Pomegranate for Prostate, Rheuma, Breast Cancer, Aromatase, Obesity, Diabetes, Inflammation, HIV, Influenza, Herpes, Crohn's, Hepatitis, Infertility ... You Name It!

Image 1: This drawing from a German 1885 compendium on the flora in Germany, Austria and Switzerland shows that other than Acai & Co, pomegranate is no exotic (expensive and useless) discovery of some fly-by-night supplement vendor.

People are always all the rave, when some clever scientist (or should I say business man?) dug up another of those exotic fruit from a godforsaken valley somewhere in the African or South-American primeval forests. With the hype around ACAI & Co they often forget that there have been real Superfoods just around the corner, right in their local grocery store for years. Pomegranate, as it becomes increasingly evident from recent research, is one of these Superfoods - one that has even been mentioned in the Book of Exodus and has been part of the Ayurevedic tradition for centuries, now. While I have been following the research for some months now, the one mind-boggling study result has always been missing so that this is in fact the first blogpost in quite some time on the "seedy apple" ("pommum", lat. "apple" + "granatus", lat. "grain, seed").

To be precise, this is a post that was triggered by a Facebook message from Lothar, who informed me about the publication of the preliminary results of a phase II trial on the effects of pomegranate extract in prostate cancer prevention (Carducci. 2011).

In all of the 104 patients, whose PSA levels were on the rise after local therapy, the PSA doubling time, which, contrary to absolute PSA values, appears to be a more or less reliable indicator of cancer progression (Semenuik. 2006; Lee. 2005), lengthened by an average of +55% and that regardless of the dosage (1g vs. 3g) the patients received.

This result is unquestionably pretty impressive, it is, however, only part of the picture that has been emerging over the past years. Even if we only include selected studies from the last three months (!), we have to add at least the following health benefits

Image 2: If you consider this pomegranate seed trail long, then you will feel that the list of their health benefits is endless ;-)

• anti-rheumatic, anti-oxidant effect (Balbir-Gurman. 2011),
  reduction in the tender joint count by -62%; -25% reduced free radical-induced lipid peroxidation
• inhibition of glucose-uptake (Kim. 2011),
  -50% Na+-dependent glucose uptake at 424 μg/ml pomegranate extract
• anti-carcinogenic and pro-apoptotic effects (Dikmen. 2011),
  reduces profileration and induces apoptosis (programmed cell death) in breast cancer cells
• cardioprotective selective estrogen receptor modulator (Sreeja. 2011)
  the methanol extract of pericarp of pomegranate is an effective and cardioprotective SERM without some of the negative side effects of tamoxifen, such as increases in uterine weight and proliferation
• anti-obesity effect in diabetics (Gonzalez-Ortis. 2011)
  stops weight and fat gain in 20 obese diabetics
• potent anti-inflammatory (Faria. 2011)
  not limited, but specifically effective in suppressing the NFκ-B pathway
• promotes bone formation in fetus (Monsefi. 2011)
  when given as an extract to pregnant mice (no human data yet)
• antiviral properties (Su. 2011)
  against HIV-1, influenza, herpes, and poxviruses, and human noroviral surrogates
• protective effect against Crohn's disease (Rosillo. 2011)
  attributed to its ellagic acid content
• antioxidant and antiartherogenic effects (Haber. 2011)
  protects from hardening of the arteries due to plaque buildup
• ergogenic and anti-soreness effect (Trombold. 2011)
  pomegranate juice attenuates weakness and reduces soreness of the elbow flexor
• nephro- and hepaprotective effect (Cayir. 2011)
  pomegranate seed extract attenuates chemotherapy-induced acute nephrotoxicity and hepatotoxicity 
• protective against diet-induced obesity and diabetes (Vroegrijk. 2011)
  dietary pomegrenate seed oil ameliorates high-fat diet induced obesity and insulin resistance in mice, independent of changes in food intake or energy expenditure
• pro-fertility effect / protection against lead poisoning (Leiva. 2011)
  due to its antioxidant activity an ethanolic extract of pomegranate reversed the damage produced by lead acetate on spermatogenesis 
• oral antiplaque effect (Bhadhabe. 2011)
  pomegranate mouthrinse could be long-term antiplaque rinse with prophylactic benefits

to a still preliminary and yet already epic list of health-benefits of an ancient superfruit that is obviously not exotic and exciting enough to compete with the mostly useless, fancy-named herb and fruit extracts people are willing to spend millions of dollars on, year by year... ah, I forgot to mention: the ripe fruit also tastes damn good!

Ripped & Buffed vs. Skinny and Sinewy: Training Velocity, not Load, Appears to be Sole Determinant of Exercise Induced Shifts from Slow- to Fast-Twitch Muscle Fibers.

Image 1: Who would you like to be?
And how do you train to achieve
his physique?

Sprinter or marathon runner? Ripped and buffed or skinny and sinewy? Although this is, after all, a question of muscle vs. fat, bone and tissue mass, it is upon closer examination as much a qualitative question, as it is a quantitative one - a question that may well be influenced by the way you train!

