Adelfo Cerame - Road to Wheelchair Nationals '12: Tweaks to Avoid Overtraining. Plus: 5 Staple Supplements and How to Effectively Combine them With Whole Foods.

Image 1: If you have followed the whole series you know that there are 6 months and tons of hard work and dedication between the pic on the left and the one on the right. Time and effort  not "the right genes" it what most people lack, or simply decide not to invest.

When I look back at the past couple of weeks, or, when I come to think about it, months, and the progress my friend Adelfo has made, it amazes me time and again how careful planning, constant tweaking and above all total dedication to training and diet can take your physique to another level - and that, on an almost weekly basis! In a way, it is unfortunate that all this will eventually not be part of the equation, when Adelfo will be showing off his totally shredded body on stage. And I am not referring exclusively to the issue of not being in form on a specific day. This is part of the sports! And in fact, I am not even thinking about the athletes, themselves. I am rather thinking of you, your friend, your son or daughter, who see bodybuilders, fitness athletes, bikini models or even "normal" celebrities on the net, magazine covers or TV and think to themselves: "I can never look like this guy/girl!" ... do the reality check, look at what it really took them to get there and realize that part of their secret is that they are well aware that you cannot "peak" 365 days a year! And now tell me: Do you really believe you cannot get there or is it rather that you do not want to invest all the efforts it would take you to get there? I suppose for most of you the latter is the case and you know what? As long as you are honest with yourself and others and don't lull yourself into believing that is it all just in your genes, that is perfectly ok! But enough of me being a smart ass, ... let's see how Adelfo is doing this week.

Six weeks out and still waiting for the brick to hit me

Image 2: I guess real foods like these are part of, if not the reason "the brick" has not yet hit me ;-)

I feel like I am sitting here, waiting... not so much for contest day, yet, but rather for that day, the day, when the brick wall is going to hit me... it is part of the game - part of the prep. That brick wall, people me (in my previous preps) included hit, whenever they diet to achieve that unnatural degree of leanness people are looking for on stage. It has not hit me yet and I cannot even tell if it will... but if it does, I will be prepared!

Looking back at the last week, I might even say that I probably barely got away from being struck. Probably not so much as a consequence of overdieting, but rather as a result of overtraining. As you will probably remember, I decided to revamp my training regimen by incorporating an intensified version of the reverse pyramid into my routine. After one week on the routine, I had to realize that as good as the idea of combining a heavy lifting and high volume approach may look on paper, doing that on four training days per week may be too much. While I was strong and felt pumped on the first two days, my strength and with it my focus began to fade on the subsequent two days: Fatigue, lack of motivation, moodiness, ... all that are pretty rare occurrences with me, especially when I just started on a new routine.

It could not get any more obvious my body was showing me the red flag!

Video 1: Wheelchair chin-ups (wheelchair = 25 lb. + 45 lb. plate = 70 lb. chins) - For a while I’ve been trying to figure out a way to stimulate my lower back and maybe even my lower trunk muscles in the back… I think I just found what stimulates them… I’ve made it a priority of mine to do weighted chins twice a week when I train my back (click here to watch).

Against that background, I decided to apply another twist to the routine and split the week into two heavy 5x5 (Mon-Tuesday) days early in the week, rest on Wednesday, and two reverse pyramid training (RPT) workouts on the following two training days (Thurs- Fri) later in the week... I think by setting it up like this, I can control the tempo, throughout the week, so I don't burn myself out to early in the week.

If I were one of my clients and not so close to competition, I would probably suggest to either take a de-load week or a complete week off from the gym, but at the moment I feel like I cannot afford doing either of these options. Although I am pretty sure a week off wouldn’t hurt me, as long as I kept my diet on point, it is precious time to make forward progress... so no, I will not take the week off! What I will do though, is start to control my training tempo from here on out to make sure that I’m not burning myself out (I mean… I have been prepping since October ;-)

Nutritional tweaks: Post-workout carbs? Yes, honey!

I made some minor adjustments with my nutrition, as well. Instead of having my carbs with my PWO meal, I switched to taking the lions share with my post-workout shake right after my workouts. I did that because sometimes, I takes me too long to get home and prepare my meal, with the insulinogenic effect of the whey potentially I sometimes felt somewhat hypoglycemic, and the subsequent surge in epinephrine and cortisol which will get my blood sugar back to normal is something I want to avoid at this time in my prep. When the whole purpose of the carbs is to refill muscle glycogen, I don't want my liver to do that by turning protein into glucose before I get home and have my carbs.

Image 3: Whey Protein + the combination of 2 ripe bananas + 1 Tbs. Raw Honey = PWO bliss!

The reason I decided to go for the ripe bananas + raw honey combi are manifold, but I would be lying if taste was not at least part of the equation. That being said, let's be honest, what better fast digesting PWO combi can you ask for, if we are talking about whole "real" foods? The combination of whey + 2 ripe bananas + one tbs. of raw honey do not only meet the macros, I am looking for in my post-workout shake, the bananas are also rich in potassium, which is necessary for muscle recovery and will help with the electrolyte balance that is so crucial to keep off unwanted water weight. And the raw honey, despite being a calorie dense high sugar food, is, unlike sugar, filled with nutrients like digestive enzymes and antioxidants. Plus, You don’t have to cough up $40- $50 as you would on other carb supplements like maltodextrin or waxymaize. An organic banana costs about 25- 35 cents, and a jar of raw honey costs around $8.

You don't need tons of supplements. Just select a few staples that work for you!

Since were on the topic of PWO nutrition and timing, I guess some of you may be interested if, how, which and when "real" supplements come into play. So here is a brief rundown on what I am currently taking and how I am timing those supps around my fasting and feeding windows.

• Fat burner (meltdown by VPX): One of the only times I ever mess with fat burners is when I get closer to show time. I like to use fat burners for the last couple weeks to help me increase my metabolism and burn a little bit more body fat to tighten me up some more, and to help with the stubborn areas where subcutaneous water likes to cling on to (in my case lower abdominals). I take my fat burner once I wake, early in the a.m. during my fast, this way I can take maximal advantage of its lipolytic effects. It does not help to liberate the fat from the fat cells if your body does not need to burn it, so taking the fat burner within the feeding window would at best be a waste of money...
   
• D-Aspartic Acid (D-Pol by PurusLabs): I was running test logs on this product a couple weeks ago, and really liked it, so when I ran out I actually decided to buy it. It worked well with improving my gains in strength and maybe size, but strength for sure! Probably due to the added nitrates, it also gave me a good pump, when I trained. I take this supplement early in the a.m. - probably like 3- 4 hours after I take my fat burner - for better absorption, so that the aspartic acid doesn't compete with other aminos and at least some of it does make it to the brain, where it is supposed to do its LH releasing magic.

Image 4: I believe in selected a hand full of supplements only. My tried and proven staples are creatine monohydrate, BCAA’s, a pre-workout and a fat burner. Purus Labs' d-aspartic acid is the only real newcomer in this prep.

• Pre-workout supp (Friction by VPX): I’m not much of a pre-workout supp junkie, but I do feel the benefits from taking them during contest prep, or cutting to help maintain strength and muscle. Most pre-workout supplements primary ingredients are creatine blends, with amino acids, and, or beta alanine. Usually each brand has its own proprietary blend and boasts of how unique it is... don't be fooled, the ingredients which actually work are the same for most of them. I take my pre-workout supplement about an hour after I ate my pre-workout meal, and about 30-45 minutes before I train. The whey + coconut oil for my pre-workout meal is digested by then, so if you will you can say, I take it on empty ;-) The main reason I chose friction was curiosity, I like to try new products once in a while and must say that I really enjoy this one.
   
