From 16% to 8% Body Fat in 10 Weeks: Crossfit Workout Gets The Leanest Shredded - But Only the Fittest Survive

Crossfit doesn't fit well with everyone. In  fact you have to be pretty fit already if you intend to benefit - specifically if you don't have someone who tailors the workouts to your specific needs. If you don't or are still miles apart from being fit, don't be bamboozled by the results of people who have been training for years.

This certainly sounds a little sadistic, but I hope you've been missing the Science Round-Up last Thursday. If that's the case, you will be happy to hear that Carl and I are back on track, and ready to talk about topics ranging from magnesium supplementation over the potentially fatal combination of NSAIDs and exercise and what's that got to do with gut health / integrity, how light therapy won't make you lighter, but help you cut body fat, how intense workouts compromise your sleep, and how intense sweeteners make you fat - at least if you add them on top of a Western diet. If we will have time, we will also take a look at how much protein it actually takes to preserve lean mass on a diet and how protein supplementation is not necessary and in a recently published study not even conducive to building muscle. And while these were only 50% of the news I've on my list of potential topics, I won't give away more... just tune in live at 1PM EST on the Super Human Radio Network.

For the time that remains and for those of you who are just arriving here after having listened to the live-stream, I still have a special goodie... have you ever pondered over the following question:

How much can you achieve within 10 weeks of training?

Even if you have already decided on a certain type of training, for example HIIT, you will have to adjust your routine to "Make HIIT a HIT" read Part I and Part II of the eponymous series and learn how to turn a HIIT workout into your HIIT workout to avoid overtraining and maximize its efficacy (learn more)

There is obviously no definite answer to this question. I mean, it goes without saying that we would first have to define, whether we are talking about muscle growth, overall conditioning, fat loss, etc. - what people often overlook, however it also depends on where you are coming from. Sometimes I feel like I am the only one who dares telling someone who's been "running" - in most cases this is rather sitting and driving - around at 2x his/her normal weight for years, is past his early 20s and has a life beyond working out and dieting is very unlikely to ever achieve a cover model physique. On the other hand, we've got the average trainee, who's been training for years has a high degree of leanness and is just about to see his sixpack shine through, who will necessarily make much smaller improvements within a given time-frame than his obese colleague who's just about to start working out for the first time of his/her life.

The previous paragraph should have made it quite clear, compared to the (overweight) beginner, an advanced trainee must invest much more thought into his/her diet and exercise regimen. That real intermittent fasting would probably be a better alternative for him/her than the "buffered every other day fat" has already been mentioned in yesterday's SuppVersity Article, but what about the exercise regimen?

Working out for fat loss and conditioning - Crossfit rules!

Fast paced high intensity workouts are gathering more and more momentum even outside of Crossfit gyms. Some of them may look somewhat "Jane Fonda", but as a previous review of the workout DVDs Insanity vs. TurboFire revealed, even hopping around in front of your TV set is more productive than the fat burning zone on the treadmill in next to your sofa (learn more)

Let's say he or she is working out primarily to increase his/her conditioning and drop a (if by any means possible) a significant amount of body fat? What would be the best way to train, then?

According to the results of a soon-to-be-published study from the  Ohio State University Health & Exercise Science in Columbus, Ohio (Smith. 2013), there is no question that this would be a Crossfit-esque workout - or, as the scientists refer to it, a crossfit-based high intensity power training (HIPT) program, they describe as follows:

"[...] a crossfit-based HIPT program using basic gymnastic skills (hand- stands, ring, and bar exercises) and traditional multiple-joint, functional, resistance exercises (squat, press, deadlift, Olympic lifts) performed as quickly as possible at a high intensity (low repetition, high percentage of 1-RM)." (Smith. 2013; my italics)

The 10-week program was varied so that some exercises were performed for a best time, and others were performed in the “as many rounds as possible” style (AMRAP; for a little more versatility check out Adelfo's EDT-CrossOver training) within anything from 10 to 20 minutes.

While there were no prescribe recovery times during the strength/skill portion of the exercise session, the WOD portion of the session did not allow for any real "rest" between the sets, as all the exercises were to be performed as quickly as possible.

Wow, who survived that? - Good question, indeed!

Only the fittest survive: Please do me a favor - If you are the aformentioned overweight person who's still carrying around another guy/gal's weight as body fat, don't even think of crossfitting, if you don't want to end up like 9 of the 11 dropouts (the study started with 54 participants), who retired willingly due to overuse or injuries, ok?

I guess you won't be surprised to hear that the 23 men and 20 women who survived and of whom the scientists state that they were "spanning all levels of aerobic fitness and body composition" were actually the typical already reaonably fit Crossfit clientele of whom Smith et al. somwhat awkwardly point out that they "had already been following a 'Paleolithic' type diet prior to and following completion of the training protocol." In other words the "levels of aerobic fitness" the participants spanned ranged from the untrained yet 100% healthy male with a VO2max of ~35 ml/kg/min to the hardcore crossfitter with a starting VOMax of >50ml/kg/min - the aforementioned heavily overweight and thus by now average (see "Obese is Going About to Become the New Normal") Westerner was yet not part of the study population.

Still, the presence of subject spanning the divide between "just healthy" and ripped and well-conditioned is in fact what attracts me as the author of a webpage that's dedicated to anyone ranging from those who just want to be / get / remain healthy and look not all-too shabby in front of the mirror to those who are looking to max out on their own physical performance and appearance. Long story short: The data you see in figure 1 is relevant for all of you. Even if you are still a couple of inches away from matching at least the initially criteria, you will sooner or later arrive at a point, where you'll find a representative counterpart of yours among the subjects of the study at hand.

Figure 1: Body fat percentage (left) and VO2Max (right) before and after the intervention (Smith. 2013)

I guess the data in figure 1 do actually speak for themselves: There is actually pretty much you can achieve within just 10-weeks of serious training: A significant (P<0.05) improvement of VO2max of 2.64% if you are a man and 11.78% if you are a women and (probably much sexier in the eyes of most of you) a 4% respectively 3% decreaes in body fat!

"To our knowledge no research on the aerobic benefits of HIPT has been conducted. HIPT focuses on high intensity resistance training usingmultiple joint exercises, with little to no focus on traditional aerobic activities. In spite of this, our results show that this type of training also provides aerobic and body composition benefits. Theincreased aerobic capacity of the subjects in our HIPT study were similar to those found in past research (Tremblay. 1994; Burgomaster. 2005). Based on the results presented here, individuals of all fitness levels and either gender can realize body composition and aerobic benefits from HIPT. Given that our subjects were following a Paleolithic diet, we cannot relate all of the observed weight loss to HIPT training. However, HIPT and Paleolithic diet in combination could be used to promote positive changes in body composition."

Now, all the scientists write is unquestionably true (also the part on the "paleo diet", as long as it is not very low carb paleo, cf. "Carbohydrate Shortage in Paleoland") and still, for me there are two things Smith et al. don't mention in the paragraph cited about and these are (A) the sex differences in terms of the VO2Max gains (maybe a result of the fact that women are not the ones who would otherwise do HIIT-esque workouts (=aerobic training at high intensities), so that the new stimulus will yield a greater results and (B) the fact that Crossfit is a workout regimen, from which even those benefit who are already fit and lean (keep in mind that the 16% in the lean group are for men and women, so that is lean!).

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Bottom line: Crossfit appears to be the high intensity workout regimen which can help experienced trainees to make the transition from lean to ripped!

Want to do some more aerobics but also stick your classic weight lifting routine and just add cardio in? Now you are asking yourself, when this would make sense? Before, after or in between? Is that's you, go back in the SuppVersity archives and learn more.

As exciting as this may seem, a brief glance at the data in figure 1 will yet also tell you that those who are not up to the intensity and athletic demands of crossfitting don't just risk getting injured (please read the red box further up in the article, as well), they are also wasting their time with a workout that's not designed for their fitness level an will thus yield suboptimal results. This may not necessarily be the case in absolute terms - after all -4% body fat reduction certainly is not bad, but that's -4% from a pretty chubby baseline of 33% and actually could be achieved with basically any well-planned nutrition + exercise regimen. The latter obviously cannot be said of the -50% relative reduction in body fat percentage in the lean subjects on the other side of the "body fat divide". These men and women are most likely people who have been working out for all their lives in one way or another.

The "gifted ones" are in fact rather the ones who are often literally accused of being "genetically gifted" by accusers who simply don't take into consideration that it is above all the epigenetic priming of years of high school, college and other sports that renders them ostensibly resistant to the "obesity virus".

If you are still infected with the obsisty virus and have just found your way to physical culture you hardly qualify as one of those individuals by whom the original Crossfit workouts were created and are therefore certainly not among those people for whom these metabolically and technically demanding workouts were and still are designed. 