Unlike our adipose tissue which has almost unlimited capacity to grow, the size of our muscles appears to limited by a number of factors, among which the individual fiber-make-up, i.e. the ratio of slow-oxidative endurance-type fibers (type I) to fast-twitch type IIA (fast-oxidative glycolytic), and fast twitch IIX (fast glycolytic) seems to play an important role, when it comes to getting big and buffed or skinny and sinewy.

Figure 1: Slow- and fast-twitch faber composition in athletes and non-athletes (data based on Carrol. 1998; Widrick. 2002)

As the data in figure 1 goes to show, athletes, unlike untrained individuals, who have about the same amount of fast and slow-twitch fibers, exhibit discipline specific adaptations in muscle fiber composition, with sprinters having the lowest and middle distance runners the highest ratio of slow to fast twitch muscle fibers. According to data from Aagard and Andersen, Bergh et al. and Fry et al. (Berg. 1978; Aaagard. 1998; Fry. 2003), the range of slow to fast twitch fiber ratios extends from ultra-endurance runners with a 90:10 slow to fast twitch ratio down to weight lifters and sprinters with a minimum of 20:80 slow to fast twitch fiber ratio.

Muscle fiber type and weight loss: Contrary to what you may have guessed, or read elsewhere, obese patients with a higher amount of oxidative slow-twitch fibers have been shown to lose weight easier than their "heavier muscled" peers. In a 2002 study Tanner et al. report (Tanner. 2002):

With weight loss intervention, there was a positive relationship (r = 0.72,P < 0.005) between the percentage of excess weight loss and the percentage of type I fibers in morbidly obese patients. These findings indicate that there is a relationship between muscle fiber type and obesity.

Image 2: For someone who already got morbidly obese, a higher ratio of type II fibers may well be counter-productive if his/her overall goal is weight loss.

Another result of the same study, which could easily be misinterpreted as politically incorrect is the genetically determined higher raio of type II muscle fibers within the African American part of the female study population, which made it increasingly harder for these women to burn the fat. And just in case, you still wonder why a type I fiber, something obviously only skinny people have in excess would help with losing fat, just think about the term "oxidative muscle fiber" for a moment, then add to that the experimental observation that type I fibers have greater mitochondria volume densities than type II fibers (Sullivan. 1978) and you will realize that a highly oxidative muscle fiber is more valuable when it comes to burning fat than a glycolitic one, reagardless of whether or not the latter may "look" better ;-)

In a recent review of the literature Wilson et al. provide the following biological explanation for the differences that exist between endurance and strength athletes (Wilson. 2011):

[...], type I fibers have been observed to have both greater mitochondria volume densities as well as capillary-fiber contact length when compared to type II fibers.  In addition, mitochondria volume density was highly correlated (r = 0.99) with O2 diffusion coefficients across three different muscle groups (retractor, sartorius, soleus) suggesting greater aerobic capacity in type I fibers.

While type I muscle fibers will thus figuratively carry their owners in 80 days around the world, type IIX and IIA fibers exhibit a 10x and 6x greater peak power and a 4x and 3.3x greater contractile velocity than their oxygen-hungry slow twitch cousins.

Figure 2: Relative peak power and contractile velocity of fast twitch fibers vs. slow twitch fibers (data based on Wilson. 2011)

The reason that the two guys from image 1 do not only perform but also look completely differently, lies yet in the greater capacity of type II fibers for exercise-induced hypertrophy (Schoenfeld. 2000). The relative number of type II to type I fibers is thus of paramount importance, if you want to look like a sprinter - not like a marathon runner and if you want to lift heavy weights instead of running cross-country. Fry et al., for example found strong correlations (r = 0.94; almost "causative") between the percentage of type IIA fibers and 1 repetition max snatch performance in national caliber Olympic athletes (Fry. 2003). Now the obvious question is: "How can I influence my individual fiber composition, or is this simply genetically determined?"

It stands to reason that genetics is a major determinant of fiber composition, but, hardgainer or not, with appropriate training and nutrition everyone can - at least to a certain degree - shift his muscle fiber make-up from a slow-twitch oxidative to a fast-twitch glycolytic type, even without the use of clenbuterol and other beta-2 agonists which hav been shown to trigger respective shifts from type I to type II muscle fibers in a rodent model (Zeeman. 1988).

Training for shifts in fiber composition

From Wilson et al.'s review of the literature it becomes quite obvious that standard exercise regimen, like jump squats at either 30% or 80% do not provide satisfactory results for someone looking to increase the number, not the size of his glycolytic muscle fibers (Wilson. 2011). In a study by Liu et al. (Liu. 2008), a 5x3RM bench press protocol, performed 3 times per week for 6 weeks, on the other hand, triggered a shift within the type II fibers. It increased the percentage of type IIA fibers from 44.9% to 66.7%, but decreased the type IIX fibers from 33.4% to 19.5%, thus leaving the percentage of slow twitch type I fibers unchanged. A second group from the same study who used a more versatile routine, with the same 5x3 regimen on Mondays, 10x concentric-repetition bench press throws at 30% of their 1RM on Wednesday and 10 stretch-shortening type push-ups on Friday for 5 sets, each, were able to increase the number of type IIA muscle fibers (from 47.7% to 62.7%) without decreases in the number of type IIX fibers, but a profound -50% reduction of slow-twitch oxidative fibers (from 18.2% to 9.2%). Wilson et al. go on and cite several other studies that were able to show the modulatory (increase in type II, decrease in type I) effects of high-velocity contractions on muscle fiber composition (Wilson. 2011) and corroborate that results with findings from other studies which corroborate these results with ...