• BCAA’s (Power Shock by VPX): BCAA’s help with muscle recovery and growth, ... but I guess the well-read SuppVersity junkie you are, I don't have to give you the lowdown on their benefits ;-)  I take mine intra-workout, to minimize catabolism and promote the exercise induced increase in protein synthesis. I mix about 2 servings in a water bottle that will last me through my whole workout. I never tried VPX’s BCAA’s, I usually use Xtend, Recoup, or Anabolic Switch, but decided to try this because of the potential benefits of the added nitrates and, most of all, the price tag ;-)
   
• Creatine monohydrate (Creapure by TrueProtein): I use to be real phobic about taking creatine while trying to cut or diet for a show, because of the “ol’ bro science” that taking creatine makes you retain water… then I thought to myself?... Well no shit!? That’s what creatine does! It draws water into your muscle tissues. Lol… As for the subcutaneous water, that people talk about they get when they supplement with Creatine? That probably has more to do with either their shitty diet, or their dump believe that creatine needs to be stacked with tons of sugary carbs to "push it into the cells". In view of the fact that my pre-workout supp already has some creatine in it, I mix 5g with my BCAA’s while I train, and take another 5g when I get home. I mix it with crystal light and drink it with my PWO-meal.

So far so good, but I still maintain that all supplement magic aside, my four whole food meals are the pillars I build my success on. And before you are bombarding me with questions in the comment area or on facebook, here is some more information on how these pillars look like:

 

Images 5-6: You know that I believe in a real food approach to dieting and this is how that could look like in the last weeks of your prep.

• Pre- workout meal: I usually break my fast at 3pm and at the gym training by 4:30pm. I don’t want to have to wait 2 hours for my food to digest, so I prefer a fast digesting protein like whey + 1 Tbs. of coconut oil for that immediate energy that my body can use. Macros= 50g protein/15g fat
   
• PWO shake + 2 ripe bananas & raw honey (cf. image 3): I eat this immediately after I train when I get into my car, because muscle tissues are primed for glucose and protein uptake right after training. Macros= 50g protein/ 75g carbs
   
• PWO meal: Since I shifted most of my carb intake immediately after training, my PWO meal is now just a P+F meal, with about 10-20g of carbs coming from strawberries, papayas or pineapples. I eat this meal around 8:30pm when I get home from the gym. Macros= 50g protein/ 10-20g carbs (fruit)/ 20g fat
   
• Last meal before fast: I like to do a shake for my last meal because my PWO meal usually gets me full, so I like to squeeze in a protein shake at around 10:40pm before I start my fast again at 11:00pm. Since I use whey protein for my shakes, I like to throw in 2 raw cage free eggs in with my shake, so the fats can slow down the digestion, since whey is a fast digesting protein. I’ll also eat about 1-2 tsp. of coconut oil to hit my macros. Macros= 50g protein/ 15g fat

That’s all I have for in stall for you, this week, but stay tuned for next week's update, when I start bringing back recipes! You're gonna love that one, I promise ;-)

Is it Your Neighbor(hood)'s Fault That You are an Obese Couch Potato? Plus: Higher Incomes Increase Obesity Risk in Men, Better Education Decreases Risk in Men & Women

Image 1: If this photo looks as if it was taken in your neighborhood, statistics say that you will have a harder time than others warding off obesity.

If you have not already been aware that the major weightloss obstacles are not so much of physio- than of psychological, or I should say behavioral natural, Monday's blogpost on the inability or unwillingness of the majority of the study participants in the Krebs study should have reminded you that there is more to losing weight than having an "optimal" diet plan. In this context, the results of a recently published paper from the University of Ottawa, Canada (Prince. 2012), comes to mind, in which Stepanie A. Prince and her colleagues report the results of a large-scale cross-sectional multi-level analysis of the association between neighborhoods, physical activity and obesity in Ottawa.

Mislead and misfed, but by no means unable to afford leading a healthier life-style

Although obviously of epidemiological nature, the study is remarkable in that it relies on relatively recent data (2006-2008) from 494,000 residents from 86 neighborhoods in Ottawa, who were part of the Ottawa Neighborhood Study (ONS). My usual advice not to confuse correlation (no matter how "significant") and causation, does yet still apply. A statement like "for each additional km² of park area per 1,000 inhabitants, the odds of being physically active increased by 17% in the female inhabitants of the respective neighborhood" (cf. figure 1, left; respective value: 1.17) does thusly signify that readily available parks areas seem to encourage women to be more physically active in their leisure time. It does not mean that moving to an apartment from which you can see the joggers doing their rounds in Central Park will turn a couch potato into a sporting ace. After all, it is at least as likely that people who like to jog try to make sure that they move to an area, where they can easily pursue their hobby.

Figure 1: Model predictions for the influence of environmental, social and contextual parameters on physical activity (left) and overweight/obesity rate (right) in men and women; * p < 0.05 (data based on Prince. 2012)

Against that background, I decided to include only factors which showed a statistically significant association with either obesity or physical activity in at least one of the two sexes in the data in figure 1. Now, you rarely have a rule without exception, and in this case, I also included the associative strength with the so-called census-based socio-economic status (SES) index, because the non-existent influence of social status on obesity rates goes just about as nicely against the notion that you cannot eat healthy if you are on a budget, as the +39% increased obesity risk of men in households with incomes >30,000$ (cf. figure 2)

Figure 2: Model predictions for the influence of the individual parameters household income and education overweight/obesity rate in men and women; * p < 0.05 (data based on Prince. 2012)

Moreover, the strong negative association -44% for men and -45% for women between having at least a college degree and being overweight/obese, would would support the argument that it is less about not being able to afford a "healthy lifestyle" than about not having learned / not being able to teach oneself to do so... or, if you will, being more susceptible to the misleading information from the food industry and less aware of the pitfalls of shopping in convenience stores (+17% increased risk of obesity in women per additional convenience store for 1,000 inhabitants) and eating at fast food outlets.

Note: Neither the age nor parameters, such as the number of indoor or outdoor recreational facilities, grocery stores, specialty stores and (normal) restaurants which, at least taken in isolation, had no statistically significant influence on either physical activity or obesity rates.

With respect to the +22% and +39% increased obesity risk per additional fast-food outlet (per 1,000 inhabitants), it should also be mentioned that this is only one out of several of the environmental factors, which had statistically significant influence only on obesity rates in women from the respective neighborhoods - a phenomenon, which could yet be a consequence of the fact that men are less likely to be in their respective neighborhood during working hours than women, so that the susceptibility to fast food stores is probably not gender-specific ;-)

The bitter or delighting truth about your neighbor(-hood ;-)

It is nevertheless quite remarkable that the associative strength of individual criteria such as age, income, education etc. showed an overall much more pronounced variation (0.98, p<0.05), than one of the area-specific variables, the variance of which did not reach statistical significance for either of the two study outcomes, i.e. physical activity level or overweight/obesity (cf. figure 1). This would suggest that environmental influences in the area we live in is in fact a more reliable indicator of our likelihood of ending up as an overweight couch potato or lean physical culturist than our incomes, education or say our age. A finding, which I would say is actually quite remarkable, don't you think so?

