Adelfo Cerame RtWC12: Shoulder Your Weaker Body Parts! Bring Up Those Lagging Delts - Exercises, Splits, Routines

Image 1: After his 2nd place at the Nationals, Adelfo wanted to bring up his rear delts and although the lighting does not really do him justice, he made use of the weeks between the Nationals (right) and the USA (left) and filled up considerably.

It is more than 3 months ago that Adelfo and I have been talking about ways to bring up his somewhat lagging delts (if you could even say that there is something "lagging" about Adelfo's physique), yet still, it seems as if it had been yesterday that I told him that he would not have to wonder that those delts were not growing, when he was working them almost exclusively with compound movements for stronger body parts, which wouldn't allow the side and, more importantly, the rear delts to reach that highly productive, growth triggering point of just too much load to handle, but still not so much load that adaptation could not make up for it. And judged by his latest progress pics, Adelfo did not just take that comment to the heart, but was also able to make the appropriate changes to his routine. Good for you that he is no magician who would never betray any of his illusionist tricks, but gives away practical advice every week ;-)

Boulder shoulder tweaks

After my Florida show, I felt that my shoulders (front, side & rear) were an area in my physique that could use some improvement. It was not a clearcut weakness of mine, but when the initial disappointment subsided and I took another look at the comparison shots, I felt that Adel (aka Dr. Andro) had been right, when he said "If anything, you lost on one maybe two of the backshots, where Neil looked somewhat more massive - his rear-delts in particular." And yeah, he had been right, those rear delts did not really keep up with the rest of my back development, which - as you may probably remember - had been one of my priorities (aside from coming in as shredded as possible) during the prep for my first competition of the year. I knew I would not make the same mistake twice, and decided to level out those imbalances in the weeks to come.

Image 2:  The left hand side is a current image of me 4 weeks out from the USA’s, and the right hand image was me 4 days out from Nationals.

And allegedly, the results, now 14 weeks later, may not be earth-shattering, but the changes are unquestionably visible and that despite the fact that the "mini-bulk" I had originally planned for in-between the shows turned out to be more of an ameliorated diet ;-)

Make changes to see changes

While I guess that it should actually not be necessary for me to point out that continuing along a way that has lead you astray is a pretty stupid undertaking, I still see people do just that day by day - and not just in the gym, but also in their private and professional lives! Often ridden by the fear to make a change for the worse they'd rather continue along a known path that won't produce the desired results than to try something new that would at least hold the chance of improvement.

My old path consisted of training my shoulders once a week, following my basic training principle to use heavy compounds wherever possible and simply rely on the fact that those would provide an intense enough stimulus to both, the primary, as well as the auxiliary muscles that are involved in the respective exercises.

According to the aforementioned primacy not to follow a path which has lead you astray before another time, I increased the training frequency a bit and made a  couple of additional adjustments with respect to the exercise selection (see table on the right) and the grouping of the bodyparts, with auxiliary shoulder work on chest day.

Barbell jammers, bent over reverse cable fly’s and lat pulls behind the neck are 3 exercises that I have added into my training. Out of the three, I really enjoyed were those jammers - I felt they really targeted all areas of my delts, plus they are less stressing on the shoulders joints, because you're pushing in a forward/upward motion rather than right over the head. What was particularly surprising, though was how effective those three rear delt exercises actually were - I have never really paid much attention to it, let alone trained them in in isolation, but the way they felt during and after each workout told me that it may have been a mistake not to do DB rows (which are certainly more difficult for me to do than for an able person), lat pulls behind the neck and bent over reverse cable flys, before.

Training shoulders twice in a bi-weekly hybrid routine cycle

Image 3: Planned changes deliver results

Consequently, all three (DB rows, lat pulls behind the neck and bent over reverse cable fly’s) have turned into staples of my routine - irrespective of whether I am training at a higher or lower training volume on my new bi-weekly alternating hybrid routine

• EDT/5x5 = 2 week phase
• Overkill/5x5 = 2 week phase
• Hypertrophy/5x5 = 2 week phase

While cycling through these basic templates, I incorporated the aforementioned additional shoulder work into my existing split on "chest-" and "back-days" which allowed me to train my shoulders - just as my chest and back - twice a week.

The following example routine (which is not intended to be copied without adaptations) goes to show you how you can reconcile all that in one routine, where you would split your shoulder workout up into front and side delts on "chest-" and rear delts on "back days" (click to enlarge):

Workout routine: No blueprint, just an example - Overkill (left), 5x5 (middle), EDT (right) hybrid

As I said before, both the volume and the intensity of these workouts are pretty insane and I am not suggesting that any beginner should simply copy this workout. The idea, however, to incorporate front and side delts on your "chest-" and the rear delts on your "back-day" is yet something that will have merit regardless of your training status or overall conditioning. So pick your favorite exercises from table one, align them into a routine with a total volume and intensity that suits your need, eat well, train heavy and get enough rest and you will see your shoulders will grow ;-)

Strength Training Ain't For Women, One Set is Not Enough and Without a 100% Dialed in Diet Lifting Weights is Useless, Anyways - Really!?

Image 1: Minimalist strength training for maximal results? In the long run even a one set strength circuit can elicit astonishing changes, if you train consistently, progressively, heavy and with picture perfect form (image Paramount Fitness).

Unconventional wisdom days at the SuppVersity: After yesterdays "news" (I hope it was not real news for the majority of you) about the superiority of high intensity interval over classic steady state cardio in at the lower end of the "fat burning zone", today's news is going to cause a couple of other set-in stone paradigms to totter:

1. resistance training ain't for women
2. low volume resistance training won't help you lose body fat
3. resistance training requires a high protein diet to work

The respective data comes from a recently published study by R. Washburn and his colleagues from the Center for Physical Activity and Weight Management at the University of Kansas and researchers from the Southern Illinois University and the Birgham Young University (Washburn. 2013).

Minimal effort, maximal adherence, ...

In their 6-month intervention trial, Washburn and his colleagues set out to evaluate the effect of a minimalist resistance training routine consisting of no more than a single set of 9 different exercises that had to performed three times per week. The sessions were supervised and the participants, overweight young men and women in their early twenties (BMI 27.2kg/m²; age 20.7y; BF% by DEXA 27.6% men, 38.9% women) performed all their exercises on standard gym equipment (Paramount Fitness, not a sponsor of the study!); an adherence of >90% was required and the supervisors made sure that all exercises were performed in the prescribed 3-6RM (85% of 1RM) with a cadence of 2s for the concentric and 4s for the eccentric period of each exercise with picture perfect form:

Tip for advanced beginners You are already training for 4-6 months? Why don't you add in a 2nd circle, 1s concentric, 2-3s eccentric, in the 8-12 rep range. I don't need a scientific study to confirm that this will be able to propel your gains. And with a couple of tweaks to your diet, e.g. 20g of quality protein with every meal and a reduced carbohydrate intake (~25-35% of total energy or 120-250g of carbs) from whole food sources, only, it won't take too long very long to see visible results.
• chest press,
• back extensions,
• lat pull down,
• triceps extensions,
• shoulder press, 
• leg press, 
• calf raise,
• leg curl,
• crunch

Whenever subjects were able to perform more than the required 6 repetitions with good form the resistance was increased by ~2.25kg. In other words the participants followed a stupidly simple linear progression protocol with a clear focus on strength, an ultra-low volume (per muscle group) and picture perfect form.

