Does the Usefulness of Vitamin E Supplementation Depend on Your Activity Level? Profound Decreases in Baseline and Peak Exercise Induced DNA Damage Would Suggest So

Image 1: If you are an athlete, let's say a competitive rower who trains 3+h per day, it appears as if 400IU of vitamin E would be nothing, but beneficial. If you are a couch potato, though, even that may hamper the small hormetic response you get from taking the stairs once a week ;-)

I don't know if you do remember, but it is actually not all too long ago that vitamin E was what vitamin D is know: The highly celebrated non-pharmacological savior of the ailing human race. Cancer? Heart disease? Diabetes? Alpha-tocopherol, which proved to be the most potent anti-oxidant in the tocopherol family, would solve all your problems and with its ability to "scavenge" the bad "free radicals" (sounds like a story from the Brother's Grimm, doesn't it?) it would also prolong your life-expectancy. After all, those mischievous reactive oxygen species were the primary drivers of the aging process... well, today we know better. Supplemental vitamin E alone does neither prevent nor cure any of the diseases of the civilization. And the "free radical theory of aging" has come under fire, as of late (cf. previous blogspots on hormesis).

Vitamin E - fallen angel or an angelic demon!?

After being disregarded by the disappointed lay-press for years, vitamin E has gotten quite a bad rep, as of late. "Journalists" claimed that scientists had found that instead of offering protection, supplemental vitamin E (+selenium) would actually increase the risk of developing cancer. Those of you who have been following my posts for more than the last two weeks, will yet probably remember that this was a similarly single-sided presentation of intrinsically questionable epidemiological data, as the latest upheaval about the life-shortening effects of multi-vitamin pills (cf. "Vitamin E & Cancer?" & "Is Your Multi Killing You?").

In view of the emerging image of the critical role of "inflammation" in the highly beneficial adaptive response to exercise, it may yet still be worth to re-evaluate the cost-benefit ratio of vitamin E supplementation. If we temporarily disregard the discussion that revolves around the use of natural vs. synthetic and isolated vs. complex forms (I would always recommend using a natural supplement with alpha-, gamma- and delta-tocopherol), and focus on the athletic or at least physically active population who is leading an otherwise relatively healthy lifestyle (whatever that may be ;-), we could probably narrow this complex issue down to the question whether or not, and in which contexts, the use of vitamin E to sooth down overall inflammation could turn out to be advantageous.

Sedentary or trained. Does it make a difference?

The first of two pertinent studies, which resurrected my personal interest into this topic has been conducted at the Warsaw University of Life Sciences in Poland (Debski. 2012). It is a 10-day rodent study in which 27 of the 54 vitamin-E deprived young male Wistar rats that were maintained on diets with 0, 0.5, 1.0 and 4.0 mg of alpha-tocopherol (as alpha-tocopherol acetate) per day, had to run on one of those funky rodent treadmills for 15 minutes a day, while the rest of the rats led their usual "sedentary" lives. The intention of the study was to elicit the effect of physical exercise on the vitamin E status and requirements of mammals and its downstream effects on insulin levels - both are issues which would obviously be important for any aspiring physical culturist, as well, since previous research has shown that low alpha-tocopherol levels impair the beneficial effects of physical activity on blood glucose management. On the other hand, you will probably remember my previous blogposts on the research of two German scientists, which suggests that very high doses of anti-oxidants could be similarly detrimental, as they could potentially impair the hormetic response to exercise / stress (cf. "Are You Stressed Enough?" and "Update on Antioxidants and Exercise").

Figure 1: Plasma vitamin E levels (in mg/L) in previously vitamin E deprived rats after 10 days on diets containing 0, 0.5, 1.0 and 4.0mg of alpha-tocopherol acetate (left) and relative change vs. baseline (left; data adapted from Debski. 2012)

If you take a closer look at the differential effects the four different amounts of supplemental vitamin E had on the alpha-tocopherol concentration in the plasma of the lab animals, you may be surprised that despite an initially greater response in the sedentary rodents, the exercised rodents exhibited a more favorable response to the highest doses of vitamin E (4mg for a rat ~1200IU for a human). Although the overall effect of exercise on the plasma level was non-significant (the amount of vitamin E in the diet was the critical determinant), the greater "vitamin E capacity" of the exercised rats could in itself be a "hormetic" response to the low grade stress. And - and this is certainly the data you are waiting for - the beneficial effects on insulin levels were present in all groups, including the high as well as the no supplementation group.

So, vitamin E is not harmful, but useless?

In isolation, the results of the Debski study would thusly support the hypothesis that the beneficial, as well as the potential detrimental effects of vitamin E, which were perpetuated by the lay-press, as of late, are largely overblown. That vitamin E was basically useless... well, if you are a rat, running on a treadmill for 15 minutes a day (which I would say is probably less "exercise" than a natural rat is "supposed to have" < attention: paleo reasoning at work ;-) that may well be the case. If you are a competitive athlete who trains 3-3.5h per day, like the rowers in a study which was recently published in the Journal of Clinical Toxicology, things may be different, however (Sardas. 2012).

Semra Sardas and her (?) colleagues obviously had a similar question in mind when they conducted a study to assess the potentially differential and hopefully beneficial effects of two months (note: for this kind of studies this is a very long and thusly meaningful study period!) of 400IU/day of supplemental alpha-tocopherol on the exercise induced DNA-damage in "recreational active" individuals (physical education students; >1h of exercise min. 2x/week) and the aforementioned competitive rowers.

Figure 2: Relative change in DNA-damage in response to 60 days on 400IU/day vitamin E in competitive rowers (highly trained athletes) and physical education students ("active individuals"; data calculated based on Sardas. 2012)

If you take a look at the relative change in DNA-damage (comparing the pre- vs. post-supplementation period) subsequent to a standardized exercise test (high intensity for the rowers, medium intensity for the students) which was performed at the beginning and the end of the 60-day study period, the first thing that will probably catch your eye are the statistically significant decreases in baseline (pre-exercise) and peak (post exercise) DNA damage in both groups. What may appear to as if it was a source of concern, though is that the relative increase in DNA damage to the acute exercise bout in the rowers was more pronounced after, than before the intervention period.

In view of the fact that the total DNA damage was yet still -9% and thusly statistically significantly reduced, it does not appear likely this would be a consequence of an inadequate ability to adapt to stressors... it is rather a consequence of the profoundly (-25%) reduced baseline DNA-damage, which in itself would suggest that especially highly trained athletes should not discard the potential benefits at least moderate doses of vitamin E could have on their overall health - even if there are no noticeable short-term effects in terms of improved body composition and / or performance... always remember: You are in this for a life-time!

Australia Day BBQ and riding really slowly up hills

Now, 7months plus. This is Mayhem doing her 'high' baby routine. She also has a 'low' baby routine (more like the 6 month pic) where she sticks a few inches further out but hangs a lot lower. She's multitalented.