TTA + Fish Oil - Fat Burning Superfats or Hepatoxic Pro-Oxidants? Why You Better Avoid Large Amounts of Omega-3 and Tetradecylthioacetic Acid in the Long Run

Image 1: Even if you align them like that, it is at least debatable whether capped fish oil is much more natural than the structurally modified 16 -carbon saturated fatty acid tetradecylthioacetic acid (TTA). As far as their effects on weight loss are concerned, the latter is certainly more potent,... the debate on the side-effects of both is yet still far from being settled. Despite the mainstream hoopla around the former...

At least for those of you who have been around the supplement world for some time, the acronym TTA, which stands for tetradecylthioacetic acid, a structurally modified 16 -carbon saturated fatty acid (SFA), which has been shown to increase fatty acid oxidation and reduce triglyceride levels via interactions with purportedly all PPAR-receptors, should ring a bell. For the rest, it will yet probably be news that, back in the early 2000s, TTA was all the rave as the new star among OTC-fat burners. And in fact, the weight loss people experienced on respective products was non-negligible... yet so were the side-effects which crept up over time (and with ever-increasing dosages): Headaches, cramps, dehydration and water retention specifically in the abdominal area were only the minor complaints. Unbearable fatigue and even palpitations were at the other extreme of the spectrum and probably the actual reason why company after company  altered the formulation of their "effective" and above all commercially successful tetradecylthioacetic acid containing fat burners.

While TTA works well, but has well-known side-effects,...

A recent long-duration rodent study that was conducted by a group of European researchers and which my friend Sean Casey from CasePerformance has brought back up onto my radar (Vigerust. 2012), did now investigate the long term (50 weeks) effects of supplemental tetradecylthioacetic acid and another purportedly saver PPAR-agonist, with similarly beneficial effects on triglycerides yet hardly noticeable effects on weight management - my all-time favorite fish oil! To this extend, the scientist kept their rats on their infamous interpretation of a "high fat" diet, which, as you will probably already have expected, had a moderate fat content of 25% tons of carbs and little protein and had thusly more of the standard American diet than of what people in the bloggosphere usually refer to as a "high fat" diet, i.e. a diet that is really high in fat (>50%) and low in carbohydrates.

Figure 1: Relative body weight (compared to identical baseline) in rats at different time points during 50 weeks on high fat diet (control) with either TTA, fish oil or both (data calculated based on Vigerust. 2012).

It is thusly not surprising that replacing 10% of the fat by fish oil (~11g EPA + 6g DHA for avg. human) had absolutely no effect on the weight gain of the hyperphagic (overeating) rodents. The miniscule amount of 0.365% TTA, which would be equivalent to a daily intake of ~912.4mg of TTA for someone consuming 2000kcal/day, on the other hand, lead to statistically highly significant reduction in weight gain over the whole 50 week feeding period (cf. figure 1).

Figure 2: Relative expression of uncoupling protein 3 (UCP3, primary axis) and enzymes involved in fatty acid metabolism (secondary axis) at the end of the 50-week dietary intervention; expressed relative to high fat control (data calculated based on Vigerust. 2012).

As evidenced by the elevations in carnitine palmitoyltransferase II (CPT II), which is necessary to shuttle the fat into the cell, HMG-CoA, which is one of the key players in ketogenesis, and peroxisomal acyl-coenzyme A oxidase 1 (ACOX1), which initiates the first enzymatic reaction during beta oxidation, the hepatic fatty acids oxidation in the TTA (and TTA + FO) group was profoundly increased, in conjunction with the exorbitant increase in UCP-3 expression (>1500x in the TTA only, and >1300x in the TTA + FO group) and the subsequent "leakage" of energy in the form of protons, this easily explains the -11% / -19% reduction in total body weight in the TTA and the TTA + FO groups at the end of the 50 week study period.

....fish oil hardly works and has less-known side-effects

In that, it is important to note, that only TTA (respectively its addition to FO), not fish oil, was able to reduce the diet-induced elevations in hepatic triacylglycerol (TAG) levels. This leads to scientists to speculate, that despite similar effects on TAG and cholesterol transport in the liver, ...

[...] animals given the FO diet are less able to metabolize the excess hepatic lipid levels [... so that] FO redistributed lipids without affecting the total lipid level and body weight.

This would also explain the detrimental effects the fish oil supplement had on hepatic cholesterol levels and lipid oxidation, which would suggest that, at least under these dietary conditions (relatively high fat + high carb + high energy = typical western diet), one would be better off taking no fish oil at all, or a combination of fish oil and TTA.

Figure 3: Relative mRNA expression of markers of protein and lipid oxidation in liver and liver mitochondrial fraction of the rodents at the end of the 50-week study period (data calculated based on Vigerust. 2012)

The latter is all the more indicated in view of the fact that the use of the highly oxidizable fish oil alone lead to non-negligible increases in protein oxidative damage (cf. GSA, alpha-AASA, figure 3) and an increase in total hepatic glyco- and lipooxidation, as evidenced by the increase in Ne-Carboxymethyl-lysine (NCL, figure 3) in the whole-liver samples and a corresponding increase in Nɛ-Malondialdehyde-lysine (MDAL), a lipid-specific marker of oxidative damage in whole-liver and the mitichondrial homogenate (liver M-fraction) of the animals in the fish oil (only) group (cf. figure 3).

These detrimental oxidative longterm effects of fish oil supplementation, which "showed a significant positive correlation with DHA content" of the liver (meaning more DHA in tissue = more oxidation), were only ameliorated, yet not totally prevented by co-treatment with tetradecylthioacetic acid (TTA), which reduced the amount of oxidizable PUFA in plasma and tissue and reduced the mitochondrial ROS production via the UCP-3 induced energy leakage and the subsequent relative reduction in oxidative energy production (remember the overall energy expenditure was still increased by TTA, yet not by FO treatment).

Bottom line: Avoid the dietary PUFA burden, eat healthy and exercise...

Image 2: "You told me to eat more protein and this burger has both meat and cheese!" - click here for more info on why dietary interventions fail

As far as the amelioration of negative side-effects of the typical Western high carbohydrate, relatively high fat diet are concerned, the results of this study would argue against the longterm use of omega-3 polyunsaturated fatty acids from fish oil (DHA in particular) and for the use of structurally modified 16-carbon saturated fatty acid TTA in order to reduce weight gain, triglyceride and liver cholesterol levels in individuals who are either unwilling or unable to make the necessary life-style-changes that would, instead of just prolonging their suffering, help them finally escape from the maelstrom of the metabolic syndrome (cf. yesterday's blogpost on "High Carb vs. High Fat, When Science Meets Real Life").

Whether the same holds true for athletes, fitness enthusiasts or at least moderately active human beings, who stick to an overall anti-inflammatory low(-er) carb (not "no carb" and not necessarily, but possibly "paleo") diet, would certainly warrant further investigation. It would nevertheless, my previously voiced concerns over the injudicious (over-)use of omega-3 supplements in the futile effort to "balance" the dietary over-indulgence of omega-6s... after all, the most straight-forward explanation for the increase in oxidative damage in the fish oil only group is the increased amount of PUFAs in the liver tissue, which are - across the board, i.e. omega-6 and omega-3 - much more susceptible to oxidative damage due to radical oxygen specimen (ROS). I thusly stick to my previous recommendation to just watch your overall PUFA intake and resort to alternative fat sources, such as coconut oil (which is, by the way, the topic of the first "non-SuppVersity" article of mine in the all-new article-section of the VPX-website; don't worry I won't neglect the SuppVersity and stick to topics without potential "conflicts of interest and objectivity" ;-), butter, dairy and meat products from grass-fed animals, eggs and obviously real fish!