[...] findings that the percentage of type I fibers may be increased with various types of aerobic training protocols such as endurance cycle training (+12% Type 1) and long distance running (+17% Type 1), [where, on the other hand] studies indicate that sprint training may facilitate the change of slow twitch fibers to fast twitch fibers.

Interestingly, Hortobagyi et al. were able to show that laziness taken to the extreme, i.e. 3 weeks of knee immobilization, also reduced the amount of type I fibers (-9%) and increased the number of type IIX fibers (+11%) in 48 recreationally active men and women (Hortobagyi. 2000). These results should yet be treated with appropriate caution and I would strongly advice against lying on the couch to increase your propensity for muscle growth by decreasing the number of slow twitch and increasing the number of fast twitch muscle fibers, because "recreational activity", for most people, consists of aerobic type of exercises, playing soccer, tennis or whatever - all sports that by and out of themselves would trigger shifts towards a more oxidative (predominant type I) muscle composition. It is thus not surprising that refraining from such activities for 3 weeks would reverse those changes.

So how should you train, then?

In view of the paramount importance of speed, not load in the few experiments which challenge the hitherto established paradigm that muscle fiber composition was largely determined by genetics and transformation was possible only within type II fibers, i.e. from type IIA to type IIX and vice versa, the incorporation of respective training techniques, e.g. concentric-repetition bench press throws at 30% of your1RM, as they were used in the study by Liu et al. (Liu. 2008), into a more versatile hypertrophy-specific routine which would

1. trigger a hypertrophy response, on "classic" strength training days (like 3x5 or 3x8-10), and
2. increase propensity for growth, on "speed-rep" days with exercises like plyometric push-ups, concentric-repetition bench press throws at 30% 1RM, etc.

would appear to be the most reasonable way to train for anyone out there, who does not belong to the "genetic elite" of born sprinters.

Increasing Adolescent Obesity Among Girls: How School Stress is the New Scapegoat When the Skinny Fat Phenomenon and Twinkie Diets Really are to Blame.

Image 1: Was it school stress that cost Michelle Obama her famous "guns" (=muscular upper arms)? Probably not - and despite contrary conclusions in the study at hand, I doubt that it is school stress that leaves our daughters fat, but undermuscled. What do you say?

According to the results of a recent evaluation of the data from the European HELENA trial, school, or rather the stress your children are exposed to within the educational system, may be one of the reasons for the increasing number of obese adolescents (age 12-18 years) - at least if we trust the statistical finesse of Tineke De Vriendt, Els Clays and 10 other scientists who recently published a paper on European adolescents’ level of perceived stress and its relationship with body adiposity in the European Journal of Public Health (DeVriendt. 2011). The study was part of the Healthy Lifestyle in Europe by Nutrition in Adolescence cross-sectional study (HELENA-CSS), the aim of which is to obtain "reliable and comparable data from a selected cohort of European adolescents concerning a broad variety of parameters related to nutrition, health, physical activity and fitness", or in other words, to provide the epidemiological back-bone for the formulation of more or less mainstream hypotheses on "why we are getting sick and obese"... be that as it may, with a sample size that allows for a confidence level of 95% and <0.3 error and 3865 adolescents from more than 10 European cities, the data from the HELENA study is probably the best we can get at the moment and thus you may nonetheless be interested to hear that ...

School-related stress was demonstrated to be a main source of stress in European adolescents, [...and] in adolescent girls (but not in boys), a positive association was observed between their level of perceived stress and measures of general and abdominal obesity.

If you have a closer look at the stress data, expressed on a 6-scale Likert scale from 1 = ‘Not at all stressful’ over  2 = ‘A little stressful’, 3 = ‘Moderately stressful’, 4 = ‘Quite stressful’ to 5 = ‘Very
stressful’ (with 6 indicating ‘Is irrelevant to me’), you will notice that school and the closely related fear of an "uncertain future" are in fact the major stressors in the life of our adolescent children (and you may safely assume that the results won't be very different in the US).

Figure 1: Overview of perceived stressors; values expressed on a Likert-scale from 1 to 5 (data adapted from DeVriendt. 2011)

In that, it is yet interesting to observe that none of the stressors is on average perceived as "quite stressful" or even "very stressful". It is also noteworthy that on 5 out of 10 scales and on the summary scores girls experienced more stress than boys. In view of the scientists previously cited conclusion (of which I do not have to tell you that it is based on one of those sophisticated *cough* statistical models) that only "in adolescent girls (but not in boys), a positive association was observed between their level of perceived stress and measures of general and abdominal obesity", it may thus surprise you to hear that the obesity rate among boys is more than 2x higher than among adolescent girls (cf. figure 2). So how is that?