If you do "qualify", however (and that is nothing you have to be born wirth, I myself once believed that I just did not have the genes to see my abs), cross fitting could fit in particularly well in your "beach-ready" plan, of which I'd hope you are already thinking about... I mean, spring is less than 3 weeks away (click here to learn more about setting up a workout routine)!

Addendum: Since I got several people asking for the lean mass changes, I thought I'd mention that there was a +1kg increase in lean mass in men and women. Unfortunately the scientists don't provide differential information for lean and heavier subjects, but if your body fat percentage decreases you do at least have  to lose much more fat than lean mass and since there was no dieting involved, I bet the lean guys and girls did not lose any muscle..

References:

• Burgomaster KA, Hughes SC, Heigenhauser GJ, Bradwell SN, Gibala MJ. Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans. J Appl Physiol. 2005 Jun;98(6):1985-90.
• Smith MM, Sommer AJ, Starkoff BE, Devor ST. Crossfit-based high intensity power training improves maximal aerobic fitness and body composition. J Strength Cond Res. 2013 Feb 22. 
• Tremblay A, Simoneau JA, Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 1994 Jul;43(7):814-8.

Buffered Alternate Day Fasting + Light Aerobics Cut Body Fat, Maintain Lean Mass & Improve LDL Particle Size. Plus: Conventional Alternate Day Fasting Detrimental for Fertility

This is how the "buffered" alternate day fast works: You eat 1/4 of the White Choc Banana Cream Pie on your fasting day and a whole pie on the next one - well, not really, but the ratios would be right ;-)

I guess at least the SuppVersity facebook friends are probably going to remember the study today's article is dealing with: "Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans." To me that sounded like Intermittent Fasting Done Wrong Does Still Produce Great Results, When You Combine It With an Aerobic Exercise Regimen", when I first read the abstract. After taking a brief look at the full-text (thx John!),  however, my perspective on the study changed from "even a dog has its day" to "that oes look interesting, let's see whether this kind of buffered alternate day fasting" is able to take bear up with a classic intermittent fast. 


A brief warning with respect to the data in figure 1: I know that a couple of you are too lazy to actually read the article and do headline + figure hopping. If you intend to to that, please keep in mind that the data in figure 1 is from another recent study, I used to illustrate the negative effects of "real" alternate day fasting.

Not all alternate day fasting is created equal

For the course of this 12-week, randomized, controlled, parallel-arm feeding trial the participants, 61 women and only 3 men aged 25 to 65 years, overweight / obese (BMI 30-39.9kg/m²) and weight stable for at least 3 months were randomized to one of the four study arms (unfortunately the data does not allow for any conclusions, whether the men and women reacted differently to the intervention or "real" alternate day fasting the data from the rodent study I discuss in the interlude surrounding figure 1 shows that this is the case, though):

• control group (C): sedentary, no diet

• exercise group (E): 25, 30, 35, 40min at intensities of 60, 65, 70, 56% of the calculated HRmax (intensity and duration were increased in week 4, 7 and 10)

• alternate day fasting group (ADF): after 4-week controlled feeding period the study concluded with an 8-week self-selected feeding period.
  

  

  As long as study subjects just have to eat what scientists serve them, every diet works. When they are however told to eat a high protein diet, for example, even the reported nutrient intake diverges massively from what the scientists had in mind, when they devised the protocol - you don't believe me? Well, then read for yourself, "What Really Happens, When Science Meets the Real World"

  "During the controlled feeding period (week 1-4) participants consumed 25% of their baseline energy needs on the "fast day” (24 h) and consumed food ad libitum on each "feed day” (24 h). [...] The diet consisted of a 3-day rotating menu plan, and all fast day meals were prepared in the metabolic kitchen of the Human Nutrition Research Unit (HNRU). Fast day meals were consumed between 12.00 pm and 2.00 pm to ensure that each subject was undergoing the same duration of fasting.[...] During the self-selected feeding period (week 8-12) subjects continued with the ADF regimen but no the fast day food was provided to them. Instead, each subject met with a dietician at the beginning of each week to learn how to maintain the ADF regimen on his or her own at home." (Bhuatin. 2013)

  During the counseling sessions the participants were also instructed to make (I quote) "healthy foodchoices on the ad libitum feed days by choosing low fat meat and dairy options and
  increasing fruit and vegetable intake." (Bhutani. 2013)

• combination group (ADF + E): combination of alternate day fasting and exercise protocol

Table 1: Nutrient composition of the fast day diet provided to the combination and ADF groups (Bhutani. 2013)

So, as you've learned from the above overview this was no "alternate day fast", as I had expected it to be, when I read the term "Alternate Day Fasting (ADF)" in the abstract of the study. With 450kcal/day and a nutrient composition providing 50% of the energy in form of carbohydrates, and 25% (each) from fat and protein the "fasting days" were characterized by a low caloric intake (see table 1), but should not have triggered a similar starvation response as the classic alternate day fasting regimen in a recently published rodent study by Kamur et al. from which the data in figure 1 is derived.

Let's briefly take a look why "real" alternate day fasting may not be a good idea

As you can see the effect of the alternate day fasting regimen in the Kumar study, in the course of which the rodents simply did not receive any food for a whole day, had profound negative effects on the hypothalamo-gypophysial-gonadal axis - especially in the female rodents.

Figure 1: Effects of every-other day fasting vs.ad libitum feeding on ovarian weight, estradiol, lutenizing hormone, leptin, and testosterone in female and male rodents (Kumar. 2013)

Now the first thing that will jump your eye is certainly the profound increase in serum estrogen in the IF group. Looks strange and certainly not anywhere near what you would have expected right? If you think that this cannot be that bad, you are probably a man, is that right? I see... so what really is bad about the estrogen explosion is actually that it is "living proof" of the total disruption of the cyclic interplay between estrogen and progesterone that's at the heart of female (in-)fertility (on a side note: the male rodents simply got skinny fat on that regimen).

Now why didn't these adverse events occur in the study at hand?

Actually I am only assuming that there were not similar negative effects in the study at hand. After all, we don't have the respective hormonal and even in the rodents it took it's time (2 cycles) until the females were totally infertile. Changes like these would thus probably have gone unrecognized. I do however suspect that the major factors contributing to the overall hormonal decline in the rodent study were the extendended time-span without food and the overall caloric deficit, which is usually ~30-40% of the habitual intake in rodents on alternate day fasting regimen, as they do not compensate for the fasting day on the subsequent day.

Figure 2: Changes in body composition in the combined, ADF, exercise and control groups (Bhutani. 2013)

With the extended fast being absent and a ~75% reduction in calorie intake on the fasting days, only (humans are unfortunately much better in "compensating" for a lack of food on a fasting day, anyway ;-) and the huge amount of adipose tissue the rodents in the Kumar study obviously did not have as an "emergency reserve", it is therefore unlikely that the beneficial changes in body composition Bhutani and his colleagues observed in their 64 subjects (see figure 2) were accompanied by hormonal deteriorations (although 61 of them were, as previously mentioned, female).

Figure 3: Changes in lipid profile (left) and glucose metabolism in the combined, ADF, exercise and control groups (Bhutani. 2013)

It is nevertheless interesting to see that there were no significant improvements in fasting glucose, insulin or HOMA-IR (the measure of long-term blood glucose levels; not shown in figure 3) in any of the groups. Moreover, the improvements in total LDL and HDL cholesterol were only significant in the combined group and that the total amount of the inflammatory marker CRP remained essentially the same in all four arms of the 12-week intervention study.

Image 2: Ramadan fasting can serve as a relatively well studied "model" of intermittent fasting. With the additional restriction of water intake and the common practice of rising early to have breakfast there are yet non-negligible differences. You can find more information about the strengths and limitations of this model in Part 2 and Part 3 of the IF series.

A brief reminder for everyone who missed the Intermittent Thoughts on Intermittent fasting series back in the day: If there is one thing we can take away from studies investigating the effects Ramadan fasting (a Muslim fasting ritual, where you eat only when the sun goes down) it is that eating the same amount of food at different times of the day alone is not going to make you lose weight. If you do intermittent fasting in order to lose weight you still have to achieve a caloric deficit. Plus, when you are doing it during a bulk, I personally suspect that you are more likely to gain body fat, simply because your body cannot make "good use" (=muscle glycogen and skeletal muscle protein) from all the food you will be cramming down in a small fasting window. So, if you insist on IF on a bulk, do at least increase your feeding window to 8h to be able to spread your energy intake more evenly.