... and you won't need TTA to lose weight or ward off unwanted body fat

Moreover, I strongly caution against a similar injudicious (ab-)use of large amounts of TTA especially over longer periods of time. The latter was probably the underlying reason for the initially mentioned side-effects, due to which most supplement manufacturers either totally removed tetradecylthioacetic acid from their products or reduced the amounts per servings to levels, where the other ingredients would give you palpitations before you would achieve dosages way beyond the 1g range, which, as previous human trials would suggest, appears to be save at least in the short term (<30days, cf. Lovas. 2009). With respect to longer durations and/or higher dosages, you should yet be aware that the very same depletion of plasma and tissue PUFAs which is partly responsible for the overall reduction in oxidative damage in the study at hand, may well backfire and produce exactly those cramps, the water retention, and the profound lethargy reports of which you will find in the archives of various health and fitness boards, all over the web.

High Carb vs. High Fat for Obese Type II Diabetics and What Really Happens, When Science Meets Real Life

Image 1: "You told me to eat more protein and this burger has both meat and cheese!" - This and other mishaps are among the reasons why calories still count in the books of most dietitians.

Today's SuppVersity post fits in nicely with the latest installment of the Intermittent Thoughts from yesterday and the post on the "heart-healthy low fat diet" from Friday, as it is about one of the few large(r) scale, long(er) term human trials on the effects of diets with different macronutrient-ratios in insulin-resistant human beings. As you would expect from an expensive nationally funded trial, a "high fat" diet (in the actual sense, not like the SAD diet from Friday) was not part of the study design and that despite the fact that not the US, but the New Zealand Health Research Council was the official financier of the multicentre (meaning that it was a corporation of several institutions) parallel design, blinded randomised control trial, the results of which have been published in the latest installment of Diabetologia (Krebs. 2011).

What turns obese diabetics into bigger losers - high protein or high carb diets?

To test the hypothesis that weight and glucose management would be effected by the protein or carbohydrate content of the diet, the 419 obese, diabetic participants (age: 30-76, mean = 58y; BMI ~36.5kg/m²) were randomly assigned to one out of two dietary regimen, both of which aimed at a reduction of total calorie intake by ~500kcal/day. As far as the actual diets were concerned, the subjects were free to make their own choices based on portion charts, "culturally appropriate recipes" and what they had learned during an initial one-to-one discussions and the first group session. 

What we are dealing here, is thusly basically the "free living individual" who tries his / her best to finally get rid of the weight by a reduction in total calorie intake. And while the latter may compromise the significance of the study results as a basis to speculate about complex underlying physiological responses to macronutrient manipulations, the 2-year study period with after all ~70% of the subjects making it to the 24-month visit at the end of the study, as well as the "I was sick of eating so much protein!"- and the "But I thought Twinkies and Dingdongs were high protein foods!"-factor provide a real-world significance neither of the controlled <30days lab experiments has.

Figure 1: Actual reduction in energy intake (vs. baseline) in high protein and high carbohydrate group in the different stages of the trial (data calculated based on Krebs. 2011)

In this regard, a brief glance at figure 1 should suffice to see that those "adherence" effects were in fact huge. The -500kcal reduction in energy intake was not achieved by either of the groups and the difference between the protein and the carbohydrate groups is more than significant. While the the average reduction in calorie intake in the protein group was ~146kcal/day and thusly <30% of the target, the high carb group with an average of ~238kcal/day did at least get close to the 50% mark... and as you may already have suspectes, things get even worse, when we take a look at the macronutrient ratios.

"High protein diet" means that I just eat some additional protein, right?

Since ours, as well as the scientists' primary interest is in the differences between the macronutrient composition of the diets of the groups (and obviously their respective effects on weight loss and glucose management), I decided to plot the relative differences in total macronutrient intake between the groups, to make it easier to see how big the differences really were. Now, before you take a look at the data in figure 2 let's briefly discuss, what we should see there, when we plot the ratio of say protein(protein group) to protein(carbohydrate group)? Right, that should be way more than 1 or 100%. And the same for carbs? Right, that should be way less than 1 or 100%!

Figure 2: Relative energy and macronutrient intake expressed as the ratio of total intake (kcal or g) in "high protein" to total intake in "high carbohydrate" group (data calculated based on Krebs. 2011)

As the data in figure 2 goes our first prediction is true, but the adherence to the high protein intake declines and at the end of the study, the "high protein" group consumes hardly more protein than the "high carb" group (only 12 out of 206 subjects, i.e. 6%, achieved the prescribed 30% of total energy from protein goal!). Our second prediction, on the other hand, does not apply for either of the study periods, because even at the end of the study, the difference in carb intake between the "high protein" and the "high carb" groups is hardly significant.

More fat, more protein, more energy, about the same amount of calories = ?

Now, given the fact that the obese diabetics in the "high protein" group obviously interpreted their diet as the "just eat more damn protein"-diet and thusly ended up consuming overall more energy from a higher protein and fat intake at about equal carbohydrate intakes, what does convential dietary wisdom tell us? Yeah, those gluttonous bastards should not lose a pound... I mean, come on -146kcal and all that fat?

Figure 3: Weight loss and reduction in waist circumference expressed relative to reduction in energy intake (vs. baseline) during the individual phases of the dietary intervention and for the whole study period (data calculated based on Krebs. 2011)

Fortunately, this is yet another instance, where the conventionally dietary wisdom with its adherence to the faulty calories-in-vs-calories-out paradigm and the notion that eating fat will make you fat, utterly fails:

1. The participants in the "high protein group" lost weight (-3.9kg vs. -6kg in the "high carb group), although they fell >70% short of the kcal-target of -500kcal/day
    
2. On a "per-kcal-energy-reduction"-base (energy expressed relative to baseline; cf. figure 3), the participants in the "high protein" trial lost on average 13.1% more body weight and 14.5% more waist circumference, than their peers on the "high carbohydrate" diet.

If we also take into consideration that the weight loss of the "high protein" group totally stalled as their compliance to the macronutrient intake plummeted from month 6 to month 12, the scientists conclusion that their study would show that ...

[...] a high-protein diet with a group-based dietician-led support and education programme easily deliverable in a real-world setting does not promote greater weight loss than the prescription of a high-carbohydrate diet

maybe true (as the total differences were statistically non-significant), the underlying reason, is however the real-world setting and not, as a cursory read of the abstract would suggest, a consequence of the fact that macronutrient modulations would not effect weight loss. The latter in turn, should remind you why you originally came here today: For a discussion of recent scientific data that goes beyond what you will find on PubMed or in the 2nd hand-information the lay-press is cooking up from press-releases ;-)

Intermittent Thoughts on Insulin Resistance: The Marathon Paradox - How Temporary Exercise-Induced Insulin Resistance Paves the Way for "Fat Burning Machines"

Image 1: Is this man temporary insulin resistant? Probably, otherwise he would hardly have made it to the finish line.

After weeks of discussing the physiological foundations of building muscle, I figure at least some of you will share my personal desire think about something else, at least "intermittently", so to say. Now, before some of you start complaining, let me say this: I will try to attack today's topic from various angles, meaning that even those of you who may now be thinking "insulin resistance" that's just for lazy fat-asses will see that a better understanding of what some people perceive to be the root cause of most if not all of the major health concerns of the western convenience society could also help you in your efforts to get even more jacked.

