Switzerland were able to show that ingestion of a "time-released" beta alanine tablet (2x800mg) did not only lead to statistically significant reductions in paraesthesia, but did also reduce the urinary excretion of the carnosine precursor (Décombaz. 2011).

Figure 1: Beta alanine (BA) serum values in µmol/L in the 6h after ingestion of 1.6 g of BA in solution or as time-released tablet (2x800mg); small graph: area under the curve (data based on Décombaz. 2011)

As you can see in figure 1, the time-released formulation avoids the rapid increase in beta alanine serum levels (solution: Cmax=248.2µmol/L; tablet: Cmax=81.9) Décombaz et al. observed with a standard solution of 1.6g beta alanine (Carnosyn TM) in aequeous solution.

Figure 2: Urinary beta alanine excretion (in µmol) in 11 healthy volunteers 0-2h and 2-6h after ingestion of 1.6 g of BA in solution or as time-released tablet (2x800mg); small graph: degree of retention (in % of intake) calculated based on urinary excretion (data based on Décombaz. 2011)

And although the area under the serum BA curve may be slightly smaller (AUC; figure 1, right), a calculation based on the decreased 6h urinary excretion in the 11 healthy caucasian volunteers (5 women, 6 men) who consumed the time-released preparation (cf. figure 2) reveals that the tissue retention from the tablet formulation was still 2.6% greater. Within the given standard deviations of 0.9% (tablet) and 2.1% (solution), I would yet be very surprised if this would actually make a practical difference as far as the ergogenic effects of beta alanine are concerned.

Figure 3: Topography of b-alanine-induced sensations. Data shown are the maximal reported values of the body
surface sensitive score (directly from Décombaz. 2011)

Of greater practical relevance is thusly the data on the incidence of "side effects" (did I mention that I like the tingling ;-), which - as the cute graphic in figure 3 goes to show - were significantly ameliorated when the subjects ingested their beta alanine in form of the hydroxypropyl methylcellulose, stearic acid, magnesium stearate, and silicon dioxide containing tablet.

... and why does it tingle? We still don't know!

What I personally do yet find more interesting than the reductions in sensory "side effects" are the speculations the scientists make as far as the underlying physiological reasons for the occurrence of the "pins and needles" (this was the prevailing description of the symptoms the study participants used) are concerned:

There are at least five recognized receptor sites for bA and the mechanism responsible for the sensitization of nociceptive neurons has not been unequivocally clarified [...] candidates include (a) bA-activated strychnine-sensitive glycine receptor sites, in association with glutamate sensitive N-methyl-D-aspartate receptors in the brain and the central nervous system, and (b) the mas-related gene family of G protein-coupled receptors, in dorsal root ganglia neurons ending in the skin, which are triggered by interactions with specific ligands such as bA.

While option b) sounds relatively harmless, option a) and previous studies reporting profound modulatory effects on brain neurotransmitter levels (esp. serotonin, cf. Murakami. 2010) keep me wondering, if beta alanine does not have more (and potentially harmful) side-effects than the minor paraesthesia.

So, in essence, we still don't know what it is that causes this feeling some people like, most people ignore and a handful of people hate so much that the time released tablets may in fact provide an adequate (yet obviously more expensive) alternative to powders or caps to max out their carnosine stores while avoiding the inconvenient sensation of "pins and needles" punctuation their flesh.

Image 2: Time released beta alanine in its natural form

Dr. Andro's tip for outsmarting the supplement industry: The wise guy (or girl) you are you probably don't really need me to tell you that by just sprinkling your beta alanine over your food or sipping on it in the course of your workout (or your daily routine) you can make your own "time-released beta alanine formula". A formula, of which you could even say that it was "invented by nature itself"... after all, poultry is the richest source of dietary beta alanine, so if you are into the whole ancestral diet concept spicing up your chicken drumsticks with another 1g of bet alanine would be the "paleo way of time-released beta alanine supplementation" *rofl*

A pros pos maxing out carnosine stores. I suggest you come back tomorrow if you are interested in whether or not doing this is actually worth it. "Unclear", "possibly", "negligible", "likely beneficial", "likely harmful" and the rest of the vocabulary that is used in a recent study from the Department of Exercise and Sport Science at the University of North Carolina to evaluate the effects the scientists observed on acute exercise performance after 28 days of beta alanine supplementation does in any case not sound that enthusiastic.

Update: Click here for the second part of this beta alanine double-whammy.

Branched Chain Amino Magic: Study Takes Another Step Towards a Better Understanding of the Anabolic & Anticatabolic Effects of BCAAs and Their Essential Cousins

Image 1: Without the other essential amino acids (EAAs), the branched chain amino acids, leucine, isoleucine and valine (BCAAs) have nothing to "build" your muscle from ;-)

Usually, I do not get very excited, when I hit upon another study into the "protein-synthetic response" that is triggered by the ingestion of branched chain amino acids (BCAAs). I mean, let's be honest... we all know that their ingestion will trigger the phosphorylation of the mammalian target of rapamycin and thusly increase protein synthesis, so why would we need another study where instead of a 17.5% increase in protein synthesis, we would see a 18.3% increase? Actually, we don't... the data Marcus Borgenvik, William Apró and Eva Blomstrand from the  Åstrand Laboratory, Swedish School of Sport and Health Sciences and the Karolinska Institutet, in Stockholm, Sweden (Borgenvik. 2011), collected goes yet well beyond what we have seen in most of the previous studies and is thus well worth an individual blogpost here at the SuppVersity.

BCCAs work! How? Little do we know...