Figure 2: Body adiposity characteristic of study sample (n=1121) of adolescents from the HELENA trial (data adapted from DeVriendt. 2011)

Well, we all know that even with a perfectly "normal" BMI, you can easily be "skinny fat". A phenomenon of which I feel that it is becoming the norm, not the exception, among adolescent girls, who - after their nth an-apple-a-day diets have lost nothing but muscle and thus have a very high body-fat percentage with a low overall body-weight.

This hypothesis would be confirmed by the regression coefficients of the statistical models from the study, according to which the association of perceived stress with the body fat level of the girls is 7x higher than the association of perceived stress and BMI, which is something that should you make reconsider, whether

1. body weight and BMI is an important biological measure, at all,
2. the real "obesity" rate, including skinny fats, among girls is not way higher than the 1.9% reported in the study would suggest, and
3. in how far school-stress, despite being the "major stressor" in this survey and not a misguided beauty-ideal is to blame for the increasingly unbalanced ratio of lean to fat mass in adolescent girls

The importance of the latter, i.e. a questionably beauty-ideal, in the etiology of (and this would be ironic if it was not so unfortunate) diet-induced obesity could also explain that the pubertal stage the girls were in and not stress or their diet had the greatest "explanatory value" (remember: we are talking of associations here) in regard of their body fat levels (cf. figure 3).

Image 2: Low self-esteem and false beauty-ideals pave the way into disordered eating and life-long misery. Something you want to spare your daughter and son, don't you?

Did you know that according to a 2000 national survey 45% of the girls, but only 20% of the boys from 5th to 12th grade reported to have tried one or more diets at some point in the past (Neumark-Sztainer)? And would you have guessed that 17% did even consider their own eating behavior as already "distorted"? Needless to say that both of these factors showed a high correlation with overweight status, low self-esteem, depression, suicidal ideation, and substance use; and certainly reason enough for you to help our children (girls and boys) not to fall victim to ill-advised beauty-ideals and false dietary recommendations.

And from the fact that the same variable had 7x less predictive value in boys, who obviously do not want to be skinny fat and refrain from Twinkie-style low calorie, low fat dieting, we can with some caution (due to hormonal effects on fat accumulation) conclude that it is not just a time factor, meaning that the older girls have more time to accumulate body fat...

Figure 3: Regression coefficients (=associative strength*100) of stress or pubertal stage with body-fat percentage in adolescent boys and girls from the HELENA trial - mind the logarithmic scaling! (data adapted from DeVriendt. 2011)

Now, what can you do about that? Well, without even knowing you probably have already done something! Assuming that you (just like every other reader of the SuppVersity ;-) are of above-average intelligence, your education has already provided your daughter, but not your son, with a better chance of staying lean than her peers from less educated parents (~80x higher explanatory value than stress!). All that is left now to make absolutely fat-proof, is to tell her that strong, not skinny fat is the new beautiful ;-)

Intermittent Thoughts on Intermittent Fasting - The Fast #2: Health & Longevity Effects of Intermittent Fasting

Image 1: Any roundworms reading this? I hope you know that by not eating enough and feeling miserable you can extend your lifespan ;-)

Thanks Caenorhabditis elegans, or "C. elegans", almost everybody who is able to read a newspaper or online magazine will have heard of the miraculous effects of calorie restriction and fasting on longevity (of this worm!). Since I assume that you possess more gray matter than this transparent nematote, you will probably have asked yourself how, or rather if these results from a worm with an average lifespan of 2-3 weeks translate to human beings,... well, all I can tell you is that leading a miserable life of lifelong dieting appears to work in non-human primates, as well (Kemnitz. 2011). Now, the obvious question is:

How does all that relate to Intermitent Thoughts on Intermittent Fasting? Obviously, none of the roundworms or rhesus monkey's followed Martin Berkhan's intermittent fasting approach, did they?

No, I have not seen pictures of abes on leangains.com, either, so I suppose they did not follow Berkhan's approach, but - and this is the likewise fascinating, as well as surprising, connection - there is scientific evidence that intermittent fasting could reproduce some of the beneficial effects of caloric reduction while avoiding a whole host of its undesirable side-effects. Reason enough for me, to devote this episode of the increasingly popular Intermittent Thoughts on Intermittent Fasting series to the non-cosmetic health effects of intermittent fasting (I know that's not as getting ripped and jacked, guys ;-)

Figure 1: Ramadan fasting leads to profound beneficial changes in inflammatory markers (left) and blood lipids (right) in 20 healthy male non-obese volunteers aged 23-39 (data calculated based on Aksungar. 2006)

We touched on one of this unsexy, yet vitally important health-benefits at the end of the last installment on the metabolic and endocrine effects of fasting, already: the beneficial effect on insulin resistance (as measured by a +44% increase in the inverse of the long-term marker of insulin resistance 1/HOMA-IR and the slight increase in QUICKI) Shariatpanahi et al. had observed in 55 ramadan fasting subjects (Shariatpanahi. 2008) for example constitutes one of these "boring side-effects", of which many dieters fail to realize that improvements in insulin sensitivity or reductions in inflammatory markers and C-reactive protein (cf. figure 1, left), as they were reported by Aksungar et al. in a 2006 study on the effects of religious "intermittent" fasting (Aksungar. 2006) facilitate weight - and more specifically - fat loss.