We had an Australia Day BBQ the other day. We should have made an attempt to take some pics but alas, we didn't. There were about 15 kids out the front yard playing volleyball, badminton and the Slip 'n' Sliding, while another 45-55 adults (at the peak of the party wave!) were hanging around the back drinking beer and cider. It was a good day, if a bit overwhelming!

Still riding, in fact I almost managed a whole 6 hours on the bike last week—that's practically training (haha)! And with 3 wind trainer sessions it sure felt like it (Arrrrrggghhhh!!). Aido went for a rainy, steamy, muggy ride with me the other day, only 1hr15. Aido rode up to the top of the Ironbark climb...must have waited for an age...then rode back down to me (I was still riding up).

He's like, 'Ummm....maybe you should not ride up hills anymore...or offroad'.
Me: 'Um, why not?'.
Aido 'What's your heart rate?'.
Me: '140, tops'. (I have no HRM at the moment, mainly cos I can't be bothered and I ride to effort rather than a number. It was HR via ESP).
Aido 'liar.'.
Me: 'I'm talking to you ain't I!?'
Aido: 'Hmpf'.

Anyway, I take it pretty easy and ride mainly fireroad. It's been pretty sketchy from all the rain—very greasy trails but I just take it slow, hopefully for just under two months I can maintain this level of exercise, we'll see. It makes me happy!

The Anabolic Effects of HIIT: 3x30s High Intensity Intervals Increase mTOR & Ramp Up Marker of Protein Synthesis by +43% in Men and +222% in Women - Even in a Fasted State!

Image 1: While the study at hand clearly shows that HIIT, even done on an empty stomach, is anabolic, not catabolic, it appears as if women respond better to sprint exercises than men. And this assumption is not based on gene-assays but dates back to the results of a 1999 study by Esbjörnsson which showed a more pronounced CSA increase in the leg muscles of female subjects.

Not all too long ago, the general accepted consensus was that anyone whose main interest is in building muscle must abstain from any strenuous cardiovascular exercise... running on a treadmill? God-forbid! You could lose muscle. Over the last two years or so, this paradigm has began to totter, though. And now, at the beginning of 2012 I would estimate that the number of (recognized) trainers and trainees who recommend doing high intensity interval training (HIIT), if not for general conditioning, then at least as a means to shed fat, initially surpasses the number of the conventionalists who maintain that "classic cardio" training in the "fat-burning zone" was the way to go. Now, if this is not your first visit here at the SuppVersity, you should be aware that the latest scientific research supports the arguments of the advocates of HIIT. And not so much to my, as to the surprise of some researchers, this holds true not only for already well-conditioned gymrats and athletes, who want to finally pass beyond the 10% body-fat barrier, but also for the obese and metabolically deranged diabetic, who is trying to get his blood sugar under control (cf. "Hitting Diabetes With A Hammer").

The advantages of HIIT reach well beyond fat loss, but...


Moreover, a 2011 study by Naito et al., the results of which I have discussed in November 2011, shortly after it was published in Acta Physiologica (cf. "HIT Your Satellite Cells to Increase Your Gains"), already hinted at the fact that the advantages of HIIT reach well beyond its fat-burning effects. Yet although the increase in both satellite cell count and incorporation into the muscle Naito et al. observed speak for themselves, there's still rumors going round that this training style could be catabolic. In that the argument usually revolves around the notion that muscle damage is a major driving force of satellite cell recruitement and that if the latter is a necessary consequence of HIIT it would counter your efforts to build muscle. Now, aside from the fact that this argument is intrinsically flawed (I mean, what to you do in the gym, when you weight train? You break down muscle tissue!), a recently published study from the famous Karolinska Institute in Stockholm, Sweden, attests to the fact that the exact opposite is the case.

... it appears as if women could derive even greater benefit from all-out sprinting than men

Image 2: The exercise stimulus in the study was a Wingate test, one of standard procedures in exercise science.

In an earlier study from 1999 Esbjörnsson and his / her colleagues had observed that the cross-sectional area of the leg muscles of women exhibited a more pronounced hypertrophy response to sprint training than those of their male peers (Esbjörnsson. 1999). With the advent of our advanced understanding of the underlying principles of skeletal muscle hypertrophy and the central, but as those of you who read the Hypertrophy 101 know, in the current discussion possibly overemphasized position of the mammalian target of rapamycin (mTOR), Esbjörnsson et al. did now set out to examine, whether a sex-specific response of mTOR and its downstream targets could explain their previous results (Esbjörnsson. 2012).

To this ends, the scientists recruited nine men and eight women who despite participating in leasure time sports were only "in good shape" and not considered to be athletes. For the experiment the subjects reported to the lab fasted and, after a brief 1min warm-up, performed the well-known Wingate-test, which consists of three consecutive 30s all-out sprints with 20min breaks between the intervals on a braked cycle ergometer (average peak power was ~645W and ~935W for women and men, respectively, on a per-lean body-mass base, the peak and mean power was yet identical)

Figure 1: Illustration of the experimental protocol used in the study.

Before the warm-up and 140min after the 3rd sprint, Esbjörnsson et al. took muscle biopsies from the quadriceps muscles of the subjects to assess the local expression of mTOR and its downstream targets.

Figure 2: Phosphorylated AKT, mTOR, p70S6K and rpS6 (a.u.) in male and female study participants before the first and 140min after the third sprint of the Wingate test (data adapted from Esbjörnsson. 2012)

If you are not well-versed in the the intricacies of the mTOR-cascade, it appears as if the data in figure 2 would disprove the scientists' research hypothesis that "mTOR signalling is more pronounced in women than in men". After all, the increase in phosphorylated mTOR (p-mTOR) and AKT (p-AKT) in response to the three 30s seconds sprints was obviously more pronounced in the male, than in the female participants (mTOR +26% and AKT +17% greater increases; a difference which did not reach statistical significance, though).

Do women just make better use of the same stimulus?

As far as the phosphorylation of p70S6K, of which the current scientific evidence suggests that is a more appropriate measure of the "real-world" protein synthetic effect of mTOR, a completely different picture emerges. While the +43% increase in the male subjects is just about statistically significant (p = 0.04), the +222% increase in p-p70S6K in the female subjects appears to confirm what Esbjörnsson et al. already  had suspected.

Figure 3: Serum leucine and growth hormone levels at rest and after the sprints (data adapted from Esbjörnsson. 2012)

The slightly greater disappearance of leucine from the skeletal muscle of the male subjects (cf. figure 3) is yet only one of three possible explanations (and one you could counter by ingesting BCAAs, for example) Esbjörnsson et al. come up with based on the results of previous studies:

Image 3: If you look at the leg muscles
of some of the female speed skaters,
it is quite obvious that the leg muscles
of women respond pretty well to short,
intense bouts of all-out sprinting.
(the image shows Claudia Pechstein)

1. Lower accumulation of lactate and ammonia and a faster recovery of ATP levels in type II fibers of women than men
    
2. Lower levels of plasma catecholamins (=stress hormones) in response to sprint exercises in women than in men
    
3. Slower disappearance of leucine and thusly more sustained elevation of protein synthesis in women than in men

Whether it is any of these, or a combination of all three factors which is responsible for the differential response to statistically (!) not significantly different activations of mTOR and p-AKT, cannot be decided based on the available data.