If we are honest, we must concede that our (=the scientific) understanding of the complex processes that are triggered when "large" amounts of BCAAs hit our bloodstream, is very limited. What we know is that we can measure increases in mTOR-expression that correlate with likewise measurable increases in protein synthesis. What we do not really know is how exactly one leads to the other and where the influences of amino acid supplementation and exercise training overlap. This is even more true for the complementary side of the protein synthetic equation of which Borgenvik et al. state that

[w]hereas extensive evidence for the stimulatory effect of amino acids, either alone or in combination with exercise, on protein synthesis has been reported, their effect on protein breakdown is elusive.

In that, it is particularly confusing that "previous investigations involving ingestion of essential amino acids (EAA) in connection with resistance exercise have revealed no attenuating effect on protein breakdown", while studies which investigated the effect of BCAA or leucine in isolation, report reduction in protein degradation in subjects at rest or performing eccentric endurance exercise (MacLean. 1994). Reason enough for the Swedish scientists to recruit a group of seven healthy, recreationally active participants (5 men, 2 women; 27 (± 2) years; height 175 (± 5) cm; weight 67 (± 7) kg), put them on a standardized diet (17% protein; 25% fat; 57% carbs; ~2100kcal for women, ~2700kcal for men) for two days and, on the subsequent morning (subjects reported to the lab fasted) and after a thorough warm-up, have them perform

• 4 sets of 10 repetitions at 80% of their predetermined 1 RM, followed by another 
• 4 sets of 15 repetitions at 65% of their 1 RM of single-legged leg presses.

The subjects used the same leg on all exercises and rested ~5min after each set. Before the warm-up, during and immediately after and 15 and 45min after the exercise regimen the subjects consumed either

• 150 mL of BCAAs (2:1:1 ratio) in flavored water, or
• 150 mL flavored water alone.

The total amount of BCAAs was 85mg/kg or 5.695g for the "average" study participant. After four weeks the experiment was repeated with each participant receiving the opposite treatment.

Figure 1: Complete analysis of serum amino acid levels in the trained and untrained leg of subjects receiving BCAA or Placebo supplement before, during and after the completion of a standardized single-legged leg press exercise (data adapted from Borgenvik. 2011)

As far as the study protocol goes this is thus certainly not an extraordinary study. If you take a look at figure 1, where I deliberately plotted all the data the scientists gathered as far as serum amino acid concentrations are concerned, you will yet realize that what makes this study stand out is the sheer amount of parameters Borgenik et al. have analyzed. Similar data is also available for the amino acid concentrations in the exercised muscle and though, the scientists, who set out to investigate the effects of BCAA supplementation on protein breakdown, would probably disagree with me, here, I feel that this data actually has the most real world significance for physical culturists, like you and me.

Figure 2: Relative increase / decrease in intra-muscular BCAAs and other EAAs in BCAA supplemented subjects vs. placebo control at different time-points before, during and after single-legged leg presses (data adapted from Borgenvik. 2011)

After all, a brief glance at the effects the ingestion of ~6g of BCAA had on the respective tissue levels of leucine, isoleucine and valine (figure 2, BCAA) and the other, "missing" essental amino acids (figure 2, EAA - BCAA) should suffice to understand that though BCAAs may be the necessary to trigger protein synthesis, they are yet obviously not sufficient to "build muscle" - or how else would you explain the

pronounced reduction in the concentration of the aromatic amino acids, tyrosine and phenylalanine, in both plasma and muscle as well as muscle EAA (BCAA excluded) during the recovery period

Borgenik et al. observed in their study? The scientists at least conclude that

[s]ince tyrosine and phenylalanine are neither synthesized nor degraded in skeletal muscle, reduction in the levels of these amino acid could be indicative of an improved net muscle protein balance, i.e. an enhanced rate of synthesis and/or decreased rate of breakdown [and] could  be explained by incorporation into protein.

The accrual of muscle mass (whatever that may eventually mean, cf. yesterday's installment of the Intermittent Thoughts) thusly obviously relies on the presence of all essential amino acids and not just the "branched chained holy grail" of protein synthesis, of which the current study revealed that they (BCAA ingestion) reduced the expression of MAFbx, which regulates the protein transcription factor MyoD and the eukaryotic initiation factor-3f (eIF-3f), which, in turn is of importance in the mTOR-p70S6k signaling pathway, by 30% and 50% in the resting and exercising legs, respectively.

Figure 3: Relative (compared to placebo) mTOR and p70S6K phosphorylation in response to BCAA supplementation in exercised (EX) and non-exercised (Rest) leg at different time-points before, and after single-legged leg presses (data adapted from Borgenvik. 2011)

As figure 3 finally goes to show, we see the "usual" increases in mTOR and p70S6K phosphorylation that are commonly held responsible for the downstream increases in protein synthesis, and which were obviously more pronounced in the exercised compared to the non-exercised leg. The latter may be ascribed to what the scientists cautiously label a ...

[...] tendency for BCAA supplementation to attenuate the elevation in the level of Rheb mRNA in both resting (1.7-fold under the placebo versus 1.2-fold in the BCAA condition) and exercising muscle (2.4-fold versus 1.5-fold).

This ameliorative effect on Rheb, the low-molecular weight GTPase located immediately up-stream of mTOR, in combination with the exercise induced reductions in REDD2 expression (another negative regulator of mTOR) the scientists observed in the exercised leg are actually where we are currently at, as far as our understanding of the complex protein synthetic machinery goes. It is here at the gene-level where amino acid supplementation and its effect on Rheb and exercise and its effect on REDD synergize and facilitate those muscle gains trainees have been making for years often without any understanding of the biological underpinnings.

And though we may eventually be able to squeeze out another 5-10% more muscle mass, when we eventually get the "whole picture", I seriously doubt that even the most thorough understanding of the underlying biomolecular processes will change such basic recommendations as "take your 25g of fast digesting whey as a bolus immediately post workout" (cf. "Never Sip Your Whey!") - or what would you say?