... results despite unaltered and obviously obesogenic eating habits

Dietary intake before and during the 6-month study period was assessed, I quote, "during one randomly selected period" each month (24hr food recalls on 2 weekdays and one day on the weekend, each) and remained at ~2300kcal. The majority of the daily energy intake came from carbohydrates (51% ~290g) and fats (33% ~95g), while the protein intake (16% ~92g) despite being at the upper level of the RDA would be considered "borderline deficient" from the perspective of most strength trainees.
Note: It stands to reason that a higher protein intake of ~120g+ could have had beneficial effects on strength gains and changes in body composition. Notwithstanding, the results of this study do confirm that not everything that has been shown to facilitate gains is actually necessary and protein intakes in the >3g/kg body weight range, despite not being as bad for your health as the medical orthodoxy would have it, will offer little to no marginal utility and may even turn against you, when you keep upping your protein intake at the expense of more readily available energy sources such as carbohydrates and fats so that the lion's share of your energy has to be derived from dietary protein via glyconeogenesis... add an energetically demanding training program on top of this, call it either adrenal fatigue or central fatigue syndrome and join the other obstinate whiners on the various overtraining, ah... I mean fitness and bodybuilding boards on the Internet.
Without any cardiovascular training, not a single change in their obviously unhealthy dietary habits (why else would these young men and women have become overweight in the first place?) the 37 formerly sedentary twens in the resistance training (RT) training arm of the study derived non-negligible benefits from their weekly workouts:

Figure 1: Changes in BMI, fat free mass (FFM) and fat mass (FM) in male and female study participants in the control and resistance training arm of the 6-months exercise-only single-set circuit training (9 exercises total, 3 training sessions per week) intervention (data based on Washburn. 2013)

I mean, as disappointing as the non-existent weight loss may seem in a society, where the majority of people is so fixated on nondescript figures on a scale, you can hardly argue that

• increasing your muscle mass by +1.5kg,
• decreasing your fat mass (women), or at least 
• ameliorating your fat gains (men) 

would not be better than losing muscle and becoming fatter and fatter as it happened to the subjects in the control arm, right? And that the anti-obesity (as defined by too much body fat, not too much body weight) effects were more pronounced in the 15 women than in their male peers goes to show you that exactly those people (=women ;-) who usually don't lift weights will benefit most from hopping of their steppers, treadmills and recumbent bikes three times a week to do nothing but a single full-body strength circuit.

Training is a nutrient repartitioner, but if the diet does not deliver those the results are suboptimal

These unquestionably favorable (compared to the sedentary control), yet hardly earth shattering results would certainly have been way more impressive, if the study participants had made appropriate changes to their diets. For most of them, it would probably have been enough to simply switch from fast-, fried- away-from-home- and ready-made foods to self-prepared meals, to double, if not triple their results (cf. Taveras. 2005; Wosje. 2010; see also red box below). With the aforementioned tip to get at least 20g of lean protein with every meal and a progression not just on the weight, but also on the volume side of things (yet to no more than 2-3 circles per training, cf. Van Etten, 1997; Shaibi. 2006; Shaw. 2006), the same simplistic full-body circuit would certainly have had a much greater impact on the chubby physiques of the soon-to-be obese type II diabetics.
Food quality? It is quite interesting that both Taveras and Wosje identify fried foods as especially problematic for children and adolescents (Taveras. 2005; Wosje. 2010). And while those were related to higher body fat levels, another common scapegoat, processed meat, showed a clearcut and unquestionably beneficial relation to high bone mass in the Wosje study (Wosje. 2010). On the other hand, dark-green and deep-yellow vegetables (eg, spinach, romaine lettuce, broccoli, carrots, and sweet potatoes), though not something you will usually see among the favorite dishes of most kids, adolescents and college students, would probably have prevented the twens in the Washburn study from being eligible to participate in the trial, in the first place. Why? Well, the BMI and, more importantly, the body fat levels of the veggie (+meat ;-) eaters would probably have been way below the obesity cut-off for the Washburn study.
If there was a single take home message from this study, one that probably won't apply to you, a seasoned physical culturist and avid trainee, though, but maybe for your sedentary niece or nephew, it would unquestionably be that physical culture does not start at the Olympia level and that doing something is better than surrendering to your "bad genes", the greatest influence of which oftentimes is inherited laziness and the stubborn adherence to a lifestyle of which even young adults should know that it will get them right into the clutches of the pharmocracy.

References:

1. Shaibi GQ, Cruz ML, Ball GD, Weigensberg MJ, Salem GJ, Crespo NC, Goran MI. Effects of resistance training on insulin sensitivity in overweight Latino adolescent males. Med Sci Sports Exerc. 2006 Jul;38(7):1208-15. 
2. Shaw I, Shaw BS. Consequence of resistance training on body composition and coronary artery disease risk. Cardiovasc J S Afr. 2006 May-Jun;17(3):111-6. 
3. Taveras EM, Berkey CS, Rifas-Shiman SL, Ludwig DS, Rockett HR, Field AE, Colditz GA, Gillman MW. Association of consumption of fried food away from home with body mass index and diet quality in older children and adolescents. Pediatrics. 2005 Oct;116(4):e518-24. 
4. Van Etten LM, Westerterp KR, Verstappen FT, Boon BJ, Saris WH. Effect of an 18-wk weight-training program on energy expenditure and physical activity. J Appl Physiol. 1997 Jan;82(1):298-304.  
5. Washburn RA, Kirk EP, Smith BK, Honas JJ, Lecheminant JD, Bailey BW, Donnelly JE. One set resistance training: effect on body composition in overweight young adults. J Sports Med Phys Fitness. 2013 Jun;52(3):273.
6. Wosje KS, Khoury PR, Claytor RP, Copeland KA, Hornung RW, Daniels SR, Kalkwarf HJ. Dietary patterns associated with fat and bone mass in young children. Am J Clin Nutr. 2010 Aug;92(2):294-303. Epub 2010 Jun 2.

Are You Still Burning Calories or Already Losing Fat? Study Shows: 5x15 Min HIIT Reduce Body Fat & Improve Fitness Twice as Effectively as 5x40min of Classic Cardio

Image 1: The number of women striving to be strong & sexy is still too skinny.

Despite the fact that the slogan "strong is the new sexy" has become increasingly popular, as of late, my personal experience tells me that women are particular resistant to suggestions, let alone well-meant advice to drop "classic cardio" training all-together. Against that background the data from a study that has been published in the latest issue of the Journal of Sports Medicine and Physical Fitness, as convincing as it may be, is probably no more than another drop in the bucket, but hey... if there is only one women who's mental bucket is already chock-full it may be the one drop that will eventually make it spill over ;-)

"But didn't they lose more weight with classic cardio!"