An alternative explanation, which would, by the way, have real-world implications for the training practice, is (and I prefer to cite this, to avoid being accused of sexism) that...

women do not exhaust themselves as much as men during each bout of exercise and thereby elicit a smaller activation of AMPK, resulting in less inhibition of mTOR.

In view of the fact that previous studies by Esbjörnsson et al. refute this hypothesis, it appears unlike that an "over-expression" of AMPK, of which I have discussed in one of the previous installments of the Intermittent Thoughts that its locally expressed alpha-2 isoform does not inhibit the exercise induced increase in protein synthesis, anyway, could explain why similar exercise stimuli (peak and mean power per fat-free mass were virtually identical for men and women) and within the statistical margin identical mTOR responses induce a more pronounced protein synthetic response in women than in men. And whether the early(-ier) rise in serum growth hormone, which is the last possible explanation the scientists mention, has anything to do with it appears questionably, as well. After all, the data in figure 3 shows quite clearly that the overall GH response was much more pronounced in the male than the female participants.

We don't know about aliens, but for earthlings HIIT is anabolic - regardless of their sex

In essence, it does not even really matter, what the underlying cause of the sex-specific response to sprint training is. As far as I am concerned, the most significant result of the study is not the gender-difference, but the simple, yet as the scientists point out "novel" finding that "repeated 30-s all-out bouts of sprint exercise, separated by 20 min of rest, increased Akt- mTOR signalling in skeletal muscle." And this effect was observed in both men and women. Now, this is allegedly not exactly your "usual" HIIT protocol, if you do yet take into consideration that it was performed after an overnight fast and went without BCAAs, protein shakes all the other "obligatory" anti-catabolics, the average gymrat uses to avoid the purported catabolic effects of high intensity conditioning work, I would dare to say that it HIITs another (if not a final) nail into the lid of the casket of the "HIIT = catabolic" myth.

Intermittent Thoughts on Building Muscle: A Preliminary Conclusion - Exercise, mTOR/AKT/MAPK, IGF-1, Testosterone, Estrogen, DHT, Nutrition, Supps & Sleep

Image 1: Arnold obviously is flabbergast that neither of the factors mentioned in the title of this blogpost was necessary to build the impressive physique of the Arnold statue which now stands in front of the Schwarzenegger Museum.

I don't know if some of you have seen it, but on January 3, 2012, ScienceDaily published a brief news-item titled "How work tells muscles to grow". It relates to a recent study by Guerci et al. who have found that the so-called serum response factor, which basically another "gene switch", is responsible, or I should say required for exercise induced satellite-cell mediated hypertrophy (Guerci. 2012). If you have been following all of the past installments of the Intermittent Thoughts from the early "Hypertrophy 101" (Part 1, Part 2), in which I explained the difference between the increase in myonuclear domain sizes as a consequence of increased protein synthesis, on the one hand and the formation of new myonuclear domains via satellite cell recruitement, on the other hand.

Do you remember myostatin?

You will probably also remember that myostatin, the legendary TGF beta protein that acts as an inhibitor of muscle growth, is something like a watchdog, who suppresses further increases in myonuclear domain size, when the latter begins to exceed a presumably fiber-type dependent maximum - with highly oxidative type I (slow twitch fibers) exhibiting less growth potential than their glycolytic (fast twitch) cousins. From analyses of muscle fibers from different athletes, we do yet know that the skeletal muscle of bodybuilders, the epitome of maximal skeletal muscle hypertrophy, are not - as some people argue - characterized by an abundance of ultra-fast highly glycolytic type II fibers (cf. figure 1).

Figure 1: 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)

As you can see in figure 1, quite the opposite is the case, probably as a result of the high training volume, the additional endurance exercise (in the 1990s, when the study was done, no bodybuilder did HIIT ;-) and the use of performance enhancing "supplements", the dominant fiber type in the skeletal muscle of the bodybuilders in the Jurimäe study from 1997 is the intermediate fast-twitch, but still highly oxidative type IIa fiber.

Protein synthesis + satellite cell recruitment = growth!?

You probably did not realize it, but with the brief reference to the recently published study on the effects of the exercise induced release of serum response factor (Srf), the subsequent reminder of the difference in the increase in myonuclear domain sizes and the increase in their number and the allusion to training (and drug) induced changes in fiber-composition, we have covered the fundamental mechanisms by which the scrawny boy on the left side of image 2 turned into a, if not the, figurehead of physical culture and bodybuilding.

Image 2: The fundamentals of skeletal muscle hypertrophy apply to us all.

Yet, although we do have a broad understanding of what happens when we train, eat, sleep, train, eat, ... the underlying physiological processes are more complex than the ostensibly straightforward interplay of protein synthesis and satellite cell recruitment would suggest. Within the follow-ups on the "Hypertrophy 101", I have thusly done my very best to tackle each of the complex physiological processes (most of which are not even fully elucidated, yet) which allegedly or effectively trigger, sustain, facilitate or drive skeletal muscle hypertrophy in separate installments:

1. IGF-1 and its Splice Variants MGF, IGF-IEa & Co - Are the growths hormones master regulators of muscle growth or just a bunch of cogs in the wheel of skeletal muscle hypertrophy?
   
   
2. IGF-1, TNF-α, IL-15 & Co and the Emerging Role of an Auto-/Endocrine-Immune Axis in Skeletal Muscle Hypertrophy  - How does inflammation factor in, is it beneficial or detrimental?
    
3. Zoning in on "The Big T" - Does testosterone (alone) build muscle?
    
4. Quantifying "The Big T" - Do increases of testosterone, which are well within the physiological range matter?
    
5. Understanding the "Big T" - How does testosterone work? What is its effect on stem cells and how come it makes you leaner?
    
6. Estrogen, Friend or Foe of Skeletal Muscle Hypertrophy? - Which role does estrogen play and why could you SERM away your growth potential, when you (ab-)use tamoxifen or potent aromatase inhibitors?
    
7. Dihydrotestosterone (DHT), The All Things Male Hormone - Will it make you bigger, stronger and faster or just balder, fatter and unhealthier? 

In case you have forgotten about the way the local and not the systemic growth hormone response is responsible for the intricate restructuring process, in the course of which the increase in myonuclei (which must not be confused with an increase in muscle cells, i.e. hyperplasia) and motor proteins keeps the growing muscle strong and functional, about how IGF acts as a door opener for the macrophages (immune cells), which then "install" the satellite cells in the inflamed muscle and about the function of testosterone and its metabolites estrogen and dehydrotestosterone in this complex interplay of intra-, para- and endocrine processes, you can read up on all that in the previous installments of this series (see list above).

A picture is worth a thousand words - tying the knots graphically 

For those of you who either remember all that or have just returned from their virtual tour through the archives of the SuppVersity, I have come up with a graphical illustration which is an attempt to sum up "all" the major players and their interactions.