Image 2: Would the issue of dehydration distort the results of Ramadan studies and thus render them irrelevant for our argumentation? (photo Offline Clinic)

As in almost every episode I want to make a few brief statements regarding the "Ramadan model of intermittent fasting". I have already discussed its advantages over "over-other day" or "alternative day" fasting in the second installment of this series and I have hinted at possible problems related to the restriction of water intake within the fasting period in the third installment of the series. Now, in view of the general recommendation to drink more and more frequently to avoid dehydration (USDA), it seems prudent to verify that potential beneficial health effects of fasting are not masked by detrimental side effects of dehydration, if we - once again - want to rely on the available data on religious fasting as part of our argumentation. In a paper published in the European Journal of Clinical Nutrition in 2003, Leiper, Molla and Molla report that despite the fact that "[d]uring the daylight hours of Ramadan fasting, practising Muslims are undoubtedly dehydrating", it is neither "clear whether they are chronically hypohydrated" nor have there been any "detrimental effects on health [...] directly attribut[able] to negative water balance at the levels that may be produced during Ramadan" observed in any scientifically relevant studies (Leiper. 2003). It is thus relatively safe for us to assume that we can neglect he influence of potential dehydration in our initial analysis of respective studies.

Now, what about the longevity effects?

Image 3: The effects the calorie restriction had on the ape on the right is certainly impressive, when you compare it to his 27.6 year old age-mate on the left - would be interesting to see how an "intermittently fasted version would end up ;-) (img. from the Irish Medical Times)

With or without the beneficial effects on cardiovascular risk markers, the question still remains: "Can intermittent fasting mimic the longevity effect of calorie restriction without the constant cravings, continuous hunger and all sorts of "human" problems that won't show in studies on yeast, worms, rodents or even apes (see image 3)?"

In order to answer this question, we will first have to give a clear cut definition of what our understanding of intermittent fasting is, in this context, because, obviously, if we coupled our (intermittent) fast with a a deliberate and severe calorie restriction we would probably end up like Canto, the ape from the the longevity study in image 3 - old, but miserable. What we want, on the other hand, is an intermittent fast, where - within the feeding window - we are allowed to eat to satiety... similar to what we are seeing in religious fasting: no calorie counting and perceived (when compared to normal meal sizes) overeating.

Now, we do already know from the studies cited above (and in previous installments of this series) that one month on a dietary regimen like that provides considerable benefits as far as weight loss, insulin sensitivity, blood lipid ratios (! this is important, because we are knowledgeable enough to give a f*** about total cholesterol & co) and inflammatory markers, all of which are associated not only with an increased life-expectancy (Danaei. 2010), but, more importantly, with an increased life-quality and neurological health (Bronwen. 2006) up into the old(er) ages. From the same studies, we do yet also know that breaking the fast, and returning to our old dietary habits returns these markers to baseline (cf. post values in figure 1). What we do not know, however, is whether ...

1. intermediate improvements in correlates of health and longevity as they can be observed during intermittent periods of Ramadan (intermittent) fasting provide any, or even significant longterm health benefits, and
2. longterm (as in for years and decades) intermittent fasting would not over months or years lose its effect, or even worse, be detrimental to our overall health and thus reduce not extend our life-expectancy and/or life-quality

From rodent studies we already know that a life-long alternate-day feeding protocol increases lifespan in the absence of any caloric reduction (Goodrick. 1990; Mattson. 2000). Evidence that similar beneficial effects, at least as far as mortality from chronic disease is concerned, would occur in human beings comes from a 2007 study by Varaday and Hellerstein (Varaday. 2007), who do yet remark that (as I already pointed out) "more research is required to establish definitively the consequences of ADF [alternate day fasting]".

The circadian clock hypothesis

A finding from alternative day fasting studies that may be of paramount importance in view of the "quality of life"-aspect, is the increase in brain-derived neurotropic factor (BDNF) that has been observed in animal studies. BDNF is involved in brain development and plasticity and its (intermittent) fasting-induced elevation could explain the neuroprotective effect of respective feeding patterns (Duran. 2001). In a review of the literature, Fory and Miskin do yet remark that (Froy. 2010)

[...] BDNF could not be [directly] linked to the neuro-protective effects in the brain of calorically restricted rats, but increased levels of another neurotrophic factor, glial cell line-derived factor (GDNF), were correlated with neuro-protection of a calorically restricted primate model of Parkinson's disease. Interestingly, BDNF is also a component of the hypothalamic melanocortin pathway that controls food intake and body weight in adult mice, and it has been implicated in the regulation of energy metabolism.