What happens if you take 60 female overweight (BMI>25kg/m² and body fat >30%) university students and tell them they got to lose weight? Well, I guess, 45 will run to the next best newsdealer get their Shape, let alone Cosmopolitan and start starving themselves according to the latest diet fat from Hollywood, while the remainder will do just the same, except that they combine the starving with some "healthy" cardiovascular exercise in the mythical "fat burning zone". Now the former, i.e. the starvation diet, was not an option for any of the 60 Chinese women, as the design of the 12-week trial required them to maintain their regular diets, the latter, and even the walking or running in the "fat burning zone" was not really part of the experimental conditions the women were randomly assigned to:

• moderate intensity continuous training (MICT): 40min of jogging or walking at 50% of the individual VO2max 
• high intensity interval training (HIIT): 5x3min of running at 85%VO2max with 3min of active rest between the high intensity bouts
• sedentary control: no exercise at all

The exercise was performed on an outdoor track five times a week for a total of 12 weeks an elicited (remember: in the absence of any dietary interventions or restrictions!) pretty astonishing results in - and this must be said for the sake of fairness - both groups.

Figure 1: Changes in body composition and fitness parameters compared to baseline (Sijie. 2013)

If you take a closer look at the data in figure 1 it is yet evident that the 15min of HIIT exercise were not only less time-consuming, they also produced more pronounced and, what's even more important, more favorable changes in body composition, i.e. a greater reduction body fat percentage and waist-to-hip ratio, greater retention in lean mass (as evident from more pronounced fat loss in the presence of slightly lower reductions in BMI) and statistically significantly more pronounced improvements in cardiovascular fitness (VO2Max and ventilatory threshold) - exactly those domains, which should (but have never been) the domain of "cardiovascular" exercise ;-)

Not just for Chinese overweight women: Another recently published study by Astorino et al. confirms that the HIIT induced beneficial effects on VO2max are not restricted to otherwise sedentary, obese subjects, but will also occur in active, young men and women (age and body fat = 25.3 ± 4.5 years and 14.3 ± 6.4%). And that despite the fact that the subjects in the Astorino study performed only two sessions per week (4-6x 30s wingate tests = all out cycling followed by 5min active recovery) and the total duration of the study was no longer than three weeks (Astorino. 2013). In this context it is also worth mentioning that Ciolac et al. were able to show that young women with high familial risk for hypertension also derive greater benefits in terms of cardiovascular health improvements from aerobic interval vs. classic aerobic training (Ciolac. 2011).

Lose weight or lose fat? Look sick or look good? Burn calories or burn body fat? LISS or HIIT?

Despite all obvious limitations of this study it should thus be obvious that "cardio", regardless of whether you do it to improve your physique or overall fitness, must neither be time consuming nor should it be conducted in the "fat burning zone". Those of you who have been following the Step By Step Guide to Your Own Workout (specifically the Fat Loss Example Routine), will yet be aware that this does not imply that you must never perform "classic" low intensity steady state cardio. As a means of recreational activity on your off days, 20-30 minutes on a treadmill may actually help you recover from the "real" training sessions which will bring about those adaptation (fat loss and muscle gain) even women should be striving for if their focus is to improve the way they look and feel about their bodies.

A note on the right type of HIIT for you: If you compare the HIIT protocol in the Astorino to the HIIT protocol in the Sije study, it is pretty obvious that we are dealing with an all-out short burst approach (Astorino) vs. an high intensity longer burst approach (Sijie). In order to find the right HIIT protocol for you, you will have to reconsider your current training status and goals - with the general rule being: The fitter you are the more you should tend towards the shorter all-out bursts, because here, outside your comfort zone, is where the magic of adaptation happens. The more body fat you are still carrying, the more you should tend to longer high intensity bouts.

References:

1. Astorino TA, Allen RP, Roberson DW, Jurancich M. Effect of high-intensity interval training on cardiovascular function, VO2max, and muscular force. J Strength Cond Res. 2013 Jan;26(1):138-45
2. Ciolac EG, Bocchi EA, Greve JM, Guimarães GV. Heart rate response to exercise  and cardiorespiratory fitness of young women at high familial risk for hypertension: effects of interval vs continuous training. Eur J Cardiovasc Prev Rehabil. 2011 Dec;18(6):824-30. Epub 2011 Feb 28.
3. Sijie T, Hainai Y, Fengying Y, Jianxiong W. High intensity interval exercise training in overweight young women. J Sports Med Phys Fitness. 2013 Jun;52(3):255-62.

Fishing for Better Wheys to Improve Your Physique and Overall Health? 6g/d Cod Protein Could Help You Cut Body Fat & Build Muscle Without Having to Change Your Diet

Image 1: This can of tuna (140g) would contains exactly 7 servings of muscle building fat burning fish protein... well, sort of. At least it contains as much protein as the subjects in the Vikøren study consumed in the form of capped cod protein isolate in the 2nd half, the "high-dose" phase of the 8-week intervention (Vikøren. 2013)

Protein days at the SuppVersity! Well, sort of... after yesterday's news on the pro-insulinogenic effects of whey protein and its not so significant negative impacts on your body composition in the absence of profoundly increased energy consumption (i.e. whey, ah... I mean "way" beyond the ~20% max. increase I suggest for a clean bulk). We will take a look at another, hitherto largely overlooked protein source: Fish! Yeah, I know, you all eat your serving of fish once or twice a week - fatty fish to be precise to derive the alleged health benefits of the latter, but did you ever remotely consider supplementing with fish protein? As a regular you may in fact have done that after reading about the superiority of cod over casein and pea as far as muscle repair are concerned, here at the SuppVersity, and if you have not the data from a recently published study from the Institute of Medicine and the Department of Heart Disease at the University of Bergen in Norway (Vikøren. 2013) could not just be an incentive for you to do so, it could in fact promote the production of fish protein isolates, which has not really kicked off before the 2011 when a Peruvian company hit the market with fat-free, membrane-refined fish protein and fish peptide products at prices of $5/kg and thus at least 38% cheaper than whey or egg protein isolates (Daniells. 2011).

Fish protein supplementation: A little goes a long way

What is so particularly stunning about the data from the 8-week double-blinded cod protein supplementation trial Linn A. Vikøren and her colleagues conducted were not so much the results,

• a decrease in postprandial blood glucose AUC,
• more pronounced, yet less sustained insulin responses (sign of increases insulin sensitivity),
• a decrease in C-reactive peptide (CRP) levels, and
• reduced LDL cholesterol, as well as
• increases in lean muscle mass, and
• decreases in fat mass,

but rather the amount of supplemental fish protein which elicited those changes: 3g/day for the first 4 weeks and 6g/day for the last 4 weeks - not much, if you relate that to the average protein intake (70-90g) of the overweight, yet healthy middle-aged study participants, right?