Figure 2: Graphical illustration of what you should have learned by now, if you read the previous installments of the Intermittent Thoughts; note: while I have used the arrows rather indiscriminately (they do not necessary mean "causes"), the stops at the end of other lines indicate an inhibition, eg. the line from exercise to myostatin indicates that exercise inhibits myostatin, which would inhibit increases in myonuclear domain sizes, if it was not "switched off" by exercise...

I bet there are still a few arrows missing here and there, but the overall message is clear: If there was one unifying factor that impacts all important aspects of (natural) skeletal muscle hypertrophy, it would be exercise. Exercise acts directly on the mTOR/p-AKT and the MAPK pathway and thusly increases muscle protein synthesis (assuming the respective substrates are present) and the accrual of motor proteins. It increases mitochondrial biogenesis via PGC-1a and induces adaptive changes in the fiber type composition of the trained muscle. It inhibits myostatin and thusly allows for further expansion of the myonuclear domain. The latter is possible because it will promote the proliferation and the recruitment of satellite cells in response to the exercise induced expression of inflammatory cytokines and local growth factors.

If you can show me another player in this orchestrate with a similarly or even more important function than physical activity with a focus on skeletal muscle overload, let me know... if not, you better make sure you do not miss your next workout ;-)

The Unsatiating Truth About Aspartame, Acesulfam K, Sucralose & Co: They Don't Induce Glucose or Insulin Spikes, But Do They Make You Hungry?

Image 1: If you plan to eat the stuff on the plate behind the coffee cup, I guess it does not really matter if you use sugar, fructose, Aspartame, Acesulfam K, Sucralose or everybody's  new darling, stevia to sweeten the coffee ;-)

If there was a yearly top 10 list of the furiously and most passionately debated topics, in the health & fitness community, the issue of "artificial sweeteners" (personally I would include high fructose corn syrup as "artificial", but I guess the FDA or rather their financiers think otherwise) would probably make it to the TOP 5 every year. All concerns about toxicity issues aside, the two main concerns people are worrying about are a direct negative effect on glucose metabolism and an indirect intake on subsequent / concurrent food intake. Both would obviously predispose consumers who buy respective products because they trust in the industry's promise that they would help the lose weight and/or ward off diabetes to the exact ailments they are intended to prevent.

Sweet taste receptors are all over the place!

My personal interest in this topic has always revolved around the issue of "sweet taste receptors" (i.e. cells that will recognize certain molecules as being sweet), the existence of which in / on all sorts of organs / tissues scientists had been overlooked for decades. I mean, isn't it revealing that the same "sensors" that are responsible for the sweet sensation you experience when you spooning your delicious full-chocolate ice cream are also present in your gut and even on your pancreas, where their activation sets the stage for the release of insulin into the bloodstream (Nakagawa. 2009)? This rather recent revelation could after all finally explain the early results of Blundell et al. who observed an increase in calorie consumption in subjects after consumption of foods containing the artificial sweeteners Aspartame and Saccharin (Coke light & Co), back in the fat-phobic 1980s (Blundell. 1986; 1989). Subsequent more sophisticated studies were yet unable to reproduce those early results (at least in humans).

Artificial sweeteners are obesogenic! Bitter truth or just another myth?

With the advent of a more sophisticated understanding of the complex physiological processes and integrated signaling systems which regulate appetite and satiety in mammals and humans in particular (I doubt we will ever be able to understand all the psychological factors that come into play with the latter), Robert E. Steinert and his colleagues from the Clinical Research Center at the University Hospital in Basel (Steinert. 2012), Switzerland, took another, more closer look at what actually happens, when we consume beverage which taste as if they contained tons of sugar, but are totally devoid of nutrients.

Figure 1: Intensity of sweetness, total amount per 250ml solution and energy equivalent of the five sweet test solutions (the sixth beverage was plain water); mind the logarithmic scale! (data adapted from Steinert. 2012)

To this ends, the Swiss scientists recruited 12 healthy, non-smoking volunteers (6 men, 6 women; mean age 23.3y; normalweight, BMI 23kg/m², min. 3 months of stable weight) to perform a randomised, placebo-controlled, double-blind, six-way cross-over trial. In each of the 6 trials, which were seperated by 3-5d the subjects reported to the lab at 8:00am after an 10h overnight fast (no alcohol, no exercise, no supplements or medication), where they received one (on each occasion) out of six 250ml test solutions containing either tap water (no problem to drink that, in Switzerland ;-), or freshly prepared solutions with concentrations of the different sweeteners, of which the scientists state that they "were comparable with the amounts found in commercially available beverages and soft drinks" (Steinert. 2012; cf. figure 1).

Note: I guess I should mention that the test beverages were administered via an intranasal feeding tube. I honestly have no clue, why the scientists chose this method over the natural route through the mouth. After all, this reduces the real world significance of their results. If, for example the sweet taste receptors in the oral cavity (which were obviously bypassed by the intranasal feeding tube) are hard-wired to the brain, while those in the gut are not, this would not only influence the "psychological" aspect of satiety, but could also induce hormonal, i.e. physiological effects... but hey, who am I to criticize the professionals? After all I am only a stray physicist in the realms of nutrition and exercise science ;-)

The intranasal feeding tube was removed immediately after the administration of the respective test beverages. Blood was drawn at regular time intervals at 5, 10, 15, 20, 30, 45, 60, 75, 90 and 120 min and the subjects were asked to rate their hunger, satiety and fullness on a visual analogue scale.

No insulin response, no glucose response to any artificial sweetener

Before we get to the significant findings, I want to address the often touted insulinogenic effect some of the artificial sweeteners are supposed to have... let me make it short and concise, so that everyone can understand it: There was NO insulin response to ANY of the ARTIFICIAL SWEETENERS!

Figure 2: Glucose and insulin response to glucose and fructose sweetened beverages; there were NO changes in either glucose or insulin in response to the artificially sweetened beverages (adapted from Steinert. 2012)

If you scrutinize figure 2 you will notice that I did not even bother to plot the "straight" lines for either Aspartam, Acesulfam K, or Succralose. The reasons for me to include the glucose and insulin responses, at all, were that...

1. there was a minimal yet statistically non-significant increase in both blood glucose as well as insulin levels in response to the fructose sweetened beverage, and
    
2. there was a huge +/- 20µU/ml (=20%!) standard deviation for the insulin response to glucose at the 20min mark.

While the former, i.e. the fructose induced increase in both blood glucose and insulin is probably a result of gluconeogensis in the liver, the latter, i.e. the huge inter-individual variation with respect to the amount of insulin that was released to a standardized beverage, which contained 50g of glucose, goes to show you how large the discrepancies wrt "insulin tolerance / resistance" actually are, even in otherwise healthy young individuals.

Sweetness alone is not satiating - neither "hormonally", ...

Apposite to the previously established non-insulinogenic effects of the three artificial sweeteners in the study, neither Aspartame, nor Acesulfam K or Sucralose led to increases in the glucagon-like peptide-1 (GLP-1, cf. figure 3), which is involved in the so-called "incretin effect". The latter is responsible for the more pronounced insulin response to an oral vs. an intravenous glucose load and is ascribed to the presence / release of GLP and GIP in the gut.