After all, the scientists believe that IF exhibits part or even all of its effects by (re-)setting clock genes, a hypothesis which despite having its merits would yet lead us into theoretic considerations with little merit to our "intermittent thoughts" on the real-world outcomes of intermittent fasting, which is why I will, at this point, skip forward to the results of a 1999 study into the relation of adipose tissue size and reductions thereof to longevity.

Is it not about eating less, but just about getting leaner?

Image 4: When we are talking about the benefits of losing body fat, this obviously does not imply you have to get in Phil Heath Mr. Olympia '11 shape to live longer (photo bodybuilding.com)

In the introductory paragraphs of this installment of the Intermittent Thoughts on Intermittent Fasting series I somewhat ridiculed the idea of changing one's whole life to get "ripped and buffed", now, after revisiting some of the studies and observing the close correlation of improvements in metabolic health markers, reductions in body fat and consequent life-extending effects of (intermittent) fasting, the central question of Nir Barzilai's and Gaurav Gupta's 1999 paper Revisiting the Role Fat Mass in the Life Extension Induced by Calorie Restriction seems by no means far fetched: What if ain't inflammation and insulin resistance & co that make us fat and reduce our lives, but being fat that leaves us insulin resistant, inflammed & co and thusly reduces our life-expectancy? The answer, according to Barziilai and Gaurav, is simple (Barzilai. 1999):

In fact, all of the benefits of CR on the neuroendocrine system and those related to the improvement in glucose homeostasis can be attributed to decrease in adipose cells and their products.

Probably too simple and above all difficult to treat with a drug and thus not profitable enough to be accepted by the medical establishment. Now, if this would be the case, intermittent fasting would in fact provide the sought-after silver bullet to leading a leaner, healthier life, as both the anecdotal reports on the Net, as well as the the majority of the studies that have been cited in this, as well as the previous installments show quite conclusively that going without food for periods <24h is capable of reducing body fat stores, while preserving lean muscle (and bone) mass. But why, or better how does that work?

Intermittent fasting, fat reduction, health improvements and the cyclicality of life

Illustration 1: It probably is the magic interplay of AMPK and mTOR that produces such remarkable transformations as Duong Nguyen's. We will delve deeper into the their reciprocal interaction in the next installment of the Intermittent Thoughts on Intermittent Fasting Series

Due to its cyclic nature intermittent fasting seems to temporarily produce similar "reductions in protein synthesis" (Barrows. 1978) as the ones which have been established as the fundamental mechanisms of the life-extending effects of calorie restriction as early as in the late 1970s and of which we know today that they partly mediated by an AMPK-induced downregulation of the mTOR pathway. In that, this transient AMPK response to intermittent fasting, which most intermittent fasters further stimulate by exercising in a (semi-)fasted state, appears to be profound enough to stimulate or, according to some recent research (cf. Canto. 2010), we should probably say "sustain" the SIRT1-pathway to an extent that allows dieters to benefit from its immediate fat-mobilizing effect on white adipocytes (Picard. 2004) and its ability to maintain telomer length (and subsequent longevity, cf. Palacios. 2010) without the unwanted muscle-wasting side-effects of prolonged fasting periods.

The fasting induced AMPK expression is yet only one part of the cycle, of which we have learned in this installment that it is responsible for both, the "cosmetic" effects on body fat, which could, after all, be causative and not just corollary or even subsequent to improvements in insulin sensitivity (cf. What Comes First: Inflammation or Obesity?), lipid profiles, and the whole string of beneficial health effects which irrefutably contribute to the longevity effect of inhumane low-calorie diets. In view of the fact that another valuable Sunday afternoon is drawing to a close, the discussion of the second player in this cycle, the mammalian Target of Rapamycin, or in short mTOR, will yet have to be postponed to the next episode of the Intermittent Thoughts on Intermittent Fasting Series - so stay tuned, keep the questions and comments coming and don't forget to check back on Thursday to see what AMPK and mTOR are doing to our man at the 2012 wheelchair nationals, Adelfo Cerame!

High and Low Dose BCAA Supplementation Have Minimal, Non-Significant Effects on Markers of Muscle Damage 24h and 48h Post Heavy Resistance Training

Image 1: Cover of the September issue of the International Journal of Wrestling Science - don't tell me you don't have a subscription, yet!

I don't know about you, but I feel that it's quite interesting to look at the highly heterogeneous dosage suggestions on the labels of the ever-increasing number of BCAA supplements on the market. Interestingly, almost every producer claims in his "non FDA-approved" statements that his supplement contains "scientifically supported" or "clinically validated" amounts of branch-chained amino acids in the "optimal" (whatever that may be) ratio of 2:1:1, 3:1:1, 4:1:1, 8:1:1, ... and all the other variations that appear to be limited only by the patent applications and lawyers of the financially more potent players in the business. From a scientific perspective, however, this "optimal" amount has still to be elucidated - at least to my knowledge, no respectable scientist has yet claimed to have found the "optimal" amount and composition of free form amino acids for a given subgroup of athletes, let alone strength athletes, bodybuilders or figure competitors, in general.