Intermittent Thoughts on Building Muscle: The Skeletal Muscle Hypertrophy 101 - Part 1: What is Hypertrophy?

Image 1: Governator, Arnold Schwarzenegger, as a teen and in his early twenties. What - puberty aside - were the underlying mechanisms of the obvious increase in sleeve-size? I mean on a strictly myocellular level, of course ;-)

Those of you, who have been following the Intermittent Thoughts series over the last weeks will probably already have realized that I finally dropped the "Intermittent Fasting" from the title... this is something I have been thinking about for quite some time now. After all, the series has evolved way beyond its initial focus on a specific dietary protocol and has become more of an educational "how do you find your way to success"-series. With the format, intermittent thoughts, being still the same, the upcoming posts in this series, which will certainly touch on the topic of intermittent fasting, again, will be titled "Intermittent Thoughts on..." whatever the topic of the week may be... and for this week's installment the latter is going to be "Building Muscle: The Skeletal Muscle Hypertrophy 101".

I can already foresee that this is only the first in yet another series of posts. An introduction into the myocellular mechanisms that turn a normal teen like into a symbol of physical culture, or, to put it simply:  

What actually is skeletal muscle hypertrophy? 

Before I even try to answer this question let me remind you of something you have learned about "growth" in one of the previous installments of this series. In "Building Muscle Starts With Losing Weight" you have learned that one of the greatest fallacies of "classical" bulking, as in "eating everything that cannot escape your ravenous hunger for mass", is adipocyte hyperplasia. You may also remember that this increase in the number of fat cells occurs, when your existing fat stores are ready to burst and your body is in need of new storage capacities. Analogously, you would expect your muscle fibers to "hypertrophy" (from mechanical overload and constant nutrient abundance) until they are "ready to burst" and then divide and form new muscle fibers. (Un?)fortunately, myocytes are not adipocytes and thusly things are working somewhat different, here.

Figure 1: Overview over the three (?) pathways by which your skeletal muscles "grow".

If you take a look at the graphical overview I have come up with in figure 1, you will see that there are two, maybe three distinct pathways which contribute to what the average trainee subsumes under "hypertrophy".

1. Pathway A - hypertrophy via satellite cell recruitment and increases in the number of myonuclei per muscle fiber,
2. Pathway B - hypertrophy via increases in myonuclear domain size within an existing muscle fiber, and
3. Pathway C - hyperplasia, which would be the increase in muscle size by cell division and thusly an increase in the number of muscle fibers

The existence of different fiber types, or to be precise, the co-existence of different fiber types (fast twitch, slow twitch and various sub-types) at varying ratios within a single muscle group complicate things even further. Instead of giving you the usual theoretical lowdown on type I and type II fibers and how the former are supposedly used for endurance and the latter for strength training, I want to discuss the matter from a more practical perspective and first pose the question: What is that we actually want? 

I mean, you do not want "hypertrophy", but you want to get big and buffed, right?

Assuming that this is the case we should initially define "big and buffed" on a myofibrillar level by taking a look at how the muscles of the forerunners of physical culture actually look like - and I promise, what you will be learning today will, once again(!), go against conventional wisdom. Or would you have expected that bodybuilding is a sport that is characterized by a loss in highly glycolytic type IIb fibers and increases in both the intermediate type IIa, as well as the "endurance type" slow-twitch muscles? No? Well, then you should have a look at the data in figure 2:

Figure 2: Fiber composition of bodybuilders, recreational lifters, endurance rowers and sedentary control; determined via myosin heavy chain (MHC) isoform content of the triceps brachii muscle (data adapted from Jurimäe. 1997)

The results of the 1997 muscle biopsies by Jurimäe et al.  (cf. figure 2) clearly show that "getting big and jacked" is by no means about maximizing the "hypertrophy-prone type II fibers", as you may have read it numerous times on one of the thousand bulletin boards, or the numerous blogs of self-proclaimed fitness experts (Jurimäe. 1997). A bodybuilder is rather a person who has maximized the expression of myosin heavy chain I and IIa. Specifically with reference to the latter, the authors write:

It is interesting to note that Kraemer et al. (1995) have reported a lack of change in the area of fibres consisting predominantly of MHC type IIb proteins (i.e. FTb fibres) as a consequence of a 12-week resistance training programme. This suggests that a shift from MHC type IIb proteins to type IIa MHC isoforms may be a necessary prerequisite for FT fibre hypertrophy to occur. Consistent with this was the significant negative correlation (r = -0.67) between the percentage of MHC type IIb isoforms and arm circumference. Similarly, the smaller arm girth of the C group may have been partially due to the greater content of MHC type IIb isoforms in this group.

Or put simply,  the "strong" type IIb fibers have a very limited (if any) propensity for hypertrophy. So that, in order to maximize growth, it is necessary to trigger a shift towards the more "intermediate" type IIa fibers. If you take into consideration, how almost all bodybuilders got, where they are now, i.e. by a volume training approach, this is actually something you should have been able to infer simply from what has been and is still working for 99% of the trainees.

Figure 3: Intercorrelations between myosin heavy chain (MHC) isoforms and isoinertial (1-RM max), isometric (extension) and isokinetic (extension peak torque) strength indices (data adapted from Jurimäe. 1997)

Moreover, the data in figure 3 shows that this does not necessarily mean that they have to sacrifice their strength, as the percentage of type IIa fibers does not only correlate with increased muscle size, but also with increased isoinertial (1-RM max, r=0.66), isometric (workload, r=0.51) and isokinetic (peak torque, 0.61). strength. Getting big and buffed and getting strong thusly both require a profound shift in the "God given" fiber composition, but why?