The whole is mostly way more than just the sum of its parts

If we go simply by the protein content that previous studies, such as , even the large dose, i.e. the 6g of cod protein isolate per day, the subjects received in the 2nd month of the intervention period, equals no more than

*Please keep in mind that Pilon et al. observed differences with respect to the physiological effects of fish proteins from different sources. In their rodent study, only salmon, yet not bonito, herring or mackerel protein had ameliorative effects on body weight and visceral body fat gain in rodents on a high-fat diet (Pilon. 2011)

• 20g of tuna
• 21g anchovies
• 22g salmon or halibut
• 23g snapper or tilapia

Now, feeding them fish, was however not a viable option. After all, it is pretty easy to distinguish a can of tuna such as the one in image 1 from a similar can with chicken, let alone "fillers and sweeteners", the sole ingredients of the placebo tablets. So in as much as you may decry the use of supplemental, instead of real fish protein, it is hardly debatable that the use of 500mg fish protein (cod) caps was necessary to effectively double-blind the study.

Figure 1: Comparison of amino acid concentration  (g/kg) of fish and whey protein (data for fish and whey from Vikøren. 2013 and Engelen. 2013, respectively)

If we take a look at the actual amino acid content (which is yet, as you should know, only one of the potential reasons we would see differences to other protein sources), it is evident that cod has a similarly high essential amino acids content as whey, but contains significantly less proline, much more arginine, glutamine and taurine.

Reminder: Just in case you have forgotten about the SuppVersity news from Friday, May 4th, 2013, I suggest you briefly go back and read up on how "Cod Protein Promotes Muscle Repair After Injury More than Casein or Peanut Protein"

What is it about fish protein that makes it so potent - arginine, taurine, or synergistic effects?

As a regular, here at the SuppVersity, you will also know that there exists a fairly decent amount of research on potential and scientifically established health effects of arginine and taurine. Whether those two individual amino acids or rather synergistic effects due to the specific protein / peptide structure of cod proteins are able to explain any of the observed health benefits (see bullet points 1-4) or the changes in body composition (see bullet points 5-6 and figure 2, below) remains yet to be elucidated.

Figure 2: Macronutrient composition of the diets at baseline, after 4 weeks and 8 weeks and changes in body composition compared to baseline (Vikøre. 2013)

Whatever the exact reasons may be, the -1.6% drop in body fat percentage (this is different from body fat mass!) is certainly astonishing given the fact that it occurred in the absence of significant changes in either the macronutrient composition or total energy content of the subjects' diets.

So what? Are fish protein isolates, the better whey?

Now without knowing the exact physiological mechanism behind the the observed effects on glucose and lipid metabolism and body composition of the 16 male and 19 female study participants, which could, as Vikoren et al. rightly point be a result of either the

• specific amino acid profile,
• the presence or formation of specific peptides (protein bonds), or 
• as of yet unknown bioactive components of fish/cod protein,

it would certainly be premature for most of you to make a switch from whey to cod, before scientific data from human trials confirms not just the efficacy, but also the supremacy of high(er) dose cod supplements over whey and other dairy proteins as the go-to muscle builders for physical culturists.

In view of the results of previous studies by by Zhang etl al. (1993), Shukla et al. (2006), and specifically van Post-Skagagard et al. (2006) on the health effects of supplemental cod protein, it may yet be prudent to make another switch in your dietary / supplement regimen, namely one from fish oils to whole fish, which has already been shown to produce superior weight-loss and health effects than supplemental fish oil (e.g. Gunnarsdotti. 2008) - results of which we know by know that they well be mediated by the synergistic effects of oil and protein from whole fish.

References

1. Daniells S. Low-cost, fat-free fish protein facility gets go ahead. Nutraingredients-usa.com. May, 27 2011. < http://www.nutraingredients-usa.com/Industry/Low-cost-fat-free-fish-protein-facility-gets-go-ahead >
2. Engelen MP, Rutten EP, De Castro CL, Wouters EF, Schols AM, Deutz NE. Casein protein results in higher prandial and exercise induced whole body protein anabolism than whey protein in Chronic Obstructive Pulmonary Disease. Metabolism. 2013 Apr 16.  
3. Gunnarsdottir I, Tomasson H, Kiely M, Martinéz JA, Bandarra NM, Morais MG, Thorsdottir I. Inclusion of fish or fish oil in weight-loss diets for young adults: effects on blood lipids. Int J Obes (Lond). 2008 Jul;32(7):1105-12. Epub 2008 May 20.
4. Lavigne C, Tremblay F, Asselin G, Jacques H, Marette A. Prevention of skeletal muscle insulin resistance by dietary cod protein in high fat-fed rats. Am J Physiol Endocrinol Metab. 2001 Jul;281(1):E62-71.
5. Pilon G, Ruzzin J, Rioux LE, Lavigne C, White PJ, Frøyland L, Jacques H, Bryl P, Beaulieu L, Marette A. Differential effects of various fish proteins in altering body weight, adiposity, inflammatory status, and insulin sensitivity in high-fat-fed rats. Metabolism. 2011 Aug;60(8):1122-30.
6. von Post-Skagegård M, Vessby B, Karlström B. Glucose and insulin responses in healthy women after intake of composite meals containing cod-, milk-, and soy protein. Eur J Clin Nutr. 2006 Aug;60(8):949-54.
7. Shukla A, Bettzieche A, Hirche F, Brandsch C, Stangl GI, Eder K. Dietary fish  protein alters blood lipid concentrations and hepatic genes involved in cholesterol homeostasis in the rat model. Br J Nutr. 2006 Oct;96(4):674-82.
8. Vikøren LA, Nygård OK, Lied E, Rostrup E, Gudbrandsen OA. A randomised study on the effects of fish protein supplement on glucose tolerance, lipids and body composition in overweight adults. Br J Nutr. 2013 May 31:1-10.

Whey More Insulinogenic Than White Bread: Insulin Spike is Mediated by GIP Secretion in the Gut & Effect of EAAs on the Pancreas + Why Whey is Still the Better Choice

Image 1: Peter Czerwinski, aka Furious Pete, certainly did not care about the pro-insulinogenic effects of whey, when he ate 900g of it within 3:30min, click here to watch his record (Furios Pete, 2010)

Among muscle heads and physical culturists, alike, whey protein has become almost synonymous with building slabs of lean muscle.What many of the protein fans - especially the low carbers - tend to overlook or ignore, though, are the pro-insulinogenic effects of whey protein, in general, and purified whey protein isolates and hydrosolates, in particlar, which do not just augment the insulin release in response to carbohydrate ingestion (Morifuji. 2010), but exert a decent increase in pancreatic insulin release in and out of themselves (Claessens. 2009). Further evidence on the hitherto not yet fully understood mechanism behind the whey induced increase in insulin comes from a recently published paper by Albert Salehi and his colleagues from the Lund University in Sweden, the University of Copenhagen in Denmark and the Oxford Center for Diabetes, Endocrinology and Metabolism in the UK (Salehi. 2013).