Based on a comparison of the data from all three groups, we can yet also conclude that it is the alternate day fasting (or probably rather the caloric deficit) that exerts the beneficial effects on what the scientists subsume under the umbrella term "CHD risk indicators":

"the combinationof ADF plus exercise decreased LDL cholesterol (12% from baseline) while increasing HDL cholesterol (18% from baseline); a change that was not noted for any other intervention. The combination group also experienced an increase in LDL particle size, and a  reduction in the proportion of small LDL and HDL particles." (Bhutani. 2013)

Only later in the discussion of their results do they mention that those "CHD risk indicators" improved to the same extend in the ADF only group - with even more significant changes in the particle profile.

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Learn why breakfast is probably not the "most", but rather the least "important meal of the day" (read more).

Bottom line: The weight and fat loss are certainly intriguing. The regimen appears to be reasonably easy to follow and the fact that the improvements in glucose metabolism were marginal could well be related to the fact that the subjects were - despite being seriously overweight (!) - not diabetic.

Keeping all that in mind I am still not convinced that a regular intermittent fasting routine (16-18h fasting window on every day; learn more about intermittent fasting here at the SuppVersity) and a combined aerobic + strength training regimen would not have yielded even superior results. The average physical culturist probably will be better of with this by now almost "classic" diet routine.

References:

• Bhutani S, Klempel MC, Kroeger CM, Trepanowski JF, Varady KA. Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans. Obesity (Silver Spring). 2013 Feb 14.
• Kumar S, Kaur G. Intermittent Fasting Dietary Restriction Regimen Negatively Influences Reproduction in Young Rats: A Study of Hypothalamo-Hypophysial-Gonadal Axis. PLoS ONE. 2013; 8(1): e52416. 

No Pain no Gain? What Can We Learn From the Time Course of Muscle Damage After Eccentric Workouts. Plus: What's that Got to Do With Your Doctor Sending You to the ER

Concentration curls are among those exercises, where eccentrics can easily be incorporate. Plus. As the EMG Series shows, this increases the biceps activity by almost 50% compared to the regular barbell curl (learn more). But will it also make you grow faster?

Just let me get this straight right away: I am well aware that it is still debated if and if so to which extend skeletal muscle damage affects or even determines the training induced gains in strength and/or lean body mass and it is not my intention to rekindle this never-ending debate. At least in my humble opinion, it does yet appear that a certain degree of "damage" is necessary for "optimal" gains. Anything that passes this threshold is however, as Schoenfeld points out in what I believe is the most recent review of the literature, not going to "further augment muscle remodeling and may in fact interfere with the process" (Schoenfeld. 2013).

The potential of negative interference is obviously particularly pronounced, when the the potentially muscle damaging physical activity is performed during the recovery phase. But how long it going to take until the repair and restructuring processes are completed?

In other words: How long would be optimal rest interval for someone who trains really intense with a focus on eccentric overload? 
 
At first sight it seems as if the results of a recent study from the State University of Campinas should help us to bring light into the darkness, but as we are soon going to see, things are (once again) more complicated than common sense would tell us.

The main intension of the researchers was to (I quote) "observe the time course of muscle damage and inflammatory responses to resistance-training with EO [eccentric overload]" (Neme Ide. 2013). To this ends, they recruited 3 women and 5 men in their early twenties who had at least one year of previous strength training experience and had them perform a standardized workout program with the following parameters:

No idea how to schedule your workouts? Learn how to do that and much or in the Step By Step Guide to Your Own Workout Routine!

• total duration: 13 sessions (total) distributed evenly across 7 weeks; 2x full body workouts trained every Tuesday & Thursday

• set & rep scheme: 4 sets of 8 reps at 80% of the 1-RM max for eccentrics; since that's more than you can "lift", i.e. move concentrically, the researchers who supervised the sessions had to help the participants on the eccentric part of the movement

• exercises: classic full body workout consisting of bench presses, 45-degree leg presses and bent-over rows

The blood samples were taken 96h after training session 2, 7, 9, 11 and 13, respectively and the creatine kinase, CRP and various hematological parameters were measured to evaluate the impact the eccentric workouts had on ...

• muscle damage - indicated by the amount of creatine kinase (CK) that leaked from the musculature into the blood,

• overall inflammation - indicated by the change in C-reactive protein (CRP) levels, 

• hemtaological paramaters - including red blood cell count (RBC), hemoglobin concentration (Hb), hematocrit (Ht), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), erythrocyte distribution width (RDW), white blood cell (WBC) count, lymphocyte (LYNF) count, neutrophil (NEUTR) count, and platelet count (PLT).

The reasoning behind the constant monitoring of CK, CRP and blood parameters was that the scientists expected that there would be an attenuation of the damaging effects of the workouts as the participants bodies got accustomed to the bi-weekly torture.

Don't let your Dr send you to the ER without letting him know that you trained the day before you got your latest bloodwork done.

If you take a look at the creatine kinase (CK) data I plotted in figure 1 (left) there are two things you should take a mental note of. Firstly, the increase in creatine kinase is "exorbitant" and could - assuming your doctor either doesn't know you are strength training or has no clue about the effects a heavy workout can have on the amount of the enzyme that "recycles" creatine into pohosphocreatine (PCr) that's floating around in your blood stream - be enough to have your physician send you to the ER - misdiagnosis: rhabdomyolysis (please bear in mind that Kraemer et al. (2004) suggest a reference interval for physically active subject of 1,309U/L; that's almost 4x more than the regular lab range that usually says everything past 400U/L would be pathological)

Figure 1: Creatine kinase (CK) levels (left) and C-reactive protein (CRP) levels (right) at different timepoints of the 7-week exercise intervention (Neme Ide. 2013)

And secondly, this increase in creatine kinase is hard to predict and varies from subject to subject (the numbers in the upper line of the label of the horizontal axis are the subject numbers):

"CK and CRP presented significant changes at specific time points, but not for all subjects. Four subjects presented significant changes in CK activity at P2 (+1719%, +1250%, +1281%, and +312% resp.), and other two at P13 (+391% and +139%, resp.). For CRP six subjects presented significant changes at P2 (+1100%, +243%, +3800%, +2500%, +1400%, and +2400%, resp.), one at P4 (+567%), other at P9 (+3200%), three at P11 (+300%, +3400%, and +3900%, resp.), and other at P13 (+1500)." (Neme Ide. 2013)

Interestingly, there was no significant correlation between the changes in creatine kinase (CK) and C-reactive protein (CRP) as you would expect if muscle damage and systemic inflammation went hand in hand.

Accommodation? yes! Unequivocal results? No.

Despite the fact that the expected pronounced initial CK response was present only in four out of the eight individuals, the scientists are confirmed that the data they gathered does support their initial hypothesis that there would be an attenuation of muscle damage in the course of the 7-week study period and ascribe the latter to the repeated bout effect a term, scientists use to refer to the protective effects a single bout of eccentric exercise has on the muscle damage during subsequent bouts (Mc Hugh. 2003).

"The potential adaptations that explain the phenomena have been categorized as neural, mechanical, and cellular. Regarding the cellular adaptations there is evidence of longitudinal addition of sarcomeres and adaptations in the inflammatory response following an initial bout of eccentric exercise, limiting also the proliferation of damage." (Neme Ide. 2013)

While a similar trend was observed for the CRP levels, the initial increase of the latter was by far less pronounced than for the CK values, so that the levels remained within the physiological norm for active people (the average CK values, on the other hand, were 2x elevated over the already high reference interval for physically active individuals).

Changes in hematological parameters were the exception

In case your workout program looks anywhere like Adelfo's Overkill Program from April 2013, you better make sure to come up with a new one after no more than max. 3-4 weeks!

If we acknowledge the reasoning Plaisance and Grandjean present in their 2006 review of the literature and take the comparatively low exercise related increases in C-reactive protein levels (CRP) as an indicator of damage in non-skeletal muscle tissue, it is also not surprising that this unquestionably intense and obviously muscle damaging exercise regimen did not have more pronounced effects on the blood panel of the study participants.

Only two subjects presented significant changes in neutrophils with an unpredictable up and down for subject 7 and a significant 60% increase after the final session in subject 6. In view of the fact that subject 7 was also the only one with detoriations in almost all other blood parameters, it's yet pretty unlikely that this was a result of the workout protocol and not the result of some sort of infection or whatever.

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Ok, so what exactly have we learned now? This is actually a pretty good question. I guess one thing we have learned is that physically active individuals can actually shock their doctors with "exorbitantly" high (yet still normal) creatine kinase levels. This does not mean that you can simply ignore constantly elevated / abnormal CK values, but it's important to realize that the 400U/L range your lab report lists is probably not sufficient for your personal CK values if you get blood drawn in the vicinity of a hard workout (on a related note: especially when you are low-carbing and eating high amounts of protein the increase in CK usually goes hand in hand with increases in the "turn protein to energy" enzymes AST and ALT, which are in this case not necessarily indicative of "liver damage").