Skeletal muscle hyperplasia - yes or  no? While there are a handful of studies which speak of hyperplastic responses to stretch or other form artificial overload, many (if not all) of them have been done on avian myofibers (Kelly. 1996), which, due to their special make-up, make it a) very difficult to distinguish between increasing overlap due to the longitudinal growth of intrafascicularly terminating skeletal muscle fibers and "real" hyperplasia and b) may not even translate to human beings. That's the reason, why I will disregard the issue of hyperplasia in the following discussion.

A very recent study by an international group of scientists from Sweden and the USA, may provide some insights, into why these fiber-transformations are necessary if you want to grow tree-trunk legs and sleeve-bursting arms. In this study, which was published on November 28, 2011, in the FASEB Journal (Qaisar. 2011), Rizwan Qaisar and his colleagues provide a detailed analysis of the the muscle fiber composition of mice who are either myostatin-negative or over-express the muscle building growth hormone IGF1 (we are talking about intra-muscular IGF1, here! More on that in future installments of the series).

Figure 4: Cross sectional area (CSA), number of mynuclei and myonuclear domain size of myostatin negative mice and mice overexpressing IGF1 relative to wild-type control (data calculated based on Qaisar. 2011)

As you would expect, both the myostatin-negative, as well as the IGF1 mice were more muscular than their wild-type cousins. There were, as you can see in figure 4, yet significant differences in fiber sizes (CSA), the number of myonuclei per fiber, and the domain sizes of the individual myonuclei in the exclusively fast-twitch extensor digitorum longus (EDL) and the predominantly slow-twitch soleus muscle.

Image 2: The balloon metaphor of skeletal muscle hypertrophy.

Note: If you picture a muscle fiber as a number of balloons which are held together by an elastic net, then the myonuclei would be within the individual balloons, which, in turn, would represent the myonuclear domains. You could thusly increase the muscle size, i.e. stretch the net, by either inflating the balloons, i.e. increasing the domain size, or simply adding more balloons to the net. The latter would then be equivalent to the recruitement of new myonuclei from the satellite cell pool in the sarcoplasma of the muscle fibers.

If you take a closer look at the data you will notice that in the IGF1 mice the predominantly fast-twitch EDL muscle growths mainly by increases in myonuclei number, a feature that is absent in the predominantly slow-twitch soleus fibers. The profound increases in myonuclear domain size that occur in the myostatin-negative mice, on the other hand, result in profound reductions in muscle function.

Figure 5: Specific force, stiffness and myosin content (secondary axes) of EDL and soleus muscle in wild-type control, myostatin negative and IGF1 overexpressing mice (data based on Qaisar. 2011)

Both specific force, as well as as muscle stiffness, are profoundly reduced in the EDL muscle of the myostatin negative mice (cf. figure 5), because they have surpassed the maximally sustainable domain size and have thusly become dysfunctional.

Figure 6: Domain sizes of EDL and soleus muscle fibers in wild-type control, myostatin negative and IGF1 overexpressing mice (data based on Qaisar. 2011)

This becomes even more obvious if we take a look at the domain sizes in isolation (cf. figure 6). It is the "uncontrolled" growth that is partly a result of a lack of satellite cell recruitment and consequent increases in myonuclei number, which cripples most of the animals with mutations in the myostatin gene.

Muscle hypertrophy = increases in myonuclear number & domain size

Healthy muscle growth, that is the intermittent take-away of this installment of the Intermittent Thoughts on building muscle, is thusly a direct result of "hypertrophy", as it is commonly associated with increased protein synthesis (and decreased or constant protein breakdown) and the subsequent expansions of individual myonuclear domains and the recruitement of satellite cells, which will then form new myonuclei.

As you may have noticed from the increasing amount of typos, of which I have probably overlooked 50% (sorry for that), my Sunday time-budget is already exhausted, so that I will have to postpone the discussion of what triggers these processes to the next installment. I do yet hope that the stuff you learned today provides enough food for thought to get you through the week ;-)

Reduced Exertion High Intensity Training - A Minimalist 2x20s HIIT Protocol For The Male Convenience Generation.

Image 1: Looks like humans are not the only lazy creatures, in these days of unhealthy convenience.

Laziness, it seems, is utterly human. If you look around, these days, it appears as if we were genetically programmed to be bone idle. And, from an evolutionary perspective, we may actually be. After all, moving around, hunting and gathering was an obligatory part of our lives in 99% of the human history. It was thus only consistent that our genes would tell us to sit down at the fireplace and relax, once we had found enough to eat on a given day... (un-)fortunately things have changed since those early days. Not only have we moved out of our caves, we have also found ways to radically reverse the ratio of activity to inactivity in our lives.

"Convenience" is the buzzword of the modern western civilization and the obesity epidemic is its unwanted consequence.

A consequence, which is yet by no means inevitable. After all, we all know that getting our behinds off our couches and into the gym, and setting the dietary recommendations of the (fast-)food industry, ahh... pardon, the government at naught would solve the problem, if ... yeah, if there was not this aforementioned genetically programmed laziness that makes the couch so much more appealing to us than the hard benches in the gym...

Sacrifice 30min per week of your TV-time and live to see your grandchildren graduate

A recent study from scientists from the United Kingdom does yet show that you could still spend more than enough time in front of your beloved television set, if you just performed what what Richard S. Metcalfe and his colleagues from the United Kingdom call the "minimal amount of exercise for improving metabolic health" (Metcalfe. 2011) - a 3x per week 10min exercise regimen with no more than two (yes, only 2x!) all-out sprints.