Whey vs. white bread and human plasma as incubation medium

In the aforementioned paper, the scientists present the results of a combined in-vivo + in-vitro trial on the effects of glucose, amino acids and amino acids mixtures (as they are found in whey) on pancreatic insulin production and its relationship to the incretin response (release of incretin hormones from specialized cells in the small and large intenstine). To this ends, the researchers had their subjects, four men and two women (healthy non-smokers, normal-weight, age 20-30y), consume test meals containing either white bread (3.7g of protein) or whey (16.7g of protein), after an overnight fast, on two different occasions. The meals had to be consumed within 12 minutes and blood samples were taken 7.5,  15, 30 and 45 min after the start of the meal.

Figure 1: GIP and GLP-1 response to whey and white bread (left, top & bottom); insulin release (%) per islet relative to glucose after incubation with different amino acids, amino acid mixtures and mixture + GIP (Salehi. 2013)

As you can see in figure 1 (left), the ingestion of  ~20g of whey protein (containing 16.7g of protein + lacose + minimal amounts of fat) produced a significantly more pronounced in increase in glucose-dependent insolinotropic peptide (GIP, see previous post "Waxy Maize Reloaded" for more information) than the white bread meal. GIP is a hormone-like substance that is produced by the enteroendocrine cells of the gut lining, amplifies the glucose-induced production of insulin in the pancreas, slows down digestion, increases glucose absorption, ramps down fatty acid oxidation and sets you into energy "storage mode" - unfortunately in both forms, skeletal and liver glycogen and fat!

Figure 2: Simplified schematic illustration of mechanism behind the EAA induced GLUT-4 increase in skeletal muscle (click here to learn more)

GLUT-4 activation - another reason, why whey is way better than sugar: If you remember Monday's blogpost on the isolated effects of essential amino acids (EAAs) on the GLUT-4 (glucose transporter = the shuttle that carries glucose from the blood stream into the cell) expression on skeletal muscle cells, it is evident that contrary to sugar or most forms of carbohydrates, whey protein, or rather the essential amino acids in whey, cod, soy, beef, pea, egg and other high EAA protein sources exert nutrient-repartitioning effects due to selectively increasing insulin induced glucose uptake in skeletal muscle and constant glucose uptake in adipose tissue (Lavigne. 2001).

Against that background it is not surprising that the combined effects of GIP (figure 1, top-left) and the amino acid induced increase in insulin production (figure 1, right, orange) lead to a more than 7-fold increase (compared to glucose control) in pancreatic insulin production after incubation of mouse Langerhans cellls (the cells of the pnacreas that are responsible for insulin mediated glucose control) with sera containing a mixture of EAAs and GIP that was matched to the respective EAA and GIP concentrations in the preceding whey vs. white bread human experiment.

Don't worry there are also benefits that can compensate for the insulin spike

Now these results certainly seem odd, after all "the experts" say that insulin is the root cause of all evil! Now whey spikes insulin and GIP and still we see study after study popping up, reporting "beneficial effects" of whey protein on glucose metabolism and overall health - how can that be? The reasons are manifold and actually quite straight forward:

1. Insulin is not the devil - Contrary to common believe the problem is not insulin, but insulin resistance and overspilling glucose stores. If your insulin spikes and you are not insulin resistant, the cells will suck up glucose, your blood sugar will drop and your insulin will drop as well; so, in terms of negative side effects, the most obvious one would be postprandial hypoglycemia in response to large boluses of whey protein (and even that is usually compensated for by increases in glucagon and consequently gluconeogensis)  - that the latter can have long-term detrimental effects on insulin sensitivity is a whole other issue, though...
2. Many studies use (pre-)diabetic subjects - In a pre-diabetics an increase in insulin release due to whey will improve postprandial glycemia and must thus be considered beneficial - it's "nature's insulin supplement", if you will, and particular helpful for non-insulin-dependent type-II-diabetics.
3. Effects on skeletal muscle are neglected - Anything that can potentially help build and maintain muscle tissue (and we all know whey can do that) will help with glycemia, obesity and lipid metabolism, because the increase or (esp. in the elderly) maintenance of skeletal muscle mass ("Metabolic Currency" - Carl Lanore) will allow for greater intra-muscular glucose stores and fatty acid oxidation (assuming you are still insulin sensitive, cf. 1)
4. The "satiety hormones" are overlooked - Similar to the muscle building effects, the increase in GLP-1, a hormone which is by no means just responsible for inducing satiety (read all about GLP-1 in my previous post "Eat More, Burn More and Lose Fat Like on Crack With GLP-1") have been hitherto largely ignored. And that despite the fact that increases in GLP-1 could be among the main reasons that whey and other EAA-rich protein sources have repeatedly been shown to help weight- and, more importantly,  fat loss and increase metabolic health (Ranganath. 1996; Baggio. 2007; Akhavan. 2011; Gerspach . 2011). 

Image 2: Real foods are better protein choices for the last weeks of a contest prep (image directly from Adelfo Cerame's kitchen)

In other words, while some of the "beneficial effects" in obese and insulin resistant individuals could actually turn against lean, active individuals, the muscle-building and "satiety hormone" induced metabolic effects make up for the potential fat storage in scenarios of energy overconsumption (remember: there is a certain margin of carloric surplus, where the laws of thermodynamics do apply, cf. "A Tale of Macro- and Micronutrient Modifications")

Whey is probably not your best choice for the final weeks of a contest prep, though

Still, if you are in the final phase of prepping for a contest and want that "paper-thin" skin conditioning, like our common friend Adelfo Cerame does, real-food protein sources like chicken, fish, lean meat etc. should be your main sources and protein shakes, an exclusive post-workout thing (in the last days, maybe not even that).

References:

1. Akhavan T, Luhovyy BL, Anderson GH. Effect of drinking compared with eating sugars or whey protein on short-term appetite and food intake. Int J Obes (Lond). 2011 Apr;35(4):562-9. Epub 2010 Aug 24.
2. Baggio LL, Drucker DJ. Biology of incretins: GLP-1 and GIP. Gastroenterology. 2007 May;132(6):2131-57.
3. Claessens M, Calame W, Siemensma AD, van Baak MA, Saris WH. The effect of different protein hydrolysate/carbohydrate mixtures on postprandial glucagon and insulin responses in healthy subjects. Eur J Clin Nutr. 2009 Jan;63(1):48-56. Epub 2007 Sep 12
4. Gerspach AC, Steinert RE, Schönenberger L, Graber-Maier A, Beglinger C. The role of the gut sweet taste receptor in regulating GLP-1, PYY, and CCK release in humans. Am J Physiol Endocrinol Metab. 2011 Aug;301(2):E317-25. 
5. Lavigne C, Tremblay F, Asselin G, Jacques H, Marette A. 2001. Prevention of skeletal muscle insulin resistance by dietary cod protein in high fat-fed rats. Am. J. Physiol. Endocrinol. Metab. 281:E62–71
6. Morifuji M, Ishizaka M, Baba S, Fukuda K, Matsumoto H, Koga J, Kanegae M, Higuchi M. Comparison of different sources and degrees of hydrolysis of dietary protein: effect on plasma amino acids, dipeptides, and insulin responses in human subjects. J Agric Food Chem. 2010 Aug 11;58(15):8788-97.
7. Ranganath LR, Beety JM, Morgan LM, Wright JW, Howland R, Marks V. Attenuated GLP-1 secretion in obesity: cause or consequence? Gut. 1996 Jun;38(6):916-9. 
8. Salehi A, Gunnerud U, Muhammed SJ, Ostman E, Holst JJ, Björck I, Rorsman P. The insulinogenic effect of whey protein is partially mediated by a direct effect of amino acids and GIP on beta-cells. Nutr Metab (Lond). 2013 May 30;9(1):48.