Figure 3: Area under the curve (AUC) and maximal value (Cmax) of GLP-1, PYY and Ghrelin in response to the administration of the six test beverages; values expressed relative to water = control (data calculated based on Steinert. 2012)

In a similar vein, the administration of the artificially sweetened beverages increased neither the "satiety hormone" peptide tyrosine tyrosine (PYY) nor the "hunger hormone" ghrelin over the levels the scientists observed for the control beverage which contained plain water, relative to which the values in figure3 are expressed. Glucose and fructose, on the other hand, led to large and small increases both the area under the curve (AUC, figure 3, left) and the maximal expression (Cmax, figure 3, right) of GLP-1 and PYY, as well as corresponding decreases in ghrelin. Accordingly, Steinert et al. conclude:

We infer from these obser- vations that sweetness per se is not sufficient to stimulate the secretion of these peptides in humans. Additional chemosensory mechanisms directed towards the structural integrity of the glucose molecule (as one of the major fuels for the body) must exist including active transport systems. Finally, potential energy-sensing mechanisms or energy thresholds might exist for the secretion of GLP-1 and PYY, although it is unlikely that the release is directly related to the energetic load in a dose–response manner.

And if we were all nothing but hormonally controlled machines, I guess this would be the end of today's blogpost, but since we are not, it is probably prudent to look at the subjective hunger, satiety and fullness ratings of the study participants before we settle this case.

... nor "psychologically", and in fact, it could even make some people hungrier!

If we had to make prediction based on the hormonal data Steiner et al. collected, what would you say, which group will feel the most satiated and the least hungry? What? The glucose group? Why? Because they consumed the largest amount of calories? But what about the insulin spike? Well, I guess, it is pointless to continue this feigned dialog... so, let's just take a look at the actual results:

Figure 3: Time (in min) until hunger, satiety and fullness after ingestion of the six test beverages returned to baseline; statistical averages, left; median, right (data adapted from Steinert. 2012)

I guess, the results won't please everyone out there, after all fructose, which has as of late been deemed responsible for whatever ailment our obesity ridden society is suffering from, induced the most profound (=long lasting) satiety effect. Fructose reduced the hunger longer than any other sweetener and the subjects felt full for a longer time period after the ingestion of the fructose-sweetened beverage than after any other sample.

A brief note: Maybe I can calm the followers of Dr. Lustig down, if I remind them of the way fructose is metabolized? Remember? Fructose is largely being processed into triglycerides by the liver. Now, the latter obviously are fats and I guess nobody will challenge the satiating effects of fat, these days, right?.

With the glucose beverage taking a close second and only non-significant (you know "statistically" ;-) differences to the artificial sweeteners, Steinert et al. thusly summarize their results as follows:

The appetite profile revealed that the (energy-containing) carbohydrate sugar loads induced the longest-lasting increase in fullness ratings above baseline, which was prolonged for fructose 108·4 (SEM 6·1) min and for glucose 90·5 (SEM 11·2) min. In contrast, water (74·0 ( SEM 13·4) min) and the AS [artificial sweeteners] acesulfame K (65·6 (SEM 15·8) min), aspartame (83·1 (SEM 15·9) min) and sucralose (65·3 ( SEM 14·1) min) induced shorter augmented fullness above initial ratings. However, due to the large data variability, these differences did not reach statistical significance. Satiety and hunger ratings showed similar trends, however, with generally smaller differences. Overall, the AS increased satiety and fullness and reduced hunger ratings to an amount that was intermediate between the carbohydrate sugars and the water control.

Now, the SuppVersity would not be the place to go to read about the latest studies, if I would content myself with someone else's analysis of data that has already undergone a selection process, in the process of which the individual responses got lost. If we do yet take a look at the difference in mean (i.e. the statistical average; figure 3, left) and median (which is the median value in an ordered list; figure 3, right) time it took for the hunger, satiety and fullness ratings to return to baseline, we have - yet again - enough evidence for the presence of a huge interpersonal variability.

Figure 4: Ratio of the statistical averages and the respective median time until the hunger, satiety and fullness ratings returned to baseline after ingestion of the six test beverages.

If we take the ratio of the average to the median as an obviously very unreliable marker of this inter-personal variability (I plotted the respective values for you in figure 4). It becomes obvious that Acesulfame K, which is the sweetener most companies who pride themselves of not using Aspartame put into their products, could in fact be a wolf in sheep's clothing. While the low median satiety scores in figure 3 (right) already suggested that it must have been significantly less satiating than plain water, let alone the other sweetened beverages, for some of the subjects, at least, the alternative representation of the data as the ratio of the average to the median in figure 4 reveals how pronounced this effect actually is.

"So, tell me: What's the unsatiating truth now?"

In spite of the fact, that I do believe that the concerns about potential insulin spikes from foods / beverages which are sweetened with artificial sweeteners only is unwarranted, the large intra-individual variation of the satiety effects of the Acesulfam K should raise your awareness of your individual response to artificial sweeteners, in general, and anything that contains Acesulfam K, in particular. If you feel that respective foods make it difficult for you to stick to your diet, just don't eat / drink them! If, on the other hand, the 1l of Coke light you consume during your fast (just an example ;-) does not make you hungrier than the same amount of water and you are not worried about the fact that rats develop cancer when you feed them with amounts of Aspartame that would equal the consumption of several truckloads of diet coke per day (and that over weeks or months), don't bother and stick to what works for you...

If you do however have trouble sticking to your diet, cannot lose weight or have existing blood sugar issues, don't use the results of this study as an excuse for your unwillingness to (at least try to) go without your beloved diet Coke for at least a month to see whether or not the latter is not part of the underlying physiological (and psychological) causes of your misery!

Button Up!

Emily and I are the proud owners of a button maker. The price is outrageous, but she plans on making money with it. I plan on making a button out of every single thing I can find. 

Here I've used an old dictionary and a 'vintage' Peanuts book.

 This is my little me that Emily drew. I see so many possibilities.

Why Smiling Is Good Business

Image Source: http://lifethroughartfoundation.blogspot.com

My first week of ninth grade, after transferring to a public school from the Christian one I'd gone to since childhood, I was approached by the friend of a boy who had a crush on me.

"He likes your smile," the friend told me. "He says you always have a big smile on your face, and he thinks it's pretty."

My ninth grade self was pretty embarrassed at this statement, that this boy who'd never even talked to me before liked my smile.  Of course, I was too awkward to ever have a conversation with my admirer, but the idea stuck: People like it when you smile.

As an adult, I've kept smiling.  I'm not always the most verbally eloquent person, but I am usually smiling and try to be engaged in what the other person is saying.  In business, I do the same.

After my recent workshop at the Idaho Business Extravaganza, I learned that several of the participants appreciated my happy disposition and the smile I had throughout most of the presentation.