Figure 1: Outline of the training protocol, the black bars indicate all-out sprints at a breaking force equivalent to 7.5% of the individuals body weight (directly adapted from Metcalfe. 2011. Fig. 1)

As you can see in the outline of the experimental protocol, the 29 healthy and normal-weight, but sedentary young (~23y) men (n=13) and women (n=16) did not even have to start with 2x20s sprints. They rather built up to it, by starting out with a single 10s all-out cycle-ergometer sprint at a braking force equivalent to 7.5% of their body weight in the first week of the 6-week study period and built their exercise capacity from there.

Image 2: "Cardio" does not have to be steady state.

Note: If you have not read my previous blogposts on HIIT, you may have missed the information that interval training (not necessarily at the maximal intensity, though) is suitable for everyone - even heart disease patients (cf. Interval, not Steady State Aerobics is the Way to Go - Even for Patients with Myocardial Infarctions!). This has been confirmed only recently by Neil A. Smart et al. who found that "[i]ntermittent exercise may improve functional capacity [of congestive heart failure patients] to a greater extent than continuous exercise" (Smart. 2011) - and that despite the fact that both continuous (30min), as well as interval training (60min, 1 min cycling, 1 min rest) were performed at the same low intensity.

The rest of the 10-min exercise sessions, the subjects were pedaling along at 60W, which is about as much as it takes so that you do not fall off the bike, because of the lack of resistance that is required to stabilize yourself on the bike. The latter would have been tragic, at least if you are a man, because that would have counteracted the surprisingly (not for who has read about the magic of HIIT here at the SuppVersity before) profound effects this regimen, for which the scientists coined the name "reduced exertion high intensity training" (REHIT), had on the glucose homeostasis of the male subjects.

Figure 2: Changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test in men and women after 6 week of "reduced exertion high intensity training" (data calculated based on Metcalfe. 2011)

As the data in figure 2 shows, the statistically more than significant decreases in the area under the glucose (-12%) and insulin (-39%) curve (AUC) measured during an oral glucose tolerance test was exclusive to the 13 male participants - and that despite the fact that both, male as well as female study participants exhibited similar improvements in their individual VO2Max (+15% in men; +12% in women).

(RE)HIIT only for men?

As far as the underlying reasons for these gender differences are concerned, the scientists are pretty much at a loss, stating that this could be due to "the low statistical power of our study, with only eight female subjects performing the REHIT", " differences in metabolic perturbations during the brief high-intensity cycle sprints",  and the 3-day delay after the last HIIT session before the glucose tolerance test was done (as a SuppVersity reader you will be familiar with the notion that the "anabolic barn door" is wide open for 24-48h), so that "insulin sensitivity was improved in female subjects at an earlier time-point". Now, I do not want to sound like a himbo, but I would say that another observation the scientists made, provides a much better explanation:

[...] we observed that some of the female volunteers struggled with the transition from 60 W to the all-out sprints, and were unable to substantially increase their pedal frequency, and thus their power output during the sprints. This may have increased the aerobic contribution to energy supply and reduced glycogen depletion.

In other words, what was supposed to be a sprint turned out to be a sluggish ordeal. The slightly, but statistically significantly higher rates of perceived exertion (+10%) in the female study participants corroborates the assumption that the women simply did not burn enough glycogen. If we do now also consider the results of a 2008 study by Hagobia et al. who report that

[...] in women, exercise altered energy-regulating hormones in a direction expected to stimulate energy intake, regardless of energy status. In men, the response to exercise was abolished when energy balance was maintained.

It appears obvious that an increase in pedaling frequency by adapting the resistance to the individual fitness levels and dietary controls may be necessary to render this minimalist "REHIT" protocol productive for the fairer sex.

Figure 2: Comparison of changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test subsequent to 6 weeks of REHIT, or 10 months of "classic cardio" exercise, or dietary intervention (data calculated based on Metcalfe. 2011 and Dengel. 1996)

The comparison of this 6 week exercise program with the results of a 10 months intervention program in likewise healthy sedentary, but older men (45y) who exercised 3x a week for 40min (steady state) at 75-85% of their maximal heart rate, goes to show that it would well be worth making the REHIT protocol work for women, as well (Dengel. 1996). After all, the steady state endurance protocol in the Dengel study was not only four times more time-consuming (plus, the intervention period was 6.6x longer) than the modified HIIT protocol in the Metcalfe study, it also failed to improve the glucose response to the oral glucose tolerance test and produced less pronounced improvements in insulin sensitivity (cf. insulin AUC in figure 3). The mild caloric reduction (-300-500kcal/day) that was imposed on another group of the study participants, on the other hand, yielded similar reductions in glucose and insulin AUCs as the REHIT protocol in the Metcalfe study that was accompanied by a body weight reduction of ~10%, a reduction in body-fat of -5.8% and essentially no loss in fat free mass!

Note: Unfortunately, Metcalfe et al. did not measure the body composition of the study participants. In view of the results of the Whyte study (Whyte. 2010), I cited in the Intermittent Thoughts on Healthy Weight Loss, where the participants lost -2.4cm of their allegedly obese bellies within no more than 2 weeks of doing HIIT, as well as the well-established correlation between insulin resistance and the size of your beer-belly, it is very well possible that the male participants in the Metcalfe study will have lost some body fat doing no more than 8.67 minutes of all out cycling spread across 18 training sessions in 6 weeks... and if they didn't their diet probably was still too convenient ;-)

The (in-)convenient truth about your future

Taken together the results of these studies suggest that a) steady state aerobic exercise is pretty pointless, b) even a minimalist HIIT regimen goes a long way, as long as c) you really hit it hard and d) adhere to your regular (hopefully non-convenient) diet, or even better e) introduce a slight calorie deficit. In other words, without at least some "inconveniences" as far as nutrition and exercise are concerned, chances are that YOU will either remain or become one of the 34,004,946 obese human beings that are now populating a planet where the US alone spend 1,550,566$ per day on the detrimental health consequences of the"convenience" of its citizens (data from Obesity Statistics).