At this point I would like to add that no respectable scientist would ever dare to make the claim that he or she has found the "optimal free form amino acid supplement" for all, or even a significantly large group of athletes, unless he or she would be interested in losing his reputation as a "respectable scientist" ;-)

In a recently published study scientists from the Department of Physical education and Sports Science University of Tabriz in Tabriz, Iran, set out to establish whether there is at least a significant difference between the effects of ~15g (210mg/kg) or 33g (450mg/kg) of branched chain-amino acids taken before and after the completion of an intense resistance training regimen comprised of 7 exercises à 3 sets of 10 repetitions (Amirsasan. 2011). Yet, despite the fact, that even the "low dose" of 15g of BCAAs (in the customary 2:1:1 ratio, i.e. 7.5g of leucine + 3.75g of iso-leucine + 3.7g of valine) was about 1.5x higher than what I have seen as "suggested dosing" or "serving size" on very high-dosed commercial supplements, the effects of this amino acid overkill were "sobering", to say the least.

Figure 1: Effects of "low" (210mg/kg) and "high" (450mg/kg) dose BCAA supplement on enzymatic markers of muscle damage relative to pre-values in the placebo group (data calculated based on Amirsasan. 2011)

As the data in figure 1 goes to show both the "low" as well as the "high" (or should I say "overkill" ;-) dose of pre- and post-workout BCAAs had only marginal, and certainly statistically non-significant effects on creatine kinase (overall - CK; muscle specific - CK MB) and lactate dehydrogenase activity, both established indicators of (exercise-induced) muscle damage.

Comparison of results between groups in mean and amplitude changes of serum indexes of cell damage (CK-LDH-CKMB), 24 and 48 hours after the exercise performance showed no significant difference between the 3 groups. In other words, different amounts of BCAA did not significantly affect the serum cell injury indexes (CK-LDH-CKMB), 24 and 48 hours after the heavy resistance activity.

These results are interesting, because they contradict previous findings by Sharp et al. who reported "significantly reduced" creatine kinase levels with BCAA supplementation in likewise previously strength-trained athletes on a similarly intense (8 exercises; 3x 6-8 repetitions) resistance training protocol (Sharp. 2010), as well as the results of studies in endurance athletes and previously untrained subjects, where the provision of BCAAs decreased creatine kinase and lactate dehydrogenase enzyme expression, across-the-board (Greer. 2007; Koba. 2007; Matsumoto. 2009).

"To supplement or not?" This question may arise if you have a look at the data from this study. Thor, in a comment to this posts poses the question whether his "personal experience" that "having the fast digesting aminos seemed to increase [his] ability to have a more successful work out" is, after all "only in [his] head" and while I cannot say for sure how much of it may be the result a placebo-effect in his case, I can provide you with the results of a 2011 study by Greer et al. who found no increases in exercise performance despite reduced perceived rates of exertion with BCAA supplementation after a 90-minute cycling bout (Greer. 2011). These results seem to confirm the "central fatigue hypothesis" according to which BCAAs exert their beneficial effects agains (perceived) fatigue via modulation of the availability of the serotonin precursor tryptophan. In a 2007 review of the literature, Meeusen and Watson do yet conclude that the "nutritional manipulation of these systems [neurotransmitter] through the provision of amino acids has proven largely unsuccessful" (Meeusen. 2007)... All that does not take away from the established beneficial effects of chronic low-dose BCAA (in particular, leucine) supplementation on endurance performance and strength adaptations to exercise (e.g. Crowe. 2006; Matsumoto. 2009). In the respective studies, dosages in the 1.5-3.0g/day range have yet been sufficient, to elicit these beneficial effects - and that in subject groups that are not particularly well-known for their exorbitantly high protein intakes ;-)

Image 2: When bought in bulk and without the addition of a ton of fancy extras BCAAs have become reasonably priced - whether they are a "necessary" part of your supplement regimen may yet depend on your dietary protein intake.

Probably - this would at least be my first guess - the outcome of these studies was not so much affected by the actual study protocol, but rather by the habitual dietary protein intake of their subjects. With endurance athletes (Koba. 2007; Matsumoto. 2009),  recreationally active (Sharp. 2010) and untrained (Greer. 2007) we usually see much lower dietary protein intake than with professional wrestlers, which prompts me to repeat my previously stated skepticism towards the usefulness of large boluses of additional free form amino acids in a group of athletes whose habitual dietary protein intake is way beyond the 1.5g/kg level, anyway... but hey, that's just the opinion of a brainy physicist; so if your brawny guru says you need those 150g of BCAAs on top of your 5x50g whey protein shakes and your 3 pound of lean meat - go for it!