In meetings, I've found that a smile can get through to even the most reserved client.  In interviews I do for writing projects, I've found that laughter and smiles make our time together much more productive and useful.

It's funny: I've also found that a simple smile can break through some of the barriers I face in the work place.  As a woman, I know that society believes I should either be like Meryl Streep's character in The Devil Wears Prada or a modern-day June Cleaver.  Frowing or smiling.  Working or homemaking.

I resist the conventional wisdom that tells me that, as a woman, I need to be stern and assertive, to "prove myself" through my demeanor and words.  I resist the idea that work can't be fun, that people can't just get along, that you can't smile through meetings (or have any other emotion, for that matter).  Now, I know that you can't always smile genuinely---firing an employee, for example, is a time when a smile might be taken the wrong way---but I do think a happy demeanor is key in business.

I also laugh.  A lot.  And genuinely, too.

So, try it: Next time you're in a meeting, at a client lunch, or doing something else professionally-oriented, add a few extra smiles into your game plan.  I bet you'll like the results.

CaffSec SITREP - Cyber Intelligence for the masses

Leveraging the power of Google Alerts, I have started posting relevant news articles, public exploit releases, and other tidbits of information related to Cyber Security and Information Assurance.

The best way to keep you and your organization prepared for unknown threats is to keep tabs on the current state of the security of the internet.

There are currently three ways to view SITREP messages:

Twitter, following @CaffSec
Tumblr through the CaffSec SITREP blog
The CaffSec Daily SITREP Online Newspaper

Please enjoy these valuable resources!

Busting the 3,500kcal = 1lbs Weight Loss Myth! A Scientific Deconstruction of a Dumb Rule of Thumb Reveals that Women Need More, Men Less Than the "Rule" Predicts

Image 1: If you are still putting your Happy Meal on a scale, you should not wonder why your weight loss falls short of your "calculations" - especially if you happen to be a woman (img. elementsofwellness.com)

While I would hope that most of you have by now embraced the notion that a calorie is not a calorie (at least, when it comes to nutritional calories), I suspect that one or two of you have still just been reviewing how much "calories" they have already eaten, or how much "cardio" they will have to do to compensate for the piece of pizza they are going to eat tomorrow at a friends party... > "STOP!" < this is what you should tell yourselves whenever thoughts like that are passing your mind (well, unless you are in the end-stage of your prep for a bodybuilding contest, I guess ;-) After all, a very recent study that is based on the results of two large-scale weight-interventions (Heymsfield. 2012), i.e. the CALERIE study, conducted at the Pennington Biomedical Research Center and the Kiel study, which was named after the German town Kiel, where the 13-week weight loss intervention took place, confirms the fallacy of number games like that.

A physicists would know: A pound of fat weighs 500g, not 3,500kcal ;-)

In order to establish the "actual" energy deficit that was necessary to elicit the loss of 1lbs of body weight in the 98 obese subjects in the CALERIE and the Kiel studies (average initial BMI of ~35 (25-43) kg/m²; mean age of ~38y and ~34y for the female and male participants, respectively), Steven B. Heymsfield and his colleagues (re-)analyzed the detailed nutritional and weight loss data from the studies and came up with the more or, I should say, less surprising result that the still widely accepted rule that a caloric deficit of 3,500kcal would result in a 1lbs reduction of body weight has to be revised ...

Figure 1: Energy deficit (in kcal) that was necessary to shed 1lbs of body weight at different time-points (in weeks) of the -25% reduced energy intake and the 890kcal/day arm of the CALERIE study (data adapted from Heymsfield. 2012)

If you take a closer look at the data in figure 1, which shows the actual amount of energy (in kcal) that was necessary to shed 1lbs of body fat, it becomes obvious that there was actually not a single time-point in the 24week dietary intervention, when the men and the women on the -25% (figure 1, left) or 890kcal/day (figure 1, right) both lost 1lbs of body weight per 3,500kcal.

Women have a harder time losing weight than men, but retain more lean tissue

If we go by the logarithmic regressions (red and blue lines; coefficients of determination see figure 1), the following important trends become obvious:

Figure 2: (a) increase in calories necessary to shed 1lbs of BW from week 1 to week 24; (b) average calories necessary to shed 1lbs in men and women over the whole study period (data adapted from Heymsfield. 2012)

1. Independent of the degree of calorie reduction (low calorie = -25%; very low calorie = 890kcal per day) and the sex of the subject, the caloric deficit that was necessary to shed 1lbs of body weight (not fat!) increased from week 1 to the end of week 3 (cf. figure 2, a)
    
2. Both, the baseline, as well as the gradual increase in calorie reduction that was necessary to shed 1lbs of body weight in the course of the 24d study period was greater in the very low calorie arm of the CALERIE study (cf. figure 1 and figure 2, a). This, btw, is clearcut evidence for the fallacy of starvation diets.
    
3. On both diets, women had a significantly harder time losing weight than men. This was even more obvious in the low calorie (-25%) than in the very low calorie arm (cf. figure 2, b).

In that it is also important to note that the relation of fat free mass to total body weight loss (ΔFFM/ΔBW) was maximal (60% for men and 50% for women) at the beginning of the study, had a nadir after about 15 weeks (~40% for men and ~20% for women) and showed a trend to increase again at the end of the 24 week study period of the CALERIE study. In other words, while women have a harder time losing weight, they maintain more of their lean muscle mass, than men do. A results that was, at least with regard to total weight loss, supported by the results of the Kiel study (no data on body fat / fat free mass loss available).

My advice: Forget about the rule of thumb, about calories and body weight!

Other than Heymsfield et al. who obviously still believe that it will by whatever means be possible to calculate the exact amount of calories to shed 1lbs of body weight, my take home message from the results of this study is that all the calorie counting, the daily disappointment, when you step onto the scale and the notoriously unreliable dietary rules of dumb... ah,  pardon "thumb", are something you banish from your weight loss inventory, right away.

Feel lost without your calories? Don't know where and how to start? Afraid of throwing the scale out of the window? Then it's time to (re-)read the Intermittent Thoughts on Stocktaking, Goal Setting, -Tracking & -Resetting to Achieve a Healthy Weight & Shed Excess Body Fat

A food log, where you record food and not calories  (I mean I still eat food, you know, things like eggs, butter, a steak, potatoes... those things without nutritional information on it!), a general understanding of the macro-nutrient (fats, carbs, protein) ratios in those foods and a measuring tape to access your progress, is all it takes access and adapt your food (not energy!) intake and evaluate the success of your diet (which does not equal weight loss!)... and I guess I don't have to tell you that the results of the very low calorie (890kcal) arm of the CALERIE study clearly suggest that dieting on a single cup of broccoli and a single serving of chicken breast sprinkled with some olive oil, is not an option, regardless of your sex, do I?

Taking full control of your life.

Mysticism tells us, everything in the world is made of an outer shell and an inner energy.

What you see, is only surface, skin deep, and, it isn’t the real deal. What is hidden from the eye after we do some scratching and digging will reveal, the reason why you see what’s perceptible to the eye. That is why in the Bible this world is called “concealed” and a “world of falsehood.” This is so, mainly, because what we see is just the surface, and the inalienable truth needs to be discovered deep inside.