When I come to think about it, the notion that "insulin resistance is just for the friends of Ronald McDonald" and the "health conscious" part of the population was immune to it, makes a particularly good starter not only because the number of "skinny fat" people with insulin resistance appears to be ever increasing, but also due to the fact that it implies that insulin resistance is unhealthy... now, I got you hooked, ha?

Insulin resistance nothing for healthy athletes like you!?

Now let's take you as an example: Let's imagine you are a 39y old man who realized a few years ago that his gut became bigger and bigger - not obese, yet but not as aesthetic as you wanted it to be. In view of the fact that the SuppVersity was not around in those days you fell for the mainstream idea that jogging would probably be the best way to get back and shape and began to work on your conditioning. Somehow you got hooked (I always say that you need to find something that you enjoy doing!) and decided that you want to run your first marathon, this year. You have been running >40km per week consistently and feel well prepared, today, the day of your run. And in fact, you made it post the finish line! The next day you go to your Dr to get a check up (this is obviously idiotic, but it is part of the story ;-) and the Dr says: "I am sorry Mr SuppVersitReader, but we will have to put you on metformin, you are pre-diabetic."

Figure 1: Glucose disposal (µmol/kg/min) and lipid oxidation (mg/kg/h) during euglycemic clamp before and after "your" marathon (data based on Tuominen. 1996)

What happened? Too many Gatorades and energy gels? Well, I cannot totally exclude this possibility, but assuming that you are following the posts here at the SuppVersity closely (and actually putting into practice what you learn), I doubt that this will be the culprit. Bad genetics? Could be part of it, but if it... but, actually you could as well say "good genetics", after all your temporary insulin resistance was what kept you and the 19 male runners in a 1996 study by Juha A. Tuominen et al. (Tuominen. 1996) from passing out during and after your 42-km run - or as the "low carbers" probably would say, you turned into a fat burning machine!

Now, the whole story is obviously somewhat far-fetched and the -12% dumb in glucose disposal in the euglycemic clamp condition, during which glucose and insulin are infused and the uptake of the former in response to the latter is measured (cf. figure 1) would not qualify as pre-diabetes, but if it helped me to drive home the main message of this blogpost, i.e. that your cells do not refuse to respond to insulin without good reason, it did serve its purpose.

Temporary, exercise-induced insulin resistance paves the way for "fat-burning machines"

Although it appears logical that your body tries to maintain blood glucose levels, this phenomenon, which by the way came to be known as the Marathon Paradox, does yet appear to violate the physiological principles we discussed in some of the previous installments of the Intermittent Thoughts (cf. "The mTOR/AMPK Seesaw"). After all, the exercise induced depletion in muscle glycogen should increase the expression of AMPK (which responds to the increase in "used ATP" = ADP) and thusly improve not reduce glucose uptake. In the presence of >3x elevated free fatty acid levels (at the end of the marathon those were even >7x over baseline!) the effective mitochondrial powerplants within the oxidative muscle fibers of an endurance athletes will yet gear up so that they produce enough energy to fuel the acute energy demands. Therefore the total glucose disposal is reduced not so much because the amount of glucose that would be sucked into the glycogen stores of the muscle was reduced, but simply because less of it is burned as fuel - in the study at hand, the decreased whole body glucose disposal is mostly a result of the -43% reduced rate of glucose oxidation at almost identical rates of non-oxidative glucose disposal.

Image 2: While it may help, temporary insulin resistance alone is not enough to run a marathon. It must be complemented by an adequate ability to burn fat for fuel if you want to make it to the finish line.

This observation does yet give rise to the question, why doing hours of steady state cardio is not getting you ripped within days, I mean, it turns you into a "fat burning machine", right? In essence this may be correct, but even the best endurance athlete is not running 24h/d 365d per week and without the exercise-induced increase in mitochondrial demand for free fatty acids, the latter will have to be restored to those adipose tissues from which they were initially liberated in response to the catecholamine and cortisol spike during the marathon.Within the following days, the "fat burning machine" will magically return to its normal highly insulin sensitive metabolically balanced self without having noticed that he/she was temporarily "pre-diabetic".

Gradually increasing diet-induced insulin resistance is the slippery slope to type II diabetes

Unfortunately, the vast majority of the population has found another, more convenient way to decrease glucose disposal and increased blood lipid (specifically triglycerides) levels than exercise: Food! The revelation that even this unquestionably detrimental form of insulin resistance originates from a by all means well-meant physical response of your body will unfortunately have to be postponed to the next installment of the Intermittent Thoughts. After all the Sunday work of the past weeks, I figured I deserved less screen time this weekend ...

In the meantime, I hope that those of you who live in the north-eastern part of Europe have made good use of the fat storing effects of insulin and have equipped themselves with a nice padding of insulating adipose tissue that is keeping you warm even when the temperature falls below -30°C ;-)

Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism

Image 1: You better make sure you don't miss out on these delicious heart- and brain-healthy cholesterol bombs.

Most of you will probably be familiar with the good old saying "An apple a day, keeps the doctor away!", right? And if you are an otherwise healthy individual the micronutrients from the apple will probably really help you maintain this status. But what if the doctor was already there to put you on the healthy low fat diet, the negative health consequences of which I have addressed in yesterday's blogpost? In that case, whole eggs probably provide a more promising escape route from that low-fat, high-carb trap - at least this is what the the results of a soon to be published study from the Huazhong Agricultural University in Wuhan, China would suggest (Yang. 2012).

Surprising(?) -9% belly-fat reduction on whole egg diet

In their 60 to 90 day experiment, the Chinese researchers put a group of 8-week old Sprague-Dawley rats (n=18 for each group) on dietary regimen which differed in either cholesterol content (control vs. experimental groups) or the source of dietary cholesterol, i.e. 17.5% lard + synthetic cholesterol, 31.25% freeze dried egg yolk or 55.56% whole egg powder.

Figure 1: Composition of the control and the three experimental diets (adapted from Yang. 2012)

If you take a closer look at the exact composition of the diets in figure 1 the you will probably notice that macronutrient-wise the three standard-chow + lard/yolk/whole egg "high cholesterol" diets are miles-apart from what the average "low carber" would consider a healthy high fat diet. Still, the idea of choosing whole eggs as a major constituent (>55%) of one's diet should ring a bell for everyone who is familiar with the practical realization of the so-called "induction phase" of the purportedly (from the perspective of the same people who recommend the purportedly "heart-healthy low-fat diet") artery-clogging Atkins diet.

Figure 2: Body weight gain, food intake, food efficiency (food intake / weight gain) and relative visceral fat weight (per body weight) in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)

Interestingly, the data in figure 2 shows that even this version of "Atkins gone wrong", with a 40% carbohydrate content in the whole egg group (cf. figure 1) lead to significant reductions in weight gain and food efficiency (weight gain per gram of chow) and, more importantly, produced statistically significant reductions in the visceral fat / total body weight ratio at the end of the 90day study period (at 60 days there were no statistical significant inter-group differences).

55.56% whole egg diet kickstarts healthy cholesterol metabolism

In view of the fact that it has never been the notion that eggs would make you fat, but rather their purported negative effect on cholesterol levels due to which eggs, in general, and yolks, in particular, have gotten a bad rep over the last years, I guess that the visceral fat argument, alone, won't suffice to convince the egg-white consumer that they are missing out on the best part of the egg. After all, it was and unfortunately still is their purported negative effect on cholesterol that is literally at the heart of the egg(yolk)-scare.