Tocotrienols: What They Are, What They Do & How They Work + Why the RDA of Palm Olein is NOT 1xCup Per Day

Image 1: If you wanted to get the tocotrienol levels a producer of respective supplements says are  "required", you would have to eat at least 200g palm fruits a day. Alternatively, you can resort to 4kg of oats, if you like those better... What? you are wondering that you are not dead by now? After so many years of tocotrienol deficiency from not getting your 4kg of oats?

The long lists of pathologies related to vitamin E deficiency include, among others, all sorts of degenerative diseases from ataxia over general muscle degeneration to degeneration of sperm and subsequent infertility. But despite the fact that there is a pretty substantial amount of evidence that would suggest that a diet rich in vitamin E could not just prevent the aforementioned pathologies, but would also protect us from many of the currently prevalent ailments of western society such as obesity and coronary vascular disease (Mishra. 2003; Rimm. 1993), respective trials with dietary supplements usually show no, or even negative effects. I have already addressed a couple of  reasons why the benefits of dietary vitamin E intake often cannot be replicated with supplements in previous posts. The most significant one, probably is the absence of the "right" mixture and ratio of alpha-, beta-, gamma- and delta-tocopherols and, as an emerging contributer, the total absence of tocotrienols in the vast majority of vitamin E supplements and almost 99.9% of the pertinent trials.

What are tocotrienols? And what do they do?

I could now rant about the structural differences between the two, with the tocotrienols being an unsaturated variety of the tocopherols with a isoprenoid side chain, but I guess it is enough to know that due to  differences in their molecular structure, they also differ in their effects on the human body, of which you may already have apprehended that their cholesterol lowering effects were the first to attract the attention from researchers (Qureshi. 1986). Within the last 26 years researchers from all around the world have identified additional health benefits, the most prominent of which are...

• Anti-cancer effects (Kato. 1985; Sundram. 1989; Weng. 2009),
• General antioxidant effects (Newaz. 1999),
• Brain specific antioxidant effects (Khanna. 2003),
• Exercise-specific antioxidant effects (Lee. 2009),
• Cardiovascular disease (Shibata 2009)
• Diabetic neuropathy (Kuhad. 2009)
• Bone health (Ahmad. 2005)
• Metabolic syndrome (Weng. 2011)
• Antithrombotic effects (Qureshi. 2011)
• Endocrine health (Yu. 2005)
• Liver health (Patel. 2013)

The purpose of today's SuppVersity article is yet not so much to compile the most extensive list of potential, purported or demonstrated benefits of tocotrienols, the major dietary sources of which are (Kobayashi. 1975; Tan. 2011)

• rice bran oil (50:50 tocopherol:tocotrienol ratio), 
• palm oil (25:75 tocopherol:tocotrienol ratio), and 
• annatto (0.1:99.9 tocopherol:tocotrienol ratio) oil
• human breast milk (!) [though this is probably no major source for you ;-]

but rather to take a look at an intriguing chart of the various molecular targets (Aggarwal. 2010) and discuss the implications:

Figure 1: Molecular targets (left) and proteins that directly interact with tocotrienols (right; adapted from Aggarwal. 2010)

As you can see  without even looking really close at the above graphic, the number of those targets is vast. Another thing you should see right away is that the effect of the tocotrienols is mostly inhibitory (red ovals in the left) and include a couple of old foes, such as:

• the inflammatory cytokines & transcription factors: IL-1, IL-6, TNF-alpha, nf-kappabeta, IL-8 (probably involved in auto-immune reactions), PF-A4 (increases platelet aggregation and thus thrombosis risk)
• factors involved in angiogenesis and cardiocascular disease: VEGF (vascular growth factor, involved in CVD) and its receptor VEGF-r, VCAM-1 (increases adhesion of immune cells to the endothelial wall)
• kinases involved in the cell cycle and apoptotic regulators: CDK's, PKC, pERK, etc. & survivin, IAP-1 & 2 etc., but also telomerase, which are all involved in the proliferation of cancer
• enzymes involved in inflammatory processes: eNOS, iNOS, COX-2, etc.

On the upregulatory side of things, we have

• enzymes from the CYP cascade, which are among other involved in the clearance of estrogen, and other hormone like substances and the metabolism of drugs,
• MAPK and JNK, which exert anti-catabolic effects on muscle tissue, or 
• GPX and SOD, two of the major enzymes involved in the antioxidant defenses

Now, if we take a look at all these, you may remember that low COX-2 levels have only recently been identified with profound overtraining (cf. "Overtraining inflammation insufficient repair"), that AKT (not mentioned above, but in figure 1) is one of the driving forces of skeletal muscle anabolism and telomerase, extends cell life in general, not just in cancer cells. Which brings us back to the issue of ...

...how much anti-oxidants do we actually need?

Figure 2: Total tocopherol and tocotrienol content of high vitamin E foods / oils (top) and tocopherol ratios (bottom) , data based on Whittle. 1967 and Slover. 1971

Or, in this particular case, how much tocotrienols are still beneficial? Neither I, nor anybody else knows the exact answer to this question. And against this fact, the recommendations I came across on the website of a major producer of respective supplements, which state that you would need

• 80g of palm oilen (cooking oil),
• 160g of rice bran oil,
• 3kg of barley,
• 1.5kg of wheatgerm, or 
• 4kg of oats

to (I quote) "achieve the required [my emphasis] level of tocotrienols" should tell any reasonable person that those "required" levels (~150mg) are probably required to generate the target revenue of the said company, yet probably not required for you or any other human being to thrive.

Do not stack one more, but take one out!