In a person, there is a constant struggle between the outer part, the body, and the inner dimension, the G-dly soul. The body wants to keep on concealing on the inner G-dly soul and its yearnings. The body seeks self fulfillment. Ego, pleasure, anything and everything for the physical self.

The soul yearns for what it naturally craves and longs for. To remain connected to its source, the infinite and the eternal. The soul looks for long term spiritual fulfillment and accomplishing its purpose, for being imprisoned in a corporeal body. The soul is constantly looking to liberate itself from the narrow confines of the short sighted body.

That is why we feel sometimes empty and hollow inside. We feel like there must be more to life. This is the G-dly soul, trying to express itself against the ever powerful force of the body, and all its hedonistic desires.

Both the G-dly soul deep inside of us, and the “animal” soul that vivifies the body are made of ten faculties, which comprise the logic and emotion of each soul. These two souls, with its strengths and weaknesses, they are what they are, and we can’t change them. Some people are born with certain tendencies and propensities to do good and to pursue outstanding and admirable goals. Others, or maybe these same people, are born with a penchant and weakness towards certain behaviors. It is what it is.

There is however a little hope, to control our destinies, and it is in our choices. How, and what, we allow to express itself, in our thoughts, speech, and actions.

A person has one brain, one mouth, and can DO one thing at a time. In mysticism these are called the garments of the soul. Garments, because, just like clothing which are not the person, but are put on and taken off at will. So too with these faculties, each one of them, it is always our choice, we have full control over what we allow ourselves to think, speak and do. And, just like garments make a statement about our personalities and character; the way we think, speak, and act, tell volumes of what is going on inside of us.

Although it is almost impossible to change the nature our souls directly, a person has total free choice over, what he decides to think, speak, and do, at all times.

Let’s say you have a feeling in your heart to think, say, or do, something bad. That may not be entirely your fault. You where born with that tendency. However, what YOU decide to indulge in with your mind, what YOU decide to talk, or do, is always and totally in your control. Unless of course you made yourself intoxicated, and you’ve lost your abilities at that moment, but it was you, who decided to drink, and therefore still remain responsible for your actions.

Harmony in our lives, is when we follow the desires of the G-dly soul. It is deeper and richer. The G-dly soul is who we are, and who we identify with. The body, is a temporary dwelling place. While we are here in this physical world, the body affords us the opportunity to earn merit and become spiritually stronger, by overcoming the superficial and shallow challenges of this materialistic world.

The more a person exercises his choice to think, speak, and do positive things, and gets himself into the habit of allowing his G-dly soul to express itself regularly, and win over the self indulgent desires of the body, the more the person has succeeded and accomplished to infuse the world with “light”, which prevails over the confusion of darkness so many people suffer from.

Soup and Stuff

I'm still keeping up to my lessons in Body Restoration. It's week 3 and I'm so happy to be caught up. It's hard but I'm enjoying the process. The lessons get you thinking about how hard we are on ourselves to look like everyone else. 

 I'm not dieting, but I'm trying to get control of my diet. I'm going to the dr. next week to see about my options, some allergy testing, and maybe medication.

In the mean time, I journal everything I've been eating and how I feel afterwards. Monday was a bad day and all I can think is that maybe I had too much dairy the day before. 

Thank goodness for things like gluten free cream of chicken with quinoa pasta soup. I'm thanking Shaun and Cobbs for the mini sour dough loaf, but my tummy didn't thank anyone for it afterwards.

 Home made clam chowder. Thank you very much. Kerry said he was never eating it from a can ever again. Cream biscuits. Yes, too much dairy. 

 Butternut squash soup, this time with a little ginger and thyme. Was a huge hit. Sour dough croutons.

 The list. I can't even pronounce what FODMAP stands for but it seems to be helping. I can eat an Arby's sandwich and fries, I can eat almost anything orange, but I can't eat a bowl of lettuce. Life is cruel. 

With all my days off, (I traded with someone so I worked a few close together but I don't work again for about 2 weeks), we have been doing the menial stuff. Washed all the cupboards, top and bottom, but didn't do the insides. Took 5 boxes of things to Salvation Army. Feels good to get that stuff out of here.

We also cleaned out 2 large boxes of the kids' school work that we'd been saving. We thought they'd want it later in life. Then I remembered I didn't want the stuff my mom had saved so whey would my kids want this stuff. We asked them and sure enough, they didn't care. We sorted it, kept a few things, and got rid of the rest. But this little gem...Emily's handy work, we had to keep it. 

 I made these for tonight. M-R's birthday was last week and she's coming over tonight. I felt like making Creamsicle cupcakes from scratch for her. I had a bite yesterday afternoon and almost instantly had stomach cramps and goosebumps. I so want one tonight. 

Adelfo Cerame - Road to The Wheelchair Nationals '12: Vince Gironda's Hawaiian Diet. Or, Caloric Zig-Zagging Intermittent Fasting Style. Plus: Crime Scene Las Vegas!

Image 1: Adelfo's trip to Vegas did not end up just as bad, but it still had some CSI-ish elements ;-)

Assuming that many of you have already been waiting eagerly to hear, or I should say, read if and how Adelfo has survived his trip to Vegas, I guess it would be best if I put you out of misery right away, but before I let Adelfo tell you his Hollywood-style story, I want to mention that in Adelfo and myself are going to be on Carl Lanore's Super Human Radio in about 2h, i.e. 7pm EST! So, in case you are reading this in time, make sure to tune in live (update: for everyone who missed the live show, click here to download the podcast)! But enough cross-marketing for now, let's hear what our common friend has gone through in gambler's paradise...

"The Good, The Bad, and the Ugly"

If you’ve ever seen the movie, that’s pretty much how I you could sum up the events in Vegas. As wild, and fun as it was, it also got pretty ugly towards the end. Someone broke into our hotel room early Sunday morning while everyone was still out and ... no, not training, but partying ;-) And when we finally came back to the hotel at around 7 am, we were so intoxicated that we didn't even realize that we got robbed. Only after we all got some shut eye, and woke up a couple hours later as we started packing our stuff to check out, one of my boys realized that someone must have had opened his bag and after had taken his iPod.

Image 2: Would you steal a Laptop
from this guy?

It took us only a few seconds to realize that all our bags had been searched through, and it struck me like a 200lbs dumbbell, when I went I looked towards the table, where my MacBook had been sitting and saw ... nothing. The damn thing was Gone! And with it 4 years of my life's work. From school stuff, research papers, personal projects, client portfolios, pictures, etc. that and much more, it was all on the hard-disk of that damn machine. What really saddened me most, though, was that my whole documentation. All the photos, nutrition and training plans, I have been documenting since late summer for my 2012 contest prep, all that was gone. I had kept an in-depth journal documenting my 2012 contest prep. It had everything from progress pictures, stats, calorie intakes, macros… Everything Gone!