Figure 3: Triglyceride, total, low density (LDL) and high desnity (HDL) cholesterol in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)

If you do yet take a look at the actual effects the natural cholesterol from the egg-containing diets had on the blood lipids of the rodents (cf figure 3), you will notice that those were statistically non-existent. In other words, only the lard + synthetic cholesterol diet had a statistically significant negative impact on the plasma lipids of the rats.

Figure 4: mRNA expression of hydroxymethylglutaryl CoA reductase (HMG-CoA R), LDL receptor (LDL-r), cholesterol 7a -hydroxylase (CYP71A), acyl-CoA:cholesterol acyltransferase (ACAT) lecithin cholesterol acyltransferase (LCAT) expressed relative to control (data adapted from Yang. 2012)

The 375x higher dietary cholesterol intake in the egg-groups, on the other hand, did not only shut down the endogenous cholesterol synthesis, as evidenced by the reduction in hydroxymethylglutaryl CoA reductase expression (HMG-CoA R, cf. figure 4) and increase its metabolization into bile acid via cholesterol 7a -hydroxylase (CYP71A), it also increased the LDL receptor expression in the liver (lack of LDL-r expression in the brain is associated with increased plaque formation in Alzheimer's, cf. Katsouri. 2011), lowered the formation and storage of cholesterol esterified cholesterol in the tissue by reducing acyl-CoA:cholesterol acyltransferase (ACAT) and increased the maturation of HDL and peripheral tissue cholesterol efflux via increased lecithin cholesterol acyltransferase (LCAT) expression.

In case you doubt that this rodent data has any significance for human beings, I just want to remind you that a 2008 study by Mayurasakorn et al., which found that "[i]n the majority of healthy adults" the addition of one egg per day to a "normal fat diet" lead to increases in HDL-c and decreases of the total cholesterol to HDL ratio (Mayurasakorn. 2008). Their conclusion that "egg consumption might benefit blood cholesterol" was however similarly ignored as the absence of scientific data to support the "eggs = increased risk of heart disease"-myth.

It is thusly not surprising that the Chinese scientists conclude that contrary to the "conventional approach to weight reduction", of which the scientists state that it is "a high-carbohydrate, low-fat, energy-deficient diet" that "has not proven to be very effective for many obese and over-weight individuals [I am not making that up, it is the exact wording from the study ;-]", an "egg diet", which "theoretically [...] would be more likely to cause obesity", could not only help those individuals finally shed unhealthy visceral fat, it could also lead to significant improvements in their lipid metabolism. If it were not for the statement that

[...] the mechanisms by which an egg diet lowers plasma cholesterol need to be further characterized and the special functional factors in egg need to be identified

one could be led to believe that Yang et al. had finally grasped the notion that just eating the right (whole) foods could solve the problem... the term "functional factors" does yet tell me that they are probably just trying to developing an "egg in a pill" that will soon be patented and sold as an adjunct to the standard statin therapy,

SAD - Human Study Shows: Three Days on "High Fat" Standard American Diet Produce Heart Healthier LDL Particle Profile Than NCEP-Approved Low Fat Diet

Image 1: SAD or just mad? It does in fact look like you better stick to Royal TS, French fries & co instead of following a low fat diet according to the guidelines of the National Cholesterol Education Program if you care about your heart health.

In view of the fact that millions of lives depend on it (literally, not just figuratively!) it is actually quite surprising, some would probably say "scandalous" that the experimental evidence (and I am talking about controlled experiments on real, healthy human beings, not about epidemiological and thusly statistical) for the purported beneficial effects of a non-calorically restricted "healthy low fat diet" in the absence of additional exercise interventions is... scarce, to say the least. I was thusly positively surprised, when I hit on a study from a group of researchers from the Institute of Nutraceuticals and Functional Foods at the Laval University and the Lipid Research Center at the CHUL Research Center in Québec, Canada, the title of which suggested that it could provide exactly that - experimental evidence in support of the purportedly healthy low fat diet (Guay. 2012).

Scientists and their interpretation of a "high fat" diet...

I guess, those of you for whom this is not the first visit to the SuppVersity will be aware that I have made a habit of looking at the data first, to make up my mind, before I even take a closer look at the scientists interpretation of the latter (this is what is usually called the "conclusion"). And, geez! The "high-fat diet", the Valérie Guay and her colleagues advertise in the title of their paper turned out to be another case of the standard American diet, the relative fat content of which (32% of total calories) is not exactly, what's on my mind, when I think of a "high fat" diet.

Figure 1: Relative macronutrient composition of the baseline and the isocaloric test (high and low fat) diets (left); total fiber, cholesterol and phytosterol content, as well as polyunsaturated to saturated fatty acid (PUFA/SFA) ratio and total fat in % of total calories (right; data calculated based on Guay. 2012)

The fact that this paper still made into the news, although the researchers' interpretation of a "high fat" diet was designed to "reflected as closely as possible current North American men averages", does yet already tell you that the results were not that the "healthy low fat diet bet the crap out of the standard American one".

SAD! Standard American Diet beats the nasty small LDL particles out of a healthy low fat diet

In fact, a closer look at the somewhat cryptically presented study results revealed that, at least as far as the measured outcome variables of this particular study are concerned, the exact opposite was the case: It was not the purportedly healthy low-fat diet which was designed according to the recommendations of the National Cholesterol Education Program Adult Treatment Panel III (cf. JAMA. 2001) which induced favorable changes in the lipid profile of the twelve initially healthy normal-weight male volunteers (~27.1y; BMI 25.2kg/m²) who took part in this 3-day randomized, double-blind, crossover study, but the calorie-, fiber- and vegetable- and animal-protein-wise identical "high fat" diet, which had been designed in the image of the infamous "standard American diet" (SAD).

Figure 2: Lipid profile (left) and its relative changes (compared to baseline, right) in response to the 3-day dietary intervention (data calculated based on Guay. 2012)

If you look at the data in figure 2 through Pfizer-ish-blue glasses you will probably say: "Wait a minute! The cholesterol level did decrease in the low fat group! So this must be the better diet." And yes, this may actually be the case, if you define better according to the same fundamentally "cholesterol is bad for you"-paradigm which has been flushing billions of dollars (and of course Euros ;-) into the coffers of Pfizer & Co over the last decades. If you have yet been following the by no means "latest" scientific research on the correlation of cholesterol and heart disease, you will be aware that neither total cholesterol, nor total LDL levels, but rather the amount of highly oxidizable small LDL particles is a relatively reliable marker of the risk of heart disease (Lamarche. 1997)- and, fortunately, Guay et al. are aware of that, as well, and measured the characteristics of LDL particles by the means of electrophoresis.

Figure 3: Relative distribution of LDL particle sizes (left), cholesterol content (mmol/L) of LDL fractions (middle), and mean LDL particle size and LDL peak particle diameter (LDL-PPD; right); * indicates p < 0.05; ** indicates p < 0.001 (data adapted from Guay. 2012)

The results of the LDL-particle analysis shown in figure 3, show quite neatly, that the unquestionably unhealthy standard American diet (Attention: Do not misinterpret these study results as a carte blanche to stick to eating your regular crappy diet!) did not only result in more favorable triglyceride (1.48 vs 1.01mmol/L, p = 0.0003) and HDL levels (1.29 vs 1.41 mg/L, p = 0.05; cf. figure 2), than its allegedly "healthy" low fat counterpart, it was ...