There is evidence that the expression of the local factions of IGF-1, MGF & Co., depends on the exercise induced wear and tear  (learn more), it would be stupid to assume that there was no turning point at which the beneficial damage turns against you.

What we unfortunately didn't learn (and I feel that the scientists really missed out on this opportunity) is what the underlying reasons of the differential CK response to the workout may have been. Would it really have been too difficult to ask the "non-responders" what kind of exercise protocol (including set + rep schemes, frequency, weights and exercises) they had been following before they enrolled in the study? I don't think so. In fact, I would rather argue that it would have been obligatory. For me, for example, the eccentrics would have been the only novel stimulus in this workout. I have however been training with a female friend of mine a couple of days ago who would certainly qualify as having been training for at least a year and following a training program consisting of 3–5 sets of 6–12 repetitions with 1-2-minute rest interval between sets, performed 4-5 times per week (these were the inclusion criteria for the study at hand), for whom all of the exercises would have constituted a whole new stimulus in and out of itself (she usually works out on those fancy machines).

Now this may be a pity, but int the end, the differential CK response could have been totally irrelevant anyway. The pertinent evidence from human studies may be more than scarce, but if we go by the few studies we have, it appears that even a 5x higher CK response to eccentric exercises as it was observed in the non-preconditioned group in a 2011 human study by Flann et al. does not result in significantly different increases in either muscle size, or strength (cf. figure 2).

Figure 2: Strength and hypertrophy (left) and creatine kinase (CK, right) response in pre-trained and naive individuals in the course of an 8-week eccentric training protocol (Flann. 2011)

The fact that Neme Ide et al. did not measure the strength and/or hypertrophy response, still baffles me. I do however believe that (most) scientists are not just clever, but also very rational beings and therefore I would suspect that there is soon going to be a follow-up paper with the respective data. Why's that? Well, in a scientific community, where the number of publications is unfortunately more important than their quality, tricks like these may eventually give you the edge over the competition on your next job application ;-/

References:

• Flann KL, LaStayo PC, McClain DA, Hazel M, Lindstedt SL. Muscle damage and muscle remodeling: no pain, no gain? J Exp Biol. 2011 Feb 15;214(Pt 4):674-9.
• Kraemer WJ, French DN, Paxton NJ, Häkkinen K, Volek JS, Sebastianelli WJ, Putukian M, Newton RU, Rubin MR, Gómez AL, Vescovi JD, Ratamess NA, Fleck SJ, Lynch JM, Knuttgen HG. Changes in exercise performance and hormonal concentrations over a big ten soccer season in starters and nonstarters. J Strength Cond Res. 2004 Feb;18(1):121-8.
• McHugh MP. Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports. 2003 Apr;13(2):88-97. R
• Neme Ide B, Alessandro Soares Nunes L, Brenzikofer R, Macedo DV. Time course of muscle damage and inflammatory responses to resistance training with eccentric overload in trained individuals. Mediators Inflamm. 2013;2013:204942.
• Schoenfeld BJ. Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy? J Strength Cond Res. 2013 May;26(5):1441-53.

Review Claims: CLA & Fish Oil Improve "Anabolic" Effects of Exercise - What Does the SuppVersity Sniff Test Say?

A bigger biceps and less body fat to cover your precious gains? At least for CLA this has in fact been observed in a human study (see figure 1).

About two weeks ago, I stumbled across an interesting paper that had just been published in the peer-reviewed journal Nutrients, filed it and got so much to do that I would almost have forgotten about it. When I was just thinking about which topic to address next, I did yet remember the auspicious conclusion to the abstract, which says "we can hypothesize that fat supplements may improve the anabolic effect of exercise." (Macaluso. 2013). "May" and "hypothesis", those are terms I like and since fish oil and CLA were implicated in the previous lines, I suppose you are going to like it as well. So what would be more obvious than to apply the "SuppVersity Sniff Test" (I am beginning to like this term, Carl often uses on the Science Round-Up) to this ostensibly well-researched review of the literature?

"May improve the anabolic effect of exercise"

Usually things that "may" do just that, namely "improve the anabolic effect of exercise" end up in a pricey and useless testosterone booster.

Check out the overview of the Intermittent Thoughts on Building Muscle and learn how testosterone, growth hormone, IGF-1, mTOR and the rest of the pack orchestrate skeletal muscle hypertrophy and why boosting your testosterone levels from mid will not translate into visible muscle gains (read more)

Personally, I don't know of any test booster though, which boasts that fish oil or CLA were it's main ingredients and without taking away too much of the results of this sniff test, I can already tell you that there is a good reason for why this is the case: It's even less likely to produce significant effects than the next best herb that "grows but in one place" in the Amazonian rain forest, where the CEO of company X harvests it at the hazard of his own life... ah, you know that spiel, so I don't have to repeat it here.

If you take a look at the tables the researchers provide as part of their review and have basic mathematical and reading skills, it's not difficult to count the number of which would remotely support the notion that fish  or CLA supplementation have any effects at all: It's 5 out of 9 for fish oil and 4 out of 7 for CLA. Certainly reason enough to "hypothesize" a bit.

Fish oil is good for your heart, but not for your physique

In the next step we need a little more than to identify those studies with the "no effect" label from the tables and take a the ones we were left with after our initial glance at the data. If we do just that the number of studies we have to look at decreases from 9 to 4 studies, as none of the fish oil studies survives the "Sniff Test", after all, neither

• 

  They probably ain't anabolic either, but could help you to stay lean on a bulk: DHA-phospholipid, as you would find them in krill vs. common fish oil supplements (learn more).

  improved cardiovascular function in the absence of increased endurance performance or recovery in football players (Buckley. 2009)

• a minimal reduction in O2 cost in the absence of effects on the endurance performance in cyclists (Peoples. 2008), 

• improvements in VO2max in previously sedentary men a non-placebo-controlled study (Brilla. 1990)

• a reduced acute phase inflammatory response in a non-randomized non-placebo controlled intervention with average Joes (Ernst. 1991) 

would qualify as convincing evidence for any "anabolic effects" - in fact, even if we were talking about ergognenic effects in general, only the study by Guezennec would survive 2nd phase of the Sniff Test.

Now, what's interesting about the Guezennec study, though, is that the "beneficial" effects (a profound decrease red blood cell deformability; RCD) were hypoxia specific and could easily turn against you. After all, one of the reasons athlete "train high and compete low" (meaning they train at high altitudes with less oxygen in the air and thus hypoxic conditions to outperform the competition at sea level) is that this will increase the production of red blood cells. Now guess why that happens!? Correct! It's a result of the hemolytic effect of hypoxic training... now, what will happens if you copy the 6g /day EPA-max supplementation regimen of the 19-38 years old guys in the Guezennec study? Right, this effect will be absent. I wouldn't go so far and call this "ergolytic", but you could certainly make a point that huge amounts of EPA are - at least in this scenario - anti-ergogenic.

So what about CLA, then? Isn't that simply a fat burner

So, if even the widely hailed fish oil has little data to support its usefulness as an ergogenic supplement for athletes and aspiring physical culturists, what about CLA, then? I mean, we all know that the benefits researchers observed in human trials were miles apart from what they had expected to happen based on previous experiments in rodents (click on the image to the right to be redirected to a study, where the CLA treated ice dropped 77% body fat and did nevertheless display statistically significant increases in endurance capacity).

Adequate dosing still remains an issue

These discrepancy in terms of the body fat reducing effects of conjugated linoleic acid supplementation, as Dilzer and Park pointed out only recently, at least in parts a result of insufficient doses:

In July 2013 I wrote about what I believe is the unquestionably most impressive study on the fat burning and endurance enhancing effects of conjugated linolic acid. 77% body fat reduction - that's bordering lipodystrophy. The dosage used in this study would be roughly equivalent to 30g/day for human being and supports the notion that profound effects are only observed with amounts of CLA that have yet not been administered to humans in controlled trials (learn more)!

"Studies with mice used diets containing 0.5 w/w%* CLA, which is equivalent to about 56 g CLA/day/70 kg (Malpuech-Bruger. 2004). Most human studies used CLA doses ranging between 0.7 g and 6.8 g per day, which is lower than doses used in mice." (Dilzer. 2013)

*Addendum: Anonymous pointed out correctly, that the figures in the above quotation (which is dirertly from the FT) are inconsistent. 0.5% would be only 5.6g. I guess that's a typo in the Dilzer study, because the Malpuech-Bruger study they reference says "a daily intake of 0.70 g/kg body mass was effective in mice". (Malpuech-Bruger. 2004) - sloppily as they are, they don't say that this is already in human equivalents, though. That becomes clear in the next sentence only, which says "A value of 0.70 g/kg body mass in humans would correspond to a daily intake of 56 g of CLA." (ibid.) The July 2013 study I reference under the image to the right used a HED of ~30g (learn more), so even if the exact figures are questionable, the argument obviously still holds.