Instead of adding another overpriced (and probably overdosed) tocotrienol supplement to your regimen, it is thus probably wiser to simply drop any superflous and potentially harmful alpha-tocopherol only supplements which do would offset the alpha- to gamma- and delta- tocopherol ratio (this could potentially be ameliorated by taking a natural blend) and limit the total tocopherol intake to reasonable levels, as the latter has also been shown to hamper the absorption and retention of tocotrienols (Ikeda. 2003). In this context it is also noteworthy that Ping Tou Gee writes in a 2011 paper with the aptly chosen title "Unleashing the untold and misunderstood observations on vitamin E" that this fact alone would suggest that "there is a need to review critically on the dietary reference intakes recommendations" for alpha tocopherol (α-T). His bold statement that

[i]t is not known whether α-T is still essential to humans in long terms, α-T₃ [alpha tocotrienol] diet appeared to produce healthy rats over five generations.

is yet probably an attribution to Palm Nutraceuticals Sdn. Bhd. (which is not the aforementioned company which wants to force-feed you either their supplements or 2 cups of rice bran oil), of which he states in the acknowledgments that he thanks them "for permission to publish this paper" and further evidence for how pathetic parts of the research in the medical field is - awful this science business, isn't it?

References:

1. Aggarwal BB, Sundaram C, Prasad S, Kannappan R. Tocotrienols, the vitamin E of the 21st century: its potential against cancer and other chronic diseases. Biochem Pharmacol. 2010 Dec 1;80(11):1613-31. Epub 2010 Aug 7.
2. Ahmad NS, Khalid BA, Luke DA, Ima Nirwana S. Tocotrienol offers better protection than tocopherol from free radical-induced damage of rat bone. Clin Exp Pharmacol Physiol 2005;32:761–770 
3. Gee PT. Unleashing the untold and misunderstood observations on vitamin E. Genes Nutr. 2011 Feb;6(1):5-16. Epub 2010 Jul 20.
4. Ikeda S, Tohyama T, Yoshimura H, Hamamura K, Abe K, Yamashita K. Dietary alpha-tocopherol decreases alpha-tocotrienol but not gamma-tocotrienol concentration in rats. J Nutr. 2003 Feb;133(2):428-34.
5. Kato A, Yamaoka M, Tanaka A, Komiyama Ka, Umezawa I. Physiological effect of tocotrienol. J
   Japan Oil Chem Soc (Yukugaku) 1985;34:375–376.
6. Khanna S, Roy S, Ryu H, Bahadduri P, Swaan PW, Ratan RR, et al. Molecular basis of vitamin E
   action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced
   neurodegeneration. J Biol Chem 2003;278:43508–43515.
7. Kobayashi H, Kanno C, Yamauchi K, Tsugo T. Identification of alpha-, beta-, gamma-, and delta-
   tocopherols and their contents in human milk. Biochim Biophys Acta 1975;380:282–290.
8. Kuhad A, Chopra K. Attenuation of diabetic nephropathy by tocotrienol: involvement of NFkB
   signaling pathway. Life Sci 2009;84:296–301.
9. Lee SP, Mar GY, Ng LT. Effects of tocotrienol-rich fraction on exercise endurance capacity and
   oxidative stress in forced swimming rats. Eur J Appl Physiol 2009;107:587–595.
10. Mishra GD, Malik NS, Paul AA, Wadsworth ME, Bolton-Smith C. Childhood and adult dietary vitamin E intake and cardiovascular risk factors in mid-life in the 1946 British Birth Cohort. Eur J Clin Nutr. 2003 Nov;57(11):1418-25.
11. Newaz MA, Nawal NN. Effect of gamma-tocotrienol on blood pressure, lipid peroxidation and total antioxidant status in spontaneously hypertensive rats (SHR). Clin Exp Hypertens 1999;21:1297–1313.
12. Patel V, Rink C, Gordillo GM, Khanna S, Gnyawali U, Roy S, Shneker B, Ganesh K, Phillips G, More JL, Sarkar A, Kirkpatrick R, Elkhammas EA, Klatte E, Miller M, Firstenberg MS, Chiocca EA, Nesaretnam K, Sen CK. Oral tocotrienols are transported to human tissues and delay the progression of the model for end-stage liver disease score in patients. J Nutr. 2013 Mar;142(3):513-9. Epub 2013 Feb 1. 
13. Qureshi AA, Burger WC, Peterson DM, Elson CE. The structure of an inhibitor of cholesterol biosynthesis isolated from barley. J Biol Chem. 1986 Aug 15;261(23):10544-50.
14. Qureshi AA, Karpen CW, Qureshi N, Papasian CJ, Morrison DC, Folts JD. Tocotrienols-induced inhibition of platelet thrombus formation and platelet aggregation in stenosed canine coronary arteries. Lipids Health Dis. 2011 Apr 14;10:58.
15. Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med. 1993 May 20;328(20):1450-6.
16. Slover HT. Tocopherols in foods and fats. Lipids. 1971 May;6(5):291-6.
17. Sundram K, Khor HT, Ong AS, Pathmanathan R. Effect of dietary palm oils on mammary
    carcinogenesis in female rats induced by 7,12-dimethylbenz(a)anthracene. Cancer Res 1989;49:1447–1451
18. Shibata A, Nakagawa K, Sookwong P, Tsuduki T, Oikawa S, Miyazawa T. delta-Tocotrienol
    suppresses VEGF induced angiogenesis whereas alpha-tocopherol does not. J Agric Food Chem
    2009;57:8696–8704.
19. Tan B. Tocotrienols: The New Vitamin E. Spacedoc.net. http://www.spacedoc.com/tocotrienols
20. Weng-Yew W, Selvaduray KR, Ming CH, Nesaretnam K. Suppression of tumor growth by palm
    tocotrienols via the attenuation of angiogenesis. Nutr Cancer 2009;61:367–373.
21. Weng-Yew W, Brown L. Nutrapharmacology of tocotrienols for metabolic syndrome.
    Curr Pharm Des. 2011;17(21):2206-14. 
22. Whittle KJ, Pennock JF. The examination of tocopherols by two-dimensional thin-layer chromatography and subsequent colorimetric determination. Analyst.1967 Jul;92(96):423-30.
23. Yoshikawa S, Morinobu T, Hamamura K, Hirahara F, Iwamoto T, Tamai H. The effect of gamma-tocopherol administration on alpha-tocopherol levels and metabolism in humans. Eur J Clin Nutr. 2005 Aug;59(8):900-5.
24. Yu FL, Gapor A, Bender W. Evidence for the preventive effect of the polyunsaturated phytolside chain in tocotrienols on 17beta-estradiol epoxidation. Cancer Detect Prev. 2005;29(4):383-8.

Less Than 15mg of DHEA Exert Identical Beneficial Effects on Insulin Sensitivity as 1h of Cardio 5x Per Week. Both Effects Mediated Via Increases in Intra-Muscular DHT

Image 1: It has long been established that diabetics have particularly low DHEA levels (Loviselli. 1994), but what's the chicken and what's the egg here?

It is quite funny, sometimes you don't hear about certain supplements, (pro-)hormones, exercise-modalities etc. in years and then, all of a sudden, there are two studies on the respective topic in one week; and moreover, two pretty interesting ones! Last Friday, exactly 7 days ago, you've read here at the SuppVersity about the muscle-protective effects of low-dose dehydroepiandrosterone (DHEA) supplementation during a 5-day intense multiple-type exercise protocol (cf. "DHEA Blunts Muscle Damage During 5 Days of Combined Endurance, Strength and HIIT Training in Young Men"). Today, I have another interesting set of data for you - data which could not just shed some light onto the underlying mechanisms of the said protective effects against skeletal muscle damage, but also on DHEA's beneficial effects on insulin sensitivity.