I could care less about my laptop, materialistic things can be replaced, but there was a lot "in" that laptop that had a lot of sentimental value to me… well, I guess this is a case of "another one of life’s lessons learned". And if there is anything that I have learned since my spinal cord injury, it is that you can't cry too long over spilled milk. You got to stop thinking about problems and begin to work on solutions. In my case this does unfortunately mean that I have to start all over again, while trying to recover as much information as I can from the last backup I have (about 50% of the data), Facebook, personal and professional email transactions and obviously my blog, here at the SuppVersity. If I am lucky I will thusly be able to recover 75% of what I have lost... and most importantly: I able to find was the "before pictures" I took, when I first started my prep...

Vodka, Tequilla and only 8 weeks to go!

A pros pos prep! Just 8 more weeks to go to the big day. My big day at the Wheelchair Nationals in Palm Beach, Florida, and I know what you are thinking now: "8 weeks out and this idiot heads to Vegas and gets so hammered that he doesn't even realize he has been robbed? What kind of bodybuilder is that?" I guess the best answer I can give you would be: "One who is passionate about training, but does not live to train, but trains to live!" And, at least judged by my latest pictures, the weekend with Vodka and Tequila Sunrise instead of protein shakes does not seem to have hampered my progress at all - wouldn't you agree (and remember contrary to political elections, bodybuilding contests are not won by the guy with wit the nicest smile ;-).?

Image 3: The Monday after… Not bad for someone whose diet consisted mostly of Vodka and tequila sunrise cocktails during his feeding hours! And since I have a brand new laptop now too. The picture resolution is a lot better ;-)

As for how my nutritional regimen went…well on Thursday night, I broke my fast with a couple shots of vanilla vodka, cocktails, a slice of pizza and a set of sexy painted toes attached to a pretty young thing for dessert ;-) [Toes are calorie and carb free with no nutritional value by the way… lol], and I think I had a burger and fries at a local burger joint at the hotel, where we were staying at for Friday and Saturday night. Overall, everything went just as planned... pretty chaotic! But I stuck to my fasting and feeding protocol and made good use of the flexibility it allows for by making a habit of braking my fast with a couple of shots of vodka, instead of food.

Getting back from Vegas and back on track

The Monday after I decided to go on a strict veggies and protein only diet for the next couple of days. I pounded a lot of water, to rid whatever excess water I may have retained during the weekend (although I honestly did not see any) and then reintroduced my post workout carbs on Wednesday night after the workout. It didn’t really hit me how close my show is and that 8 weeks is not that long, so I started playing with my caloric intake and macros again while trying to update everything on my new laptop. When I was reasoning about the macronutrient ratios, I realized how much of a difference the reintroduction of carbohydrates had made in terms of the way I looked and the intensity with which I trained.

When you are getting into the single-digit body-fat realm, small dietary (or supplement) changes often make a big difference.

For me the ~100g of carbs make me feel much fuller and tighter. The increase in glycogen content goes hand in hand with an increase in vascularity and my muscles look overall much grainer. At the same time, I know I have to keep gradually dropping my calories to lean out, if I want to be beyond shredded by show time. I will therefore start to cycle my calories between 1500 kcal to 1200 kcal - with the higher, 1500 kcal intake on workout days, and the lower 1200 kcal on non-training days.

Table 1: Energy intake and macronutrient composition on workout days; * trace carbs, # starchy carbs & fruit.

The 10g of carbs are trace carbs from my whey protein; I usually wouldn’t count it but when it gets down to the final weeks, it gives me the peace of mind that is necessary to keep cortisol at bay ;-) All 65g of my PWO carbs will come from organic russet white potatoes (about 55g), and the rest of the 10g I’ll use on light fruits like berries, papayas or pineapples (about ½ a cup to add to my cucumber salad that I make… I still don’t count veggies by the way).

65g of starch carbs is all it takes to let make muscle pop

"Only 65g of starchy carbs?" Is probably something the carboholics out there are just asking themselves!? For me it is plenty to get me full and satisfied. The cucumbers and zucchinis will then do their share to fill up my tummy, while the carbs from the potatoes find their way right into the bellies of my muscle, so that I can even feel the muscle contractions pop, when I flex! An unexpected yet very appreciated side effect, by the way, is that along with increased vascularity, even the excess skin that I can pull in my lower abs magically disappears when the muscle beneath it gets its share of the glucose that is floating through my veins.

Table 2: Energy intake and macronutrient composition on non-training days.

The zigzagging, as far as calories goes (cf. workout and non-training days in tables 1-2) is actually an old trick of Vince Gironda. He called it the Hawaiian Diet. The Hawaiian diet consists of red meats, chicken or fish, with either pineapples or papayas. The macronutrient foundation of every meal is protein + fat meal - the exact food combination vary, though. In that Vince deliberately selected pineapple and papaya for their high enzyme content, of which he believed that it would help with fat loss.

Image 4: Vince Gironda,
the Iron Guru

The reason this protocol appealed to me is that both the macronutrient composition (mainly fat + protein), as well as the foods you are supposed to eat, are pretty much identical to the interpretation of intermittent fasting I have come up with in the course of the past weeks and months. And although I am repeating myself here, all geeky science, AMPK and mTOR stuff aside (I'll leave that to Dr. Andro ;-), it's major advantage over your usual contest-prep diet is its ingenious simplicity and convenience... 50g of meat, 20g of fresh pineapples, and 15g of raw coconut oil - how much easier could dieting for fat loss possibly get? Having the total caloric intake and the macronutrient ratios in check, I am pretty confident that the caloric zig-zagging and the weekly re-feeds on Sunday will compensate for the overall borderline low calorie intake and prevent my metabolism from slowing down over the course of the next week.

When adaptation occurs, stagnation begins

Obviously, my training will have to complement what I am doing diet-wise and thusly I have revisited the results from the 5x5 routine I have been following as of late and decided that it may be about time to switch to a higher volume / rep range program for some time. Aside from the higher rep ranges I have been using on a few auxiliary exercises, I stuck to the 5-6 rep range for the whole contest prep. And although it has worked fine for now, I start to notice that both the escalating density training (EDT, cf. "Things Begin to Escalate"), as well as the 5x5 training don't feel as intense or tiring as they used to. I have gotten stronger, my stamina has increased and my body has adapted... and while adaptation means progress, it will entail stagnation, whenever you fail to provide new stimuli to which your body will have to adapt. For me, an increase in training volume will hopefully do just that. I will yet still have to figure out how I can make sure that the intensity of my training sessions does not suffer from that. So, in essence, I will try to lift as heavy as I can, but with 8-12, instead of 5-6 reps. The exact training schedule is yet still in the works, but I will have it nailed down before next week.

Just wanted to let everyone know: My Facebook page is always open to anyone who has questions or needs pointers or advice on anything! Don't be shy, I won't charge you ;-)

So, with all my pictures and recipes being on the laptop that was stolen from my room in Vegas, the promise that I will address my revised higher rep, higher volume training regimen in next week's installment of my weekly contest prep blog, here at the SuppVersity, is the only thing I have in store for you this week.