Green Tea Extracts for Building Strength & Size and Losing Weight - Fact or Fraud? Or, Why It is Always Worth Taking a Look at the Data that Is NOT in the Abstract.

Image 1: If the watery green tea is healthy, then a potent extract must be even more healthy, right? This may well be just another instance of "supplementational idiocy"...

I know people love their Green Tea! After all, Camellia sinensis is one of the staples that has not yet been debunked as another hoax of the supplement of pharmaceutical industry - a real healthfood, right!? Well, you will probably be familiar with my skepticisms towards the notion that taking tons of the polyphenols you are "supposed" to get in relatively small quantities from 2-3 cups of green tea in supplemental form must necessarily be a good thing, just because epidemiological data suggests that people who consume green tea (for those who only now this stuff in capped form: Green tea is actually a beverage ;-) in moderation are overall healthier than people who abstain from drinking hot water extracts (=tea) from minimally oxidized (=green) Camellia sinensis leaves.

Did you miss my previous blogposts on the negative effects of high dose green tea extracts on testosterone levels and male fertility? If so, I suggest you read up on that one before adopting the (stupid) more-is-more principal and popping the whole box of green tea caps at once.

Two recent studies do confirm the notion that green tea, even as a supplement, may be a worthwile addition to your dietary (I suggest you drink the tea not use the supplement) or supplemental (if you cannot stand the taste of the brew) regimen. The first one comes from scientists from the University of Warsaw in Poland (Jówoko. 2011). In a small-scale study with 35 subjects, Ewa Jówoko and her co-workers investigated the effect of 1280mg of green tea polyphenols (from a standardized GTE supplement by Olimp Sports) had on the adaptational response to a standardized 4-week strength training regimen (cf. figure 1)

Figure 1: Summary of the study design - participant characteristics, training and supplementation regimen.

If you look at the summary of the study protocol in figure 1, you may notice that there are two factors which contribute to the real-world significance of the study. Firstly, the subjects followed a semi-standardized diet (90g protein; 270g carbs; 104g fat), because they had to eat at the University's cafeteria. Secondly, the training, as well as the supplementation protocol are similar to what a real beginner would be doing in the gym, when he strives to build lean muscle tissue. On the other hand, this also means that we will probably see different (I would bet even less pronounced) results in trained athletes / advanced strength trainees with an optimized diet and a highly sophisticated supplement regimen - so bare that in mind, when you interpret the following results.

Figure 2: Changes in back squat and bench press 1-RM max and repetition max after 4-weeks of strength training with and without GTE supplement (data calculated based on Jówoko. 2011).

It should not surprise you that 4 weeks of training led to increases in squat and bench press performance. The inter-group differences, as well as the increase in maximal repetition number on the bench, however, did not reach statistical significance. In other words, what we are seeing here are effects of the exercise regimen, independent of GTE supplementation.

Figure 3: Changes in blood pH, base excess and lacate subsequent to the initial (Term I) and post (Term II) muscular endurance and max strength tests (data calculated based on Jówoko. 2011).

Similarly, the changes in blood ph, base excess and lacate subsequent to the initial (Term I) and post (Term II) muscular endurance and max strength tests (cf. figure 3), were not statistically different between groups. But if you followed the SuppVersity news lately, you will already know that blood ph is the domain of plain baking soda... so why even bother with green tea in this regards? After all its not even supposed to be a H+ buffer, but a powerful anti-oxidant, so what we should see are decreased rates of oxidation...

Figure 4: Lipid hydroxyperoxides at rest, 5min and 24h after a strength and endurance test before and after the 4-week intervention (data based on Jówoko. 2011).

And in fact, if you take a very close look at the data in figure 3, you may be able to see (I highlighted the bar for you ;-) why the title of the study, "Green tea extract supplementation gives protection against exercise-induced oxidative damage in healthy men", is not totally off: The degree of lipid peroxidation at rest(!) remained constant (within statistical margin) in the GTE group, while it increased by +27% in the non-supplemented group. In view of the non-existent differences in terms of strength or endurance gains between the groups, it is yet very questionable whether this "protective" effect is worth the 16$ (based on the price of the original supplement used in the study that is only available in Europe) it would cost to mimic the supplementation regimen used in the study - especially for someone who does meet the dietary requirements for vitamin E, which is something the study participants with their cafeteria food didn't.

Scientific fraud in the name of marketing

The results of the second study, which investigated the effects of decaffeinated green tea extract (DGE: 2x530mg per day; 800mg catechins per day, total) on body weight changes in 69 overweight subjects (sedentary males, aged 40–69 years, with BMI > 28 and < 38 kg/m²) are similarly dazzling. In their abstract, A. L. Brown and his collegues from Unilever (do I have to say anything else) summarize the results of their 6-week placebo controlled cross-over study as follows (Brown. 2011):

Despite a similar increase in estimated energy intake during intervention period 1, body weight decreased by 0.64 (SD 2.2) kg and increased by 0.53 (SD 1.9) kg in the DGT and placebo groups, respectively (P< 0.025), suggesting a protective effect of green tea catechins on weight gain.

Does not sound earth shattering, but -0.6kg weight loss does at least appear to be more desirable than +0.53kg weight gain. But even if you do not have access to the full-text (as I do) and are thus able to debunk this as a blatant manipulation of the facts (which, by the way, is the result of selecting data from the more favorable 2 weeks of the 6-week study period), the standard-deviations of 2.2kg in the DGE and the 1.9kg in the placebo group should ring an alarm. If you do have the full-text, and take a closer look at table 3 (cf. excerpt)...