Not younger, but leaner with a minimalist dose of DHEA?

In a 6 week trial, and thus over a more than eight times longer timespan than in the previously mentioned human study on skelatal muscle damage, Koji Sato and his (or her?) colleagues from the Ritsumeikan University, the Senshu University and the University of Tsukuba (all in Japan, as you probably already suspected) investigated the effects a low dose of DHEA (human equivalent: 0.16mg/kg per day => 10-15mg/day) supplementation on the insulin, QUICKI (=quantitative insulin-sensitivity check index) and intramuscular DHEA and DHT (dihydrotestosterone) levels in sedentary or exercised dietary obese male rodents.

Figure 1: Relative insulin levels, QUICKI, intramuscular DHEA and DHT content in obese male rodents after 6 weeks of DHEA or combined DHEA + exercise (1h, 5days/week) treatment (data adapted from Sato. 2013)

As you can see in figure 1 the effects of both 5x/week running on a treadmill (ETA: 1h) and orally administered DHEA were profound. If you compare the "exercise only" group (red) to the two DHEA groups (green and violet), you will yet notice interesting parallels. Not only were the decreases in serum insulin and the increases (=improvements of insulin sensitivity) in the QUICKI test very similar, the exercise regimen alone yielded a +56% increase skeletal muscle DHEA content and a +71% increase in DHT.

Exercise increases intramuscular DHEA & DHT...
 

Figure 2: Hormonal cascade from DHEA to DHT; all enzymatic conversions can take place on a systemic and intra-cellular level!)

At least the latter, i.e. the increase in DHT should not be news to you if you have been following the in-depth articles at SuppVersity over the past couple of months. From the Intermittent Thoughts on DHT you know that exercise in general and HIT endurance exercise in particular has been found to boost intramuscular dihydrotestosterone levels, as well. The bros, or friends of bros among you, will probably also have heard the horrific stories about creatine monohydrate leading to increased levels of DHT (van der Merve. 2009), of which every reasonable person must actually assume that they are nothing but a downstream effect of increased training loads and/or improved adaptation... I mean, think about it "paleo style": Why would the mammalian body (rodent and human appear to react alike here) increase the DHEA and, via 5-alpha reductase (cf. figure 2), the dihydrotestosterone levels in response to high volume exercise, if not as a means of adaptation?

Oral DHEA + exercise = double-whammy against obesity

The combined treatment, or I should say the exogenous support of the exercise induced changes had - and this is not visible from the data in figure 1, astonishingly profound effects on the diet induced weight gain of the lab animals. While all other rodents became fatter, those in the exercise + DHEA group remained at a steady body weight level; an observation the researchers comment as follows:

Although DHEA administration and exercise training each produced beneficial effects, 6-weeks of combination treatment were more effective for obesity. The precise mechanisms that reduced abdominal fat weight in the combination group remain unclear, yet we can propose several plausible hypotheses. 2 weeks of DHEA administration has been shown to activate fatty acid metabolism-related enzymes, such as long-chain fatty acyl-coenzyme A synthase, and to increase free CoA levels in liver (Mohan. 1998; Mohan. 1990). In addition, exercise training is  known to reduce adipogenesis via upregulation of fatty acid metabolism and increased energy expenditure (Hou. 2003). Therefore, 6-weeks of combination treatment may have promoted additive reductions in abdominal fat volume.

In other words, while DHEA increases the efficacy of fatty acid oxidation, exercise takes care of the increase in energy expenditure which is - all convictions wrt to "calories don't count" and the "calories in vs. calories out"-hypothesis aside - still a fundamental prerequisite that the fatty acids do actually get burned and are not released into circulation to be restored or replaced a couple of hours later.

"Ok, I am just ordering some DHEA, how much should I take?"

Before you head over to the online vendor of your choice to make sure you get your share of DHEA before the FDA hears that it could hamper the sales of diabetes drugs and removes it from the OTC market, I would like to remind you that despite the fact that Sato et al. rightly claim that a "combination treatment [with DHEA and DHT] may be more beneficial than either therapy alone", a cursory glance on the data in figure 1 should suffice to tell you that those additional benefits as statistically significant as they may be are just that "additional" and that exercise alone yielded about equal results, is free of negative and full of beneficial side effects (update: as long as you don't overtrain; thanks Stapedius for this important note) and does not have the same host of studies refuting its efficacy as DHEA has (Clore. 1995).

It is nevertheless intriguing that a hormone the medical orthodoxy has, more or less all of a sudden, dropped like a hot potato and declared "questionable" and "ineffective" is now, roughly 15-20 years being rediscovered... and I am pretty sure that this was not the last DHEA study you will see and read about here at the SuppVersity ;-)

References:

1. Clore JN. Dehydroepiandrosterone and body fat. Obes Res. 1995 Nov;3 Suppl 4:613S-616S. Review.
2. Hou CW, Chou SW, Ho HY, Lee WC, Lin CH, Kuo CH. Interactive effect of exercise training and growth hormone administration on glucose tolerance and muscle GLUT4 protein expression in rats. J Biomed Sci. 2003 Nov-Dec;10(6 Pt 2):689-96.
3. Loviselli A, Pisanu P, Cossu E, Caradonna A, Massa GM, Cirillo R, Balestrieri A. [Low levels of dehydroepiandrosterone sulfate in adult males with insulin-dependent diabetes mellitus]. Minerva Endocrinol. 1994 Sep;19(3):113-9.
4. van der Merwe J, Brooks NE, Myburgh KH. Three weeks of creatine monohydrate  supplementation affects dihydrotestosterone to testosterone ratio in college-aged rugby players. Clin J Sport Med. 2009 Sep;19(5):399-404.
5. Mohan PF, Cleary MP. Effect of short-term DHEA administration on liver metabolism of lean and obese rats. Am J Physiol. 1988 Jul;255(1 Pt 1):E1-8.
6. Mohan PF, Ihnen JS, Levin BE, Cleary MP. Effects of dehydroepiandrosterone treatment in rats with diet-induced obesity. J Nutr. 1990 Sep;120(9):1103-14.
7. Sato K, Iemitsu M, Aizawa K, Ajisaka R. Testosterone and DHEA activate the glucose metabolism-related signaling pathway in skeletal muscle. Am J Physiol Endocrinol Metab. 2008 May;294(5):E961-8. Epub 2008 Mar 18.
8. Sato K, Iemitsu M, Aizawa K, Mesaki N, Ajisaka R, Fujita S. DHEA administration and exercise training improves insulin resistance in obese rats. Nutr Metab (Lond). 2013 May 30;9(1):47. [Epub ahead of print]