[...] also associated with a significant increase in LDL particle size (255.0 vs 255.9Å; p = 0.01) and a significant decrease in the proportion of small LDL particle (<255.0 Å) (50.7% vs 44.6%, p = 0.01).

And although Guay et al. are quick to point out that "because the present study was only conducted in men, the results cannot be generalized to the whole population", I would say that these results should at least.make you reconsider if following a "healthy low fat diet" in accordance with the dietary guidelines of the National Cholesterol Education Program will help you lower your risk of heart disease... unless, of course, you have already popped so much Lipitor & co that the chronic lack of cholesterol is already hampering your cognitive abilities -.what? Ah, yes... of course, the favorable results occur only if you take you daily dose of statins with your low fat meals... right, how could I forget that ;-)

Adelfo Cerame - Road to Wheelchair Nationals '12: Reviving an Ancient Training Technique - Intensified Reverse Pyramid Training For "Disgusting" Graininess and Vascularity!

Image 1: "The Rock", Dwayne Johnson, certainly looked less "disgusting" as the Scorption King in The Mummy Returns ;-)

If I had not seen his latest pics, which were taken after my friend Adelfo went on his new torture ... ah, pardon... I mean, training regimen, I would certainly voice more concerns about the latest increase in training volume by which he intends to bring his physique to yet another "next level", or as he would probably put it: "To make my muscle look even more disgusting"... I guess, in this regard, it is actually a very smart move to borrow some "torture techniques" from the past. I mean, the mummies from the pyramids are unquestionably "disgusting", right? But before I delve deeper into the history of ancient Egypt, I better hand over to Adelfo and let him tell you what kind of pyramid he had on mind, when he planned his latest routine...

7 weeks out and getting closer: Separation, veins and grainy muscle

I am now 7 weeks out and I have been very pleased with my progress. Day by day, I'm seeing more and more separation in my muscles and in certain parts of my muscle, the fibers begin to show through the the skin. In view of the current low carb craze and the notion that even the slightest amount of sugar will make you hold tons of water it is quite ironic that it was the re-incorporation of carbs into my post workout meals, which made my muscles not only look fuller, but also much harder. And while I cannot tell whether this is simply a result of the increase in muscle glycogen, the measuring tape tells me that my arms have grown! Last I checked they were 17 ¼ and when I measured today, they are now 17 ½ …  whatever the reason may be, it certainly feels and looks neat ;-)

Here are some current progress pictures, and will probably be the last that I post in a while until I get closer to show time. I feel I can still make some significant changes in my physique, and I want you, my dear readers to be able to see the difference from now and 7 weeks later…

Image 2: 7 weeks out - my arms are now at 17 ½ inches from 17 ¼ and my waist is down to a 28" from a 29". My BF% reads 4-5 % on my digital calipers but I’m pretty sure it’s a bit off so I’d like to say 6% or 7%... maybe 8%? Just to be on the safe side. Don’t know my weight either; last I checked during the holidays, it was 141 lbs.

As I already pointed out in several of my previous blogposts, here at the SuppVersity, I am a firm believer in constant progress. There is always room for improvements, and here are those I know I can and am determined to make in the seven weeks to the show:

• Although I am starting to notice that my lower back is coming up the way I want it (you may remember the issue if you listened to Dr. Andro's and my interview with Carl Lanore, last week). Still it seems like a long shot, but I’m making it a priority to do weighted chin-ups 2x a week to try and really stimulate my lower lower lats and maybe even the lower trunk muscles in the back... well, at least that part of those muscles, that actually still respond to the signals my brain is sending. It's somewhat awkward not to know if the whole problem is a result of the spinal cord injury or just me not paying enough attention to a muscle, I rarely use, as I simply cannot do those exercises which are the most demanding for the stabilizing muscles of the lower back.
   
• Despite the fact that my muscle separation has improved significantly over the last couple of days, I am positive that I can still improve it - particularly in the area where my biceps, triceps and side deltoids meet and tie together.
   
• The same is true for my abdominals. They look neat, already. The separations are showing, but still... I have even begun to include regular ab exercises in my regimen, this week. I know that I have mentioned before that you don't actually have to train your abs to get a six pack, and that diet alone will bring your abs out and shine in their full glory. For someone who cannot to squats or deadlifts, however, a few crunches could in fact make a difference. And since I don't want to leave anything to chance, I rather spent the additional five minutes on ab work then later see an "L" instead of a "Win" in the column on the score boards.
   
• At the same time, I am still trying to perfect that "super" vascular, grainy and disgusting look *lol* I got 7 weeks to make that happen and certainly will spare no effort.
   

I guess, it goes without saying that I am not going to achieve all that without some changes and those of you who have read last weeks installment, will be aware that I already felt that my body was getting use to the EDT and 5x5 regimen that I have been doing for the past couple months now. The intensity of the workouts just didn’t feel like earlier in my prep. And while I was not sure if my body just needed any type of change, or whether it actually needed to be pushed harder, the signals were pretty clear: There was something to be done to (re-)intensify my workouts, if I wanted progress, not stagnation - let alone regress.

A brief note for those who have not followed the whole series: For the past months my training regimen consisted of escalating density (EDT) and 5x5 training - low reps, heavy weights. Aside from what my diet obviously did, I feel that the low(-er) reps and heavy(-ier) loads have helped me a lot to increase my strength and gains, while still being able to cut significant amounts of body fat, something, which is obviously not common, when you are on a non-negligible caloric deficit.

So, I thought to myself… "How can I increase the volume in my training, yet still maintain lifting a heavy load as I did with EDT and 5x5 training?" From my experience with high volume training, you often think that you lift as hard as you can, but with the high amount of reps and sets on your mind, you are always leaving some gas in the tank, so to say, and end up settling for moderate weights and ever-increasing amounts of half-heartedly executed reps.

Reverse pyramid training - a routine about as ancient as the Pyramids on the Giza Plateau

I was not looking for a concrete routine, as you know that I like to build those around the moves that work best for me, but rather for a "training style", something like EDT, or 5x5, a "training paradigm", if you will, that would allow me to train at a higher volume, but still at maximal intensity. The thing that eventually caught my eye is something many of you will probably call an old hat: reverse pyramid training (RPT).

Image 3: In case you think there is something wrong with this picture, you probably have not heard of the famous "reverse pyramid",  right?

If you are familiar with pyramid training, (which, I assume, the average SuppVersity will be ;-), you already now what RPT is: It is basically just the opposite of the classical pyramid. Instead of beginning with your lightest weight, to then gradually increase the load, you start with the heaviest weight you can handle for 4-6 reps, then just pyramid down by dropping the load while increasing the reps, while continuously pushing yourself to list as heavy and do as many reps as you can... pretty straight forward, right? What attracted me to this regimen is that I can start out lifting really heavy. Compared to starting with a lighter weight, this allows for an overall greater workload (as in amount of weight x reps) and that was what I was looking for, eventually.

Making a routine "my routine": More sets, more reps more exercises

At least those of you who are not new to this series will yet know that whenever I "apply" a new method, be it diet or, as in this case, training-wise, I make a few tweaks and adjustments according to my contemporary goals. Therefore, you may be surprised to hear that the only real "adjustment" I made, is to add in even more sets and reps... and I know what you are thinking now: "Still more? Adelfo is going crazy! That's too many exercises, the sessions will be too long and at best this is going to be un- at worst counter-productive." In that, you are probably making some good points, but like I said: This is what I feel will work for me at this point in time... and if I am wrong? Then I will keep tweaking until it works ;-)

Tables 1-2: My new RPT routine; due to the fact that I do the Gironda dips unweighed, I don't use the pyramid in this particular exercise.