Table 1: Excerpt from table 3 in Brown, 2011

... you should start sensing fraud. After all, the table clearly states that the mean body weight loss over the whole study period was -0.038kg for the placebo and -0.327kg for the decaffeinated green tea group. If you now scroll a few pages down and read the last paragraph...

The authors are all employed by Unilever Research & Development, which is a division of Unilever plc, a company which has a significant commercial interest in tea. Unilever plc provided all funding for the study.

... it should become obvious that, even in the case of something as "innocent" as green tea, you better not believe everything you hear and read about "superfood" and respective extracts on the Internet. So, instead of buying decaffeinated capped bullshit from Unilever, you better go to your local grocery store, get yourself some quality green tea and make tea-time a relaxing part of your probably hectic daily routine ;-)

Adelfo Cerame - Road to The Wheelchair Nationals '12: Back From Thanksgiving and in Better Shape Than Ever!

Image 1: Some people just know how to improve their physique even when pigging out on thanksgiving. Or can you see any collateral damage the turkey, the pie and the pie and the turkey from last week have done?

Assuming that all of you have eventually overcome the physical and psychological consequences of your thanksgiving festivities, you should be about as ready as can be to kickstart the last three serious training weeks of the year. It alway amazes me how long some days (especially those without lectures and tons of paper work in the office) appear to be, when weeks and months fly by like nothing. I remember back in the day, when I first contacted Adelfo on behalf of the Suppversity Student Spotlight and we came up with the idea for this series, I was thinking to myself: "Damn, 2012? That is a going to be a hell long series of blogposts! Let's hope people will like it..." And now? Well, the title of the email I just received from Adelfo is "2 months down! And 3 1/2 more months to go!" And the positive feedback we are receiving week by week is overwhelming (keep it coming ;-). So what more can I say? I guess I better say nothing and let just Adelfo tell you what he has been doing the last days to make sure to pocket his pro-card at the 2012 Wheelchair Nationals...

Time flies by! 16 weeks out and keepin' it rollin'!

I am 16 weeks out from my show. Man! Am I glad that I started my prep 2 months ago, because it feels like the next 16 weeks are going to fly by. Today is the first of December and, as I mentioned in my last blogpost,  I have cut back another 200kcals from my diet and am now at daily caloric intake of only 1600 kcal. I actually have already the first day with 1600kcal under my belt, and it felt.... it felt like this is going to be a walk in the park! Although my carb-, and with the latest cut, even my fat-intake are pretty low, now (160g protein/ 50g CHO/ 75g fat per day), I still manage to get my schoolwork done, help my clients throughout the early part of the day and still have tons of energy to burn when I train later in the afternoon. Two years ago I would’ve been dead tired by the time 4 o’clock pm came around and would have just gone through the motions at the gym.

Figure 1: Adelfo's current macronutrient breakdown. Since December 1st, he is at a 1600kcal/day level.

I feel that I have been able to perform efficiently throughout the day and train optimally in the gym ever since I realized that my body prefers fat as a better fuel source than carbohydrates. I also feel that my body has adapted to using fats more efficiently, the reason why I really don’t get affected when I have to drop my carbohydrate intake. Since my body is now adapted to being a fat burning machine, it does efficiently utilize its own body fat stores as a source of energy, when carbohydrate and dietary fat intakes are low. And while I have deliberately not gone all the way, now, i.e. I have not yet dropped my carbohydrate to zero and my fat intake to similarly low levels, this may still happen in the last week(s) of the prep and I am confident that, even than, I won't be the walking Zombie I have become in the course of classic high-carb preps, where your energy levels plummet when you eventually have to drop the carbs to get stage ready.

Intermittent fasting gives me balance - physiologically and psychologically

In that, I am convinced that the high(er) fat approach aside, my decision to switch to an intermittent fasting protocol also has a lot to do with how smooth my prep and dieting has been going so far. I honestly can say, that I rarely feel hunger pangs, if any at all. I’m not pre-occupied with what I’m going to cook or eat next. My mind is not distracted with thoughts of food. I can even go a whole day without eating and I feel fine. When I take a look back, it’s amazing how much my diet controlled my everyday life. Don’t get me wrong, I love the science of nutrition, eating smart, making healthy food decisions and preparing for bodybuilding shows, but when you start getting OCD and letting the diet determine and control how you live your life. Dieting sometimes even goes so far that it starts to alter your personality! And this is, when you should now: It's time to make a change!

Natural hormone optimization - a new asset in my portfolio!?

Video 1: Mike Mahler's "Hormone Optimization" seminar on YouToube (click on the navigation on the right to see all parts). Big kudos to Mike for sharing so much great information for free!

So far everything from diet and training is going great. The one thing though that I’ve noticed that needs improvement in my prep is sleep. For some reason I’ve been having trouble sleeping…while searching for a solution to my issue and trying to find a reason why my sleeping patterns were so out of whack, I ran into a YouTube video by Mike Mahler, where he discusses hormone optimization in quite some detail. Leptin, insulin, adrenaline, cortisol, ... he covers them all and I thin that I may have found possible reasons for my suboptimal sleep patterns. In particular, I realized that my cortisol and adrenaline levels might be too high during the night. I try to get 7-8 hours of sleep but most of the night I’m tossing and turning. I don’t necessarily feel that it’s from stress, well nothing negative at least. I do think about a lot things at night though… like I said nothing negative, more like thoughts of future endeavors, excitement to compete, how I can make my business successful, ways I can improve training and nutrition… like thoughts of that nature.

Eventually I found myself digging deeper into this subject of hormones and hormone optimization trying to learn and educate myself on a topic I know nothing about, but yeah… anyway, I think I’ve found a subject that peaks my curiosity and will probably keep me busy for a couple of weeks trying to learn as much as I can and will most likely distract me from my school work ;-)

End of November: 4 weeks paying off...