Since the same goes for studies investigating the "anabolic" effects the abstract to Macaluso et al.'s review explicitly mentions, chances are that increases in endurance performance, as they were observed in the previously mentioned rodent study (read the full story, here), were likewise species or at least dosage specific.

Is CLA "anabolic" or at least ergogenic?

If we take a look at the 7 studies the researchers included in their review (I guess you will be hard-pressed to find more than those seven, as CLA is not exactly the typical supplement researchers use as an ergogenic), we can easily exclude three of them. In these studies that were conducted on healthy young women, trained male bodybuilders and physically active men and women, supplementation with 3g, 6g and 3.9g/day of CLA did exactly nothing.

This leaves us with a set four studies to take a closer look at - three of them report improvements in body composition, two of them also observed increases in endurance performance and a single one even found "slight increases in testosterone":

• Improvements in body composition were observed by Thom (2001), Colakoglu (2006) and Pinkonski (2006); all studies were placebo controlled and the participants were physically active or at least healthy men (only in the Thom study) and women who consumed 1.8, 3.6 and 5g of CLA per day.
  
  While the former two studies by Tho and Colakoglu used exhaustive and medium intensity endurance programs, the study by Pinkonski et al. used a stardardized full-body workout with 12 exercises ranging from leg presses, bench and shoulder presses, to lat pull downs, biceps curls, and some core exercises. Each exercise was performed three times per week consisting of 3–4 sets of 4–10 repetitions at approximately 75–90% of one-repetition maximum (1RM).

  

  Figure 1: Relative changes in body composition biceps and quadriceps size and strength parameters after 7 weeks of serious strength training with or without 5g of CLA per day (Pinkoski. 2006)

  This protocol and the high number of study participants (76 men and women) and their training status - the majority had more than 2 years of weight training experience under their belts - make the results of the Pinkoski study so interesting for us. The results, on the other hand (cf. figure 1), are not exactly earth shattering, especially in view of the fact that only the fat loss and the increase in biceps size reached statistical significance and that despite a pretty high number of participants. Whether or not CLA really is "anabolic" and not "just" a mediocre fat burner has thus still to be determined.

Figure 2: Increases in cortisol (top) and testosterone (bottom) and respective increases in lean body mass in response to a 12-week hypertrophy oriented resistance training program (West. 2013)

• Increases in testosterone, as Macaluso et al. observed them in 10 "physically active" male subjects (age, 27.4) in a previous study in response to 6g CLA per day, on the other hand, would probably qualify as "anabolic" if the latter had not been measure right the workouts, as part of a short 3-week study with no corresponding effects on body composition (Macaluso. 2013).
  
  The latter should actually not come as a surprise to any seasoned SuppVersity student. After all you've learned that (1) endocrine induced changes in body composition take their time in the Intermittent Thoughts on Building Muscle, that (2) the role of  testosterone levels in the normal range in the whole process is fundamentally overrated and (3) that the seminal paper by West & Phillips, on which the data in figure 2 is based, clearly refutes the notion that post-workout increases in testosterone have any impact on skeletal muscle hypertrophy.

If we also take into account that numerous rodent studies do in fact support the notion that CLA posses "ergogenic",  yet not necessarily "anabolic" qualities. Macaluso et al. are certainly correct, when they conclude their paper with the scientific equivalent to "And they lived happily ever after" stating that "additional research".

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Milk from pastured cows has a relatively high amounts of both, CLA and DHA + EPA. The absolute amounts are however so low that you would probably have to drink more than the notorious gallon of milk per day to see any effect - and let's be honest, even if CLA + DHA make a good fat burner, the gallon of milk certainly makes a better weight gainer ;-)

Bottom line: I guess, you'd like to hear a supplement recommendation now, right? Well, as far as ergogenic and/or anabolic effects are concerned, CLA is unquestionably the more promising fatty acid off the "two" (actually we are talking about four fatty acids, here: DHA + EPA = fish oil and cis-9,trans-11 and trans-10,cis-12 CLA). CLA's anti-PPAR-gamma effect, which is probably responsible for the reductions in insulin sensitivity and detoriations of the lipid metabolism that have been observed in numerous studies (only trans-10,cis-12 CLA), is probably not so much of a problem for lean, physically active people and the upside of the PPAR-gamma blockade is a reduced rate of fat storage....

Ah, you see I am diverting to the fat loss effects again. And if we are honest, the results of this review do actually only confirm that what you've read here at the SuppVersity roughly 3 months ago the combination of CLA + DHA could turn out to be a safe and effective fat burner (learn more), if we would finally see adequately doses, long(er) term supplementation trials in humans.

As ar as the "anabolic" nature of either of them, i.e. EPA + DHA or cis-9,trans-11 and trans-10,cis-12 CLA. The jury may still be out there, but the verdict is - at least in the case of regular fish oil almost certainly "not guilty", .. ah I mean, "not anabolic".

References:

• Brilla, L.R.; Landerholm, T.E. Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. J. Sports Med. Phys. Fitness 1990, 30, 173–180.
• Buckley, J.D.; Burgess, S.; Murphy, K.J.; Howe, P.R. DHA-rich fish oil lowers heart rate during
  submaximal exercise in elite Australian Rules footballers. J. Sci. Med. Sport 2009, 12, 503–507. 
• Colakoglu, S.; Colakoglu, M.; Taneli, F.; Cetinoz, F.; Turkmen, M. Cumulative effects of conjugated linoleic acid and exercise on endurance development, body composition, serum leptin and insulin levels. J. Sports Med. Phys. Fitness 2006, 46, 570–577.
• Dilzer A, Park Y. Implication of conjugated linoleic acid (CLA) in human health. Crit Rev Food Sci Nutr. 2013;52(6):488-513.
• Ernst, E.; Saradeth, T.; Achhammer, G.  n-3 fatty acids and acute-phase proteins.  Eur.  J.  Clin.
  Invest. 1991, 21, 77–82.
• Guezennec, C.Y.; Nadaud, J.F.; Satabin, P.; Leger, F.; Lafargue, P. Influence of polyunsaturated fatty acid diet on the hemorrheological response to physical exercise in hypoxia.  Int.  J.  Sports Med. 1989, 10, 286–291.
• Lenn, J.; Uhl, T.; Mattacola, C.; Boissonneault, G.; Yates, J.; Ibrahim, W.; Bruckner, G. The effects of fish oil and isoflavones on delayed onset muscle soreness. Med. Sci. Sports Exerc. 2002, 34, 1605–1613. 
• Macaluso, F.M.;  Catanese, P.; Ardizzone N.M.; Marino Gammazza, A.; Bonsignore, G.; Lo Giudice, G.; Stampone, T.; Barone, R.; Farina, F.; Di Felice,  V. Effect of conjugated linoleic acid on testosterone levels in vitro and in vivo. J. Strength Cond. Res. 2013, 26, 1667–1674. 
• Macaluso F, Barone T, Catanese P, Carini F, Rizzuto L, Farina F, Di Felice V. Do Fat Supplements Increase Physical Performance? Nutrients 2013; 5:509-524.
• Malpuech-Brugère C, Verboeket-van de Venne WP, Mensink RP, Arnal MA, Morio B, Brandolini M, Saebo A, Lassel TS, Chardigny JM, Sébédio JL, Beaufrère B. Effects of two conjugated linoleic Acid isomers on body fat mass in overweight humans. Obes Res. 2004 Apr;12(4):591-8.
• Oostenbrug, G.S.; Mensink, R.P.; Hardeman, M.R.; De Vries, T.; Brouns, F.; Hornstra, G. Exercise performance, red blood cell deformability, and lipid peroxidation: Effects of fish oil and vitamin E. J. Appl. Physiol. 1997, 83, 746–752.
• Peoples,  G.E.;  McLennan,  P.L.;  Howe,  P.R.;  Groeller,  H. Fish oil reduces heart rate and oxygen consumption during exercise. J. Cardiovasc. Pharmacol. 2008, 52, 540–547..
• Peoples,  G.E.;  McLennan,  P.L.;  Howe,  P.R.;  Groeller,  H. Fish oil reduces heart rate and oxygen consumption during exercise. J. Cardiovasc. Pharmacol. 2008, 52, 540–547. 
• Pinkoski, C.; Chilibeck, P.D.; Candow, D.G.; Esliger, D.; Ewaschuk, J.B.; Facci, M.; Farthing, J.P.; Zello, G.A. The effects of conjugated linoleic acid supplementation during resistance training. Med. Sci. Sports Exerc. 2006, 38, 339–348.
• Thom, E.; Wadstein, J.; Gudmundsen, O. Conjugated linoleic acid reduces body fat in healthy exercising humans. J. Int. Med. Res. 2001, 29, 392–396.
• Toft, A.D.; Thorn, M.; Ostrowski, K.; Asp, S.; Moller, K.; Iversen, S.; Hermann, C.;  Sondergaard, S.R.; Pedersen, B.K. N-3 polyunsaturated fatty acids do not affect cytokine response to strenuous exercise. J. Appl. Physiol. 2000, 89, 2401–2406.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2013 Jul;112(7):2693-702. 