As you can see in table 1-2, each workout consists of 7 exercises total and 6 sets for each exercise, with a rep scheme starting from 4 reps, 6 reps, 8 reps and so on... increasing the reps while gradually decreasing load. For my first two sets of 4 reps, and 6 reps, I lift as heavy as possible - just as I would during an EDT or 5x5 session. And being able to do just that, is what makes the beauty of this routine. On the flat bench, for example, I start my first set with 275 lbs, then gradually drop the load by 5 lbs, each set, so that by the time I hit my 6th set, I am lifting 225 lbs for 14 reps. I try to drop the load by as little as possible (in this case 5lbs steps) from set to set, to ensure that the intensity does not drop and I still lift as heavy as I can.

My body was done after Monday and Tuesday’s workout! I haven’t felt that sore in a while.

Image 3: Adelfo during his firefighting days before the accident. While he was not exactly athletic, he never had weight issues with all the physical labor. If you want to know more, read up on Adelfo's SuppVersity Student Spotlight

In case you decide to try that out, yourself, you will notice that as you go through your sets, reps and exercises, the volume and the load begin to wear you down and muscular fatigue sets in, so that it is becoming increasingly harder to stick to just dropping 5 lbs if you want to really feel the muscle on your next set and not just to partial reps to get the work done. Mid-way through the workouts it is thusly advisable to start dropping the weight faster - like 10-15 pounds or more per set. Eventually you get to a point in the latter part of your workout where even the lightest load becomes unbearably heavy… I guess, you know this feeling you get when your mind tells you that you’ve lifted this weight time and time again with no problem, but your muscles just wont budge?! This is the price you have to pay, if you, just like me, want to increase pace and volume, without having to sacrifice the intensity of your workouts...

Even when I started out doing EDT training, I wasn’t that sore. The last time my body felt this... I guess, "painfully good" is the right way to describe it, was when I came home from work after a day of hiking mountains, digging fire lines, and fighting forest fires. So, in case you are someone with a masochistic vein, I suggest you grab your gymback and give my routine a try... ah, and if you can, let me know how you feel when you are done. A pros pos, I am done for this week, at least as far as my weekly blogpost is concerned. Until next Thursday, then - same time, same place!

Cardio Before or After Weights? While Both are Suboptimal. Greater Reduction in Leptin With Cardio Before Strength Training Would Yet Suggest "Weights First!"

Image 1: Spinning before or after weights? While none will be "optimal" the leptin and cortisol responses in the study at hand would suggest that lifting weights first, will produce more favorable results - especially with respect to improvements in body composition.

"Cardio before or after strength training?" This was and still is one of the most debated questions among both amateur and professional trainees who want to combine the muscle building effects of weight lifting and the fat burning effects of classic cardio (LISS) or high intensity interval training (HIIT). And although it may be debatable, whether or not this practice is advisable, or generally inferior to doing "cardio" and "weights" on seperate days, it does stand to reason that for most non-professional athletes and those, who cannot make of living off their passion, daily, let alone morning + evening sessions, are simply not feasible. And while the difference between the two regimen may not be as earth-shattering as the proponents of either position would have it, the results of a recently published study from the Laboratory of Human Kinetics at the University of Rio de Janeiro would suggest that, at least as far as the leptin and cortisol responses are concerned, the option to do "cardio after weights" could be slightly advantageous (Rosa. 2012).

Before or after - more than a question of personal preferences?

The subjects of the respective study were 10 randomly selected male volunteers (27.1 ± 4.8  years,  74.89 ± 0.30 kg;  172 ± 0.03 cm; BMI 25.38 ± 0.09)who had engaged in regular physical activity 3 times per week for at least 6 months and thusly represent the "average aspiring gymrat", who often wants a Mr. Olympia or Men's Health cover model physique, but whose schedule allows for no more than max. three training sessions per week.

Figure 1: Graphical illustration of the experimental protocol; the OMNI values refer to the OMNI scale on which the subjects rate the intensity of the exercise from 0:"extremely easy" to 10:"extremely hard".

On three separate occasions, with 5-day rest periods in-between, the subjects had to report to the lab in the morning, fasted. After a standardized breakfast, consisting of 200 ml fat-free yogurt, 2 slices of light whole-wheat bread, 30 g of fresh cheese, 10 g of margarine and one medium-sized banana, the subjects either sat around idly for 2h at the lab (control session) or performed one of two cardio + strength training regimen which differed only in the order in which the indoor cycling (cardio component) and the weight lifting (strength component) were performed (see figure 1 for more details on the exercise intervention). Before and after the combined strength + endurance (or vice-versa) programs and in the control trial blood samples were collected at ~6:45am (pre) and ~8:45am (post). Other than 500ml of plain water, no fluids or solid foods were allowed during this ~2h period.

Figure 2: Absolute leptin and cortisol levels in control (no exercise), endurance first or strength first sessions before and after the 2h rest / workouts (left); relative changes from pre to post during each of the three sessions (right; data adapted and calculated based on Rosa. 2012)

As the data in figure 2 goes to show, the overall effect of the training regimen on the plasma leptin and cortisol levels of the subjects was identical. Regardless of whether the subjects cycled first and weight lifted afterwards, or vice versa, both leptin and cortisol levels declined significantly (p < 0.05) compared to the non-exercised control (which shows only minor natural fluctuations).

The smaller reduction in circulating leptin levels speaks in favor of lifting weights first

If we take a closer look at the relative changes from pre to post within the individual groups (figure 2, right), it does yet become obvious that the "strength first" session produced an overall more favorable hormonal response than its "endurance first" counterpart. After all, the human body interprets a reduction in leptin (at least in the absence of a profound upregulation of leptin sensitivity) as "starvation signal" to which it will respond with adequate reductions in overall calorie expenditure and fatty acid oxidation.

A brief note on cortisol: Whether the concomitantly more pronounced reduction in cortisol is a good, or in view of the increasing number of people with chronically low cortisol levels and "adrenal burnout" or "central fatigue syndrome", is something everybody would probably have to answer for him-/herself as an individual. In view of the fact that both regimen lead to a significant reduction  (-26% and -34%), the results of the study at hand would yet underline my general recommendation to refrain from any type of exhaustive exercise when you notice that your adrenal glands cannot cope with whatever stressors they have been exposed to any longer. After all, chronically low cortisol levels impede weight loss and performance just as profoundly as the dreaded opposite extreme - an established fact which is unfortunately commonly overlooked in the cortisol-phobic fitness community.

In this context, it is also worth mentioning that according to a 2003 meta-analysis by Hulver et al. (Hulver. 2003) all the studies investigating "long" (>1h) duration exercise bouts

[...] convincingly [...] indicate that serum leptin concentrations are reduced with exercise durations ranging from one to multiple hours [, probably] due to alterations in nutrient availability or nutrient flux at the level of the adipocytes.

This, in turn, would support the earlier voiced objection that doing weight and cardio on separate days would be the optimal, yet for many trainees simply impracticable option. So, in case you are part of this group of trainees, it appears prudent to schedule your "cardio" sessions right after your strength workouts. And if you also replace the arduous light-to-medium intensity steady state exercise by a very brief (!) high intensity interval session (HIIT; 4-6 intervals, 10-15min max), you can well be in and out of the gym in <1h and could thusly get away without any significant reductions in leptin.