A pros pos work, it's also time to evaluate where a hell lot of hard work in the gym has gotten me in the past couple of week. So here are some recent progress pictures that I took yesterday, as well as comparisons from the beginning of the month.

Image 2: Picture on the left hand side was taken on November 15, 2011, and the picture on the right hand side was taken yesterday on November 30, 2011 (photos by Adelfo Cerame, 2011).

As you can see with the most recent picture, the 2-day Thanksgiving holiday feasting I engaged in last week did nothing to hamper my forward progress.With the front pose, I definitely can see a difference especially my abdominals. Since I don’t have the luxury to weigh my self often, I always use my abdominals as marker to gauge and monitor my progress… and I advice that you should do so, too. Don’t get too pre-occupied on scale weight. The smaller your waist gets, the lower your body fat gets. Losing body fat and maintaining lean muscle mass is what’s important, not what the scale reads.

... yet a still not at my short-term goal of outperforming my friend Duong ;-)

To be honest from looking at the comparisons, I feel that I certainly could afford to stay at 1800 calories and still make some good progress by the end of December. In fact, I was tempted for about 5 minutes, but then I reminded myself of  the short-term goal that I set for myself, which is to achieve or better outperform Duong's already phenomenal physique by Christmas, which also happens to be the 12-week mark in my contest prep (sorry Duong, just my competitive nature ;-)

Supplement reviews: Since this past weekend there was a black Friday/Cyber Monday sale online @ TFSupplements (by the way, although I do not even get a discount there, I still want to mention that this is a very cheap place to shop for supps ;-) I picked up a bottle of Liquid Clenbutrx by VPX (yeah I know… the name sounded pretty sketchy to me also!), and a tub of Anadraulic State by LG Sciences. Both were at a very affordable price compared to retail.

Note: I just started on both supplements this week,
so you’ll have to wait until I finish them for a full review.

Image 3: VPX Clenbutrx, a solid product with a more than questionable name, which will yet have to showcase its fat burning magic in the weeks to come.

Liquid Clenbutrx: My initial thoughts were…  name and bottle alone of the VPX product (with the little injection dispenser) looked and sounded suspect to me. I mean look at the name… rhymes with clenbuterol right? And look how they make the bottle look all-pharmaceutical like with the injection dispenser to the side… "It looks like it can be illegal, so I guess it must work!" *rofl* Even with all the signs directing me to stay clear, the price was right, the majority of the reviews were positive (on a side note… when I read supp reviews I take into consideration the physique of the one making the review. You usually can find their profile picture on the left hand side of reviews), and even Mr super-critic Dr. Andro considers VPX among the most reputable companies in a business, where shady names of obviously have become part of the game...

• Taste: Tastes like shit and Nyquil mixed together! It’s gotta work if it tastes this bad right?
  
• Energy: So far for the past 3 days since I’ve been taking it… my energy is literally through the roof. In fact this elixir kept me up all night for the first day, because I took the 2nd dose to late in the afternoon… and I guess taking anadraulic state 30 minutes after does not help either - though this is actually a "non-stim" pre-workout product. I am, by the way, curious on how long these potent effects are going to last and whether they will have worn off before I will have gone through the whole bottle. Keep checking back for more info in the posts to come.
• Fat Loss: Don’t know yet, until I finish the bottle, but I get a good sweat in the gym.
• Side notes: So far no jitters throughout the day or while I workout. And so far it hasn’t ramped up my metabolism in the Ferrari-like way it claims to do. But hey - should I really have believed that? I guess no. So, not a bad product, so far.

Image 4: LG Sciences' Anadraulic State GT - for the 14$ I would hardly have gotten the 720g of ingredients in bulk.

Anadraulic State: My initial thoughts… Another pre- workout supplement that’s worth a try because 720g for $14 and a really sound ingredient profile, this was obviously a bargain!

•  Taste: Strawberry lemonade, well at least that is what the label says. I guess it's a good thing that it does not taste as if it was mixed with battery acid, though ;-)
• Energy: I did not buy it for the energy factor. It's a non-stim and with the potent effects of the Clenbutrx I really can't tell if you would feel some kind of energy rush from Anadraulic State, as well.
• Pump/ vascularity: I can’t really tell either because my body gets a good pump or gets pretty vascular even when I don’t take pre-workout supplements.
• Strength/ performance: So far it’s all me. But given the fact that the ingredients are meant to do their magic over time, I did not expect to notice it until being on it for at least 2-3 weeks.
• Side notes: Nothing to really report or rave about yet.  

I will keep you updated on the impact these two have on the results I am seeing in the mirror, as well as the gym in the future installments of this series. Every Thursday, right here at the SuppVersity - remember that ;-)

Image 5: Not exactly hitting the macro ratio is an issue only OCD bodybuilders will worry about... and as Dr. Andro likes to say "The stress due to too much thinking about what to eat and what not to eat is much worse than the one wrong food choice you could make".

If you want to know how this little precontest-contest turns out, I suggest you come back next Thursday and see how far I've gotten already, because, for today, that is all, folks! And with the supplement feature being this week's special, I will skip the weekly recipe and just leave you with a picture of 2 big ass turkey legs from the last of my holiday leftovers that I’m about to eat before I begin my fast.

I usually like to track my macros and actually don’t mind doing it, but since my last meal before I start my fast and hit the sack are P+F meals. It’s usually pretty easy for me to eye it and guesstimate my macros. My macro meal split for my protein and fat are around 50g protein, and 25g fat. I’m guessing these 2 turkey legs are a bit under my protein and fat, but I’m not too worried about it... buon appetito!