Light Weights, Low Oxygen: Hypoxia & Vascular Occlusion Training Yield Similar Increases in Neuromuscular Activation & Maximal Voluntary Force Generation in Female Athletes

The left part of the image shows what scientifically proven hypoxic training looks like. You wear a mask with an exogenous supply of low oxygen air. The right part of the image shows you what the fitness industry will try to sell you as "hypoxic training". That being said, did you know that at least the left version could also help you shed 11%% of your body fat in three weeks (learn more)?

Based on the feedback I got on the mini-summary of the latest review on "Kaatsu" aka blood flow restricted training I posted as part of last Monday's Exercise Science Round Up, I gather that many of you will be interested to hear about the results of a pertinent experiment that has been conducted only recently at the Lincoln University in Christchurch; New Zealand (Manimmanakorn. 2013).

To elicit, whether a combination of resistance training and vascular occlusion would modify the patterns of muscle activation, the development of muscle strength and hypertrophy, and whether these effects could be replicated by training under hypoxic conditions, the scientists who were involved in this research recruited 30 female netballers (age 20.2 ± 3.3 years, height 168.4 ± 5.8 cm; body mass 65.2 ± 6.5 kg, mean ± SD).

Ladies, hold your breath ;-)

The women were in their pre-competition training phase, and matched on their netball ability (had equal training volume, and were trained by the same physical conditioner). They were randomly assigned to either hypoxic training (HT), vascular occlusion (=Kaatsu; KT) and control training (CT) and had them perform bilateral knee extensions and flexions from 0 to 90° on a regular leg extension machine.The detailed experimental protocol for the three groups looked like this:

If you don't intend to suffocate yourself or at least your leg muscles, but still have (for whatever reason) to use lighter weights, you may be interested in another recent study, which was able to show that ballistics lunges activate muscles to the same extent as 34% lighter standardlifts and that this effect can be improved by using elastic band & dumbbells (learn more)

"During each set of knee extensions and flexions, participants in the HT group received normobaric hypoxic gas from a face mask via a hypoxicator system . The fraction of inspired oxygen (FIO2) was automatically adjusted by the hypoxicator using a biofeedback control system to maintain saturation of peripheral oxygen (SpO2) at *80 % (normal SpO2, approximately 99 %). The KT group performed training with restricted leg vascular blood flow in both lower limbs. During training, the pressure exerted by the Kaatsu cuffs (which were approximately 5 cm in width) at the root of the thigh,was gradually increased by 10 mmHg each day, starting from 160 mmHg at Day 1 going up to 230 mmHg at Day 8. The pressure then remained unchanged throughout the remaining of the training (Abe 2006). Heart rate and SpO2 were monitored by a pulse oximeter at the end of each exercise set. The CT group performed knee extension and flexion exercises with the Kaatsu cuffs on but not inflated (<5 mmHg) and breathed normal ambient room air." (my markups in Manimmanakorn. 2013)

In the course of the 5-week training period the participants completed three training sessions per week. Each training session consisted of three sets of knee extensions followed by three sets of knee flexions to failure (unable to complete the exercise successfully). The total number of sets was thus six, with 30s rest between sets and 2-min rest between exercises and a TUT (time under tension) of 1 0 1, which means that the women performed the exercise with a 1s concentric, 0 seconds rest at the top and a 1s eccentric contraction.

"Building strength with 20% of the 1-RM? You are kiddin' me, right?"

The resistance used was light - very light in fact: 20 % of the 1-RM. And as if that was not already light enough, the HT and CT groups of which the scientists expected that they would be able to perform more reps were advised to match the repetitions performed by the KT group "to ensure equal training load between groups" (during the tests the subjects were obviously required to perform as many reps as they could). Against that background, it's actually not surprising that there were no increases in any of the measured parameters in the control group:

Figure 1: Relative changes (in %) in the peak maximum voluntary contraction in 3 s,  area under the 30 s MVC curve,the number of repetitions able to be performed at 20 % 1-RM (left) and changes in surface electromyogram (EMG) amplitude (root mean square RMS %) during the Reps20 test before (pre) and after (post) 5 weeks training (Manimmanakorn. 2013)

As you can see in figure 1 the hypoxia training turned out to be the most effective if training methods - at least, if we go by the absolute increases in maximal voluntary contraction. The difference to the Kaatsu condition, however was trivial for all three parameters: The MVC3, the MVC30 and the total number of reps at 20% of the 1-RM.

The gym of the future a torture chamber or just an "old-school" gym in the basement?

Whether the gyms of the future will hand out cuffs at the door or "simply" have a low oxygen environment... wait a second: Now I know why all the strong guys train in these non-air-conditioned old-school gyms. It's to create a hypoxic environment, one of which the researchers say that it furthers "substantial increases in strength and endurance", which were "undoubtedly" brought about in part due to increased skeletal muscle hypertrophy.

Takarada et al. found that low inten- sity occlusion training can induce greater increases biceps CSA than regular high intensity training even in trained subjects (Takarada. 2000)

"However, indications of specific neuromuscular adaptation were also detected in the form of an increased EMG signal during the MVCs, particularly in the vascular occlusion group, indicating that increased motor unit activation probably also played a role in enhanced force production in these participants. Additionally, during a dynamic fatiguing exercise (Reps20) improvement in performance by the hypoxic and vascular occlusion groups post-training was in part due to improved efficiency of the force production machinery of the muscle." (Manimmanakorn. 2013)

Unfortunately, the actual increases in muscle cross sectional area (CSA) were not measured in the study at hand, but based on the findings of previous studies, which did report (in some cases) pretty impressive increases in CSA (see image next to the citation for one impressive example), I guess the scientists assumption that the ladies in the hypoxia and Kaatsu groups will also have gained more muscle than their peers is more than plausible.

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Looking for readily available intensity techniques? "Unleash the Neanderthal Within" with Adelfo Cerame's "Fav Five Intensity Techniques" (learn more)

Bottom line: Now, let's get back to the "gym of the future" - I am not yet convince that we are soon going to see the air being sucked out of the gyms, but I am more and more convinced that blood flow restriction, Kaatsu, vascular occlusion or whatever else you may be using to reduce the oxygen supply to the muscle and thus increase the amount of eu-stress (=beneficial stress, learn more), will probably become the "intensity technique" of the future - if not on a "whole gym level", then maybe in form of one or two of those neat cages (see image at the bottom of the article).

Whatever the future may hold, I still feel that it is very unlikely that Katsuu and hypoxic training with light weights are ever going to replace "regular" strength training completely. 

After all, working out should be more to you than just a means to develop sleeve bursting biceps. Honestly, if you seriously can say for yourself that you would not miss lifting heavy weights and would willingly content yourself with the knowledge that you should be able to do that, it's no wonder that you are clutching to any straw to finally make those gains you have been chasing for years.

Kaatsu training on methodological dope: Where is the level playing ground?"

You should also keep in mind that neither the study at hand, nor the previously mentioned and unquestionable impressive study by Takarada offered a level playing ground for the contestants, i.e. classic hypertrophy vs. Kaatsu or training in hypoxic conditions.

Is this how the gym of the future looks like? I guess, the results of the study at hand are still not enough to predict the future, but when I was looking for a nice video to go with this article, I found an ABC report that underlines that Victor Conte (yep, the "Balco guy") believes in the success of hypoxic training (watch video)

The "high intensity" condition in the Takarada condition prescribed training loads from 50-80% and would be considered "moderate" by the majority of muscle heads. Manimmanakorn study, on the other hand, the fact that the "HT and CT groups were then instructed to match the repetitions performed by the KT group to ensure equal training load between groups" (Manimmanakorn. 2013) is a major downside to its real world significance and makes me wonder what the ladies in the HT group could have achieved, when they would not have had to stop "before their time"...

... ah, and I don't have to mention that not having a high intensity group in the Manimmanakorn study reminds me of those sponsored pre-workout supplement studies, here the placebo is either plain water or simple sugar - when you want to prove something is superior to common practice you better test it against common practice or your data is of highly questionable practical value. 

References:

• Abe T, Kearns CF, Sato Y (2006) Muscle size and strength are increased following walk training with restricted venous blood flow from the leg muscle, Kaatsu-walk training. J Appl Physiol 100:1460–1466 
• Manimmanakorn A, Manimmanakorn N, Taylor R, Draper N, Billaut F, Shearman JP, Hamlin MJ. Effects of resistance training combined with vascular occlusion or hypoxia on neuromuscular function in athletes. Eur J Appl Physiol. 2013 Feb 15.
• Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000 Jun;88(6):2097-106. 

Magnesium vs. Diabetes - Which Form is Best? Exercise, Energy Intake & the HPTA. Glutamine & CHO For Sprinters & HIITers. Mercury & Diabetes, Amalgam, Se, Zn & Detox

Won't take long until China is the world economy #1 and not much longer until they are the fattest economy, as well ;-)

Let's see which one do I pick? Oh, ok... The SuppVersity Figure of the Week is 0.19. This is the correlation coefficient that describes the statistical relation - which is as every SuppVersity student knows no evidence of causal relationships (!) - between the per capita gross domestic product (GDP) and the prevalence of obesity as it was calculated by Mario Siervo and colleagues from the Newcastle University and the UCL Institute of Child Health in London as part of their analysis of country-specific prevalence estimates of overweight, obesity and hypertension and their relation to nutrient and food intakes and (and this is new!) the economy (Siervo. 2013).

The scientists used the WHO Global Infobase database, year- and country-specific Food Balance Sheets (FBS) and information on urbanization rates, per capita GDP and physical inactivity and did so much statistical shenanigan that of all the baseline correlations (incl. milk consumption and egg consumption, as predictors of obesity and high blood pressure) only the already mentioned per capita GPD, as well as physical inactivity (PA) and cereal consumption (CE) remained as highly significant predictors of being overweight (GPD), being obese (PA) and not being obese (CC). Statistical significant, but very low correlations were also observed for obesity and the relative energy intake from sugar (regression coefficient B = 0.03).

Makes me wonder what the addition of the average population-based magnesium intake would have had to contribute to the results... why? Well, the diabesity-protective role of magnesium is the first topic of today's installment of On Short Notice.

The importance of adequate magnesium intake can hardly be overestimated

The latest issue of the Journal of Nurtition (US) features yet another article showing how important adequate magnesium intakes are for an optimal glucose metabolism. Since a messed up glucose management it one of the root causes of most of the features of the metabolic syndrome, the results Adela Hruby and a ton of colleagues present in their latest paper are of great importance not just for individual, but also for public health. The latter is particularly true in view of the fact that the researchers who started out with the hypothesis that single nucleotide polymorphisms (SNPs ~= minimal genetic differences between person A and B) would explain / influence the potential differences of the association between magnesium intake and fasting glucose and insulin on an individual level.

It's not going to work for everyone but there is scientific evidence that 500mg/day magnesium can help with headaches (learn more)

To verify / disprove this hypothesis the researcher analyzed data from fifteen studies from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) Consortium . The studies provided data from up to 52,684 participants of European descent without known diabetes. In a fixed-effects meta-analyses, they quantified

1. cross-sectional associations of dietary magnesium intake with fasting glucose (mmol/L) and insulin (ln-pmol/L) and 
2. interactions between magnesium intake and SNPs related to fasting glucose (16 SNPs), insulin (2 SNPs), or magnesium (8 SNPs) on fasting glucose and insulin. 

After adjustment for age, sex, energy intake, BMI, and behavioral risk factors, the found that each  50-mg/d increment in magnesium intake was inversely associated with fasting glucose (β = −0.009 mmol/L, P < 0.0001) and insulin (−0.020 ln-pmol/L, P < 0.0001). Plus - and this is the actual news - these improvements (within a "normal" intake of magesium wa below the  2xRDA dose of 720mg) was not generally  related to the individual genetic make-up of the healthy stud participants.

However, rs2274924 in magnesium transporter-encoding TRPM6 showed a nominal association (uncorrected P = 0.03) with glucose, and rs11558471 in SLC30A8 and rs3740393 near CNNM2 showed a nominal interaction (uncorrected, both P = 0.02) with magnesium on glucose.

Now what's interesting, here, is that previous studies investigating the effects of familial TRPM6 polymorphisms showed that a mutation / loss of the former SNP, i.e. TRPM6, will disrupt the regular magnesium flux in the kidney and epithelial tissue an is accompanied by hypo- (=low) not hyper-(=high) glycemia (Schlingmann. 2003; Chubanov. 2005).

Are there other reasons you may be set to be obese (learn more)?

These observations, as well as results from a case-controlled study by Romero et al. who did not find gene variations in TRPM6 and its cousin TRPM7 to "be useful predictors for T2DM risk assessment" (Romero. 2010). Clearly point towards the negligent effects genes have on the magnesium <> diabetes connection. In other words: Keeping an adequate magnesium intake is one of the easiest ways to reduce your risk of developing type II diabetes regardless of your genetic make-up.

What's the best magnesium supp? Cap, tablet or powder? Oxide, citrate, lactate, ...?

Speaking of solutions, magnesium and glucose management - Did you know that no-calorie sweeteners disrupt early response to glucose ingestion, reduce GLP-1 expression and could thus promote overeating (learn more)

Although the urinary excretion of magnesium after the ingestion of equal amounts of magnesium oxide in the form of everescent tablets vs. regular powder-filled caps is not a direct quantitative indicator of tissue accumulation (t's still better than the serum mg / creatinine ratio; cf. Bøhmer. 1990), the +100% increase in this parameter Siener et al observed in 2011 with the former preparation is still good evidence for the superiority of the highly soluble tablet preparation (Siener. 2011).

In a similar study, Marcelín-Jiméne et al. found that the pharmacokinetics of a single 500mg oral dose of Mg-valproate 500-mg ingested eiher as a solution, suspension, or in form of enteric-coated tablets were identical (Marcelín-Jiméne. 2009). So, if we discard  the initial surge in magnesium with the solution an suspension that was absent with the enteric-coated tabs (they took ~2.5h to fully kick in)  it is probably not necessary that you crush your tabs to make a "crushed  tab magnesium suspension" out of them ;-)

I do yet suspect that you will probably be more interested in the results of one one of the most comprehensive evaluations of the consequences of chronic supplementation with different types of magnesium supplements, namely the inorganic magnesium salts MgCl2, MgSO4, MgCO3 and magnesium-acetate and their organic cousins in which the magnesium is bound to pidolate, citrate, gluconate, lactate or aspartate from a 2005 rodent study by Coudray et al.:

Figure 1: Plasma an bone (primary axis) as well as red blood cell (RBC; 2ndary axis(!)) content after 14 days of supplementation with identical amounts of magnesium in different organic and inorganic forms (Coudray. 2005)

Now regardless of which of these magnesium supplements you pick, one thing probably holds for all of them, if your levels are already saturated you will only increase the workload on your kidneys (Altura. 1994). Or put simply, if you pick one of the expensive versions such as mg-lactate the result is expensive urine (matches well with the tons of B-vitamins you hopefully peeing out and not retaining from your 12x overdosed "high potency B-supplement") - So, if you eat tons of magnesium rich foods already, save the money for more of those goods foods.

Review underlines the importance of adequate energy intake in reproductive function 

Figure 1: Reproductive hormone changes in exercising cynomolgus monkeys undergoing energy restriction (Williams. 2001)

Everyone who has read all parts ot the SuppVersity Athlete's Triad Series has hopefully absorbed the message that "under-eating" is the main reason for the endocrine disturbances in both men and women. The latter and the non-significance of cortisol outside of its function as a glucocorticoid (=hormone that does everything to keep your blood glucose from dropping) is also what Fuqua and Rogol emphasize in their latest review of the literature (Fuqua. 2013):

The data in figure 1, which shows parameters of the endocrine . function of female monkeys who were placed on a fixed caloric intake and then trained to run on a treadmill for increasing lengths of time, shows that after only 2 blocks, the reproductive function was totally lost (again, usually male mammals remain fertile, but often loss of libido, sexual dysfunction, as well as depression and the obvious weight loss and exercise performance plateaus are non-sex-specific).

As Fuqua et al. point out, the onset of amenorrhea was accompanied by  decreases in gonadotropins, estradiol, and progesterone. In that, the endocrine hormones are yet nothing but "slaves" to the changes in ghrelin, leptin and PYY, of which particularly the former, i.e. ghrelin suppresses pulsatile LH secretion in adult men and women. If you are interested in learning more, check out the Athlete's Triad Series, if you haven't done that already.

Glutamine & maltodextrin keep anaerobic power up to the last sprint

It wasn't part of the post of PWO glucose repletion, but theoretically glutamine could help here as well.

In an article that was published ahead of the next print issue of the Asian Journal of Sports Medicine Roohi and Khorshidi, two researchers from the Tehran University of Medical Sciences report that the ingestion of both 50 mg of maltodextrin and/ or 0.25g/kg body weight glutamine has significant ergogenic effects on repeated sprint performance.

What's interesting about this study is that the participants were all "well-trained physical education students who were participating in a training regimen (three or more days a week for at least an hour)" and not the next best sedentary volunteers the scientists were able to find (most importantly, they were not smoking water pipe - you got to love those cultural differences ;-)

As you can see in figure 2 the provision of the supplements two hours before the first of three RAST test, which consisted of 6x35m discontinuous all-out sprints, with 10 seconds rest between the individuals sprints (all six sprints are one bout), did yield ergogenic effects from the very first exercise bout on.

Figure 2: Minimal and maximal power on subsequent 6x35min sprints (1h in between bouts) with or without matlodextrin and/or glutamine supplementation 2h before the workout (Raahdi. 2013)

Statistical significant were yet only the difference between the placebo supplement (water) and the combined treatment during the third of the RAST tests. What's particularly interesting is the additive nature of the effects about which the Iranian researchers speculate that it could be "due to greater storage of carbohydrate in sites other than skeletal muscle, the most likely candidate being the liver" (Roohi. 2013), as well as glutamine's own role as a substrate for gluconeogenesis in the liver.

"Real world" evidence: Early exposure to mercury precipitates diabetes in man

From rodent studies, we already know that early mercury exposure increases the susceptibility to develop diabetes later in life. With the soon-to-be-published results from a prospective cohort of 3,875 American young adults who were 20-32 years old and free of diabetes in 1987, when the first data-set was acquired, the number of subjects who had abnormally high toenail mercury levels was extraordinarily high in the 288 incident cases of diabetes that occurred in the years up to the 18 years of follow-up.

Did you know that there is no correlation between amalgam fillings and Hg levels in the toe nails? At least according to a 2007 study by Björkman et al. who analyzed brain, blood, muscle and toenails of 30 deceased individuals the statistically non-significant correlation between the surface area of amalgam fillings and toenail mercury is even negative (meaning more fillings = lower Hg levels in the nails; Björkman. 2007). This is yet no reason to be relieved. In fact, it's rather the exact opposite: While the Hg levels in the toenails may have been low, the levels of the hardly less toxic inorganic mercury in the brain, as well as the total mercury concentrations in the pituitary and thyroid were significantly correlated with the surface area of amalgam fillings.

After adjustment for age, sex, ethnicity, study center, education, smoking status, alcohol consumption, physical activity, family history of diabetes, intakes of long-chain n-3 fatty acids, as well as serum magnesium, and toenail selenium levels the toenail mercury levels were still positively associated with the incidence of diabetes. With a probability of only 2% that we are dealing with a statistical outlier and an increased diabetes risk of 65% this provides another reason to give all mercury containing stuff an extra wide berth (He. 2013).

Against that background it appears to be all the more important to keep an adequate dietary intake of nutrients such as selenium and zinc, which have only recently been shown to useful adjuvants to a standard treatment of thiol chelator (DTT) regimen in a rodent model of acute mercury exposure (Deepmala. 2013) . The latter is obviously the extreme version of the slow, but constant onslaught of mercury most of us are exposed to, but our bodies' very own detoxification mechanism rely on the presence of adequate amounts of zinc (for the necessary metallothioneins; cf. Durnam. 1997) and selenium (for glutathion repletion; read more about selenium).

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Since these "Short News" got a little longish, I have just updated the facebook news with a couple of shorter items, influcing among others...

• 

  Man or woman, trying to build muscle or get ripped, always prefer whole proteins (and whole foods in general) over isolated nutrients. That this is particularly true for amino acids has been addressed in way more than the two most recent posts on the repartitioning effects of isoleucine and respective peptides in whey (learn more) and the related post "Don't Judge a Protein By Its Amino Acids" (read it) here at the SuppVersity

  EAA induced protein synthesis - Additional energy from carbohydrates or alanine does not increase protein synthesis beyond what 10g of essential amino acids alone will do (read more)
• Human data on ergogenic effects of fish oil "inconclusive" - Scientists also point towards problems with increased immunosuppression and prolonged bleeding times (read more)
• Probiotics for bone health -An exclusively male thing? At least in rodents their beneficial effect on bone density appears to be sex-specific (read more)
• Alternate day fasting and exercise make a perfect match - 2x higher weight loss exclusively from body fat and greater improvements in cholesterol particle distribution in the combination group (read more)

There are as usual more sort news for you to spend the hours to whatever you have planned for Saturday night, so I suggest you briefly surf over to www.facebook.com/SuppVersity check out the rest and comment and discuss the latest news. 

References:

• Altura BT, Wilimzig C, Trnovec T, Nyulassy S, Altura BM. Comparative effects of a Mg-enriched diet and different orally administered magnesium oxide preparations on ionized Mg, Mg metabolism and electrolytes in serum of human volunteers. J Am Coll Nutr. 1994 Oct;13(5):447-54.
• Björkman L, Lundekvam BF, Laegreid T, Bertelsen BI, Morild I, Lilleng P, Lind B, Palm B, Vahter M. Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study. Environ Health. 2007 Oct 11;6:30.
• Bøhmer T, Røseth A, Holm H, Weberg-Teigen S, Wahl L. Bioavailability of oral magnesium supplementation in female students evaluated from elimination of magnesium in 24-hour urine. Magnes Trace Elem. 1990;9(5):272-8. 
• Coudray C, Rambeau M, Feillet-Coudray C, Gueux E, Tressol JC, Mazur A, Rayssiguier Y. Study of magnesium bioavailability from ten organic and inorganic Mg salts in Mg-depleted rats using a stable isotope approach. Magnes Res. 2005 Dec;18(4):215-23.
• Chubanov V, Gudermann T, Schlingmann KP. Essential role for TRPM6 in epithelial magnesium transport and body magnesium homeostasis. Pflugers Arch. 2005 Oct;451(1):228-34. 
• Deepmala J, Deepak M, Srivastav S, Sangeeta S, Kumar SA, Kumar SS. Protective effect of combined therapy with dithiothreitol, zinc and selenium protects acute mercury induced oxidative injury in rats. J Trace Elem Med Biol. 2013 Feb 18. 
• Durnam DM, Palmiter RD. Analysis of the detoxification of heavy metal ions by mouse metallothionein. Experientia Suppl. 1987;52:457-63.
• Fuqua JS, Rogol AD. Neuroendocrine alterations in the exercising human: Implications for energy homeostasis. Metabolism. 2013 Feb 14.
• He K, Xun P, Liu K, Morris S, Reis J, Guallar E. Mercury Exposure in Young Adulthood and Incidence of Diabetes Later in Life: The CARDIA trace element study. Diabetes Care. 2013 Feb 19.
• Marcelín-Jiménez G, Angeles-Moreno AP, Contreras-Zavala L, Morales-Martínez M, Rivera-Espinosa L. A single-dose, three-period, six-sequence crossover study comparing the bioavailability of solution, suspension, and enteric-coated tablets of magnesium valproate in healthy Mexican volunteers under fasting conditions. Clin Ther. 2009 Sep;31(9):2002-11.
• Romero JR, Castonguay AJ, Barton NS, Germer S, Martin M, Zee RY. Gene variation of the transient receptor potential cation channel, subfamily M, members 6 (TRPM6) and 7 (TRPM7), and type 2 diabetes mellitus: a case-control study. Transl Res. 2010 Oct;156(4):235-41.
• Schlingmann KP, Waldegger S, Konrad M, Chubanov V, Gudermann T. TRPM6 and TRPM7--Gatekeepers of human magnesium metabolism. Biochim Biophys Acta. 2007 Aug;1772(8):813-21. Epub 2007 Apr 3. Review.
• Siener R, Jahnen A, Hesse A. Bioavailability of magnesium from different pharmaceutical formulations. Urol Res. 2011 Apr;39(2):123-7. 
• Siervo M, Montagnese C, Mathers JC, Soroka KR, Stephan BC, Wells JC. Sugar consumption and global prevalence of obesity and hypertension: an ecological analysis. Public Health Nutr. 2013 Feb 18:1-10.
• Williams NI, Caston-Balderrama AL, Helmreich DL, et al.Longitudinal changes in reproductive hormones and men-strual cyclicity in cynomolgus monkeys during strenuous exercise training: abrupt transition to exercise-induced amenorrhea. Endocrinology 2001; 142(6):2381–9