Things that Belong into Your Gymbag: A Well-Adjusted Boil & Bite. Study Shows Decreased Cortisol Response After Intense Exercise with Custom-Fit Performance Mouthpiece

Image 1: An Under Armour Performance Mouthpiece - hitherto not a bodybuilder's 1st choice from the Under Armour line-up; something that may change when Cutler & co get wind of its effects on post exercise cortisol levels ;-)

Any (semi-)professional boxers out there? No? Football players? Ice-hockey? Lacrosse? Did you ever think of wearing your mouthpieces in the gym? No? Well, I guess then you have not heard about the surprising performance enhancement the stabilization of your temporomandibular joint by a well-adjusted mouthpiece may have on exercise performance and recuperation, have you? Studies into the effects of mouthpieces on exercise performance date back to the late 1970's and early 1980's, when Stephen David Smith published two studies on the effects of mouthguards and jaw posture on strength and exercise performance in the New York State Dentist Journal (Smith. 1978; Smith. 1982). In spite of that, a proper, experimentally verified explanation for the underlying mechanism by which the proper alignment of temporomandibular joint could have influenced muscular strength in these early studies had still to be provided.

In a very recent paper that is soon to be published in the Journal of Strength and Conditioning Research, Dene P. Gardner, Wesley D. Dudgeon and Erica J. Mc Divitt, from the Department of Health, Exercise and Sport Science at The Citadel in Charleston, South Carolina, report the results of an experiment that may well provide some insights into the performance enhancing effects of a piece of equipment that was originally invented to protect the teeth and jaws of boxers, football players and other athletes engaging in full-contact sports (Garner. 2011).

Illustration 1: Exercise protocol used in the study (adapted from Garner. 2011)

Based on animal studies by Hori et al. (Hori. 2004) and human data from Tahara et al. (Tahara. 2007) the scientists knew that biting or chewing could reduce the stress-induced release of corticotrophin releasing hormonen (CRH) from the hypothalamus and thus reduce the ACTH-stimulated release of well-known stress hormone cortisol from the adrenal glands. Garner et al. thusly speculated that they would find statistically significant differences in the cortisol response to 1h of intense resistance exercise (for details on the exercise protocol see illustration 1, on the right) in a group of 28 division I football players, who were randomly assigned to the use of a custom-fit mouthpiece in one of two identical training sessions (=within subject-design). Salivary cortisol samples were taken during both exercise bouts immediately before and at 25min, 45min, and 60min during, as well as 10 minutes post exercise.

As the data in figure 1 goes to show, there was indeed a direct interaction between mouthpiece-use and cortisol levels.

Figure 1: Cortisol response (expressed relative to pre-values) to identical 1h exercise bouts with and without a custom-fit Under Armour Performance Mouthpiece in 28 collegiate football players (data calculated based on Garner. 2011)

Unlike the slight amelioration of the immediate cortisol response during the 1h exercise bout, the difference in cortisol levels at 10 min post exercise is statistically highly significant and would validate the hypothesis that the correct alignment of the temporomandibular joint (TMJ)

Image 3: The temporomandibular joint

[...] leads to the activation of the motor area of the cerebrum, which then resulted in a decreased hypothalamic–pituitary response and thereby a reduction in cortisol release

as it has already been proposed by Hori et al. (Hori. 2004). Another possible explanation is related to earlier findings from Garner's laboratory, which showed that

[...] this product [the custom-fit Performance Mouthpiece] specifically creates a forward movement and increased space between the upper and lower teeth leading to improved airway dynamics.

which is why the scientists cite "the repositioning of the mandible and the improved airway response" as another possible explanation for the favorable post-exercise cortisol response.

Image 3: Although this is common practice and nothing shady, it is important to note that this research was "partially supported" by BiteTech, the manufacturer of the mouthpiece used in the study

There are two things I still want you to know before you skip to another of the highly educative SuppVersity posts ;-) Firstly, the study was "partially supported" by Bite Tech Incorporated from Minneapolis. In view of the fact that scientists have known about the potential benefits of mouthpieces for decades, now and considering the fact that the scientists openly declare that the financial support by Bite Tech, I do not doubt that the data they presented is 100% accurate. That being said, "sponsorship", and this may sound like an unfortunate truth, is becoming more and more essential for scientists (in all fields) and there is absolutely nothing wrong with that, IF (as it is the case with Garner et al.) the scientists explicitly state the involvement of the third party.... ah, you are waiting for secondly? Ok, here we go - I want to give a shout-out to my buddy Sean Casey from CasePerformance and wish him all the best for the upcoming exams ;-)

So, while it is now increasingly clear that the performance benefits, which by the way are not restricted to strength training, but have also been observed in endurance athletes by Garabee back in 1981 (Garabee. 1981), are related to the modulatory effect the use of a well-adjusted (!) mouthpiece has on the stress-response to (intense) exercise. In the end, I suppose, few athletes will be interested in whether this is due to a direct connection of their jaw muscles to some areas of their hypothalamus or improvements in airway dynamics, as long as it could give them the 0.1% edge that makes the difference between victory and defeat.

Adelfo Cerame - Pre-Contest-Prep: Back Training 101!

Image 1: An impressive back of which Adelfo feels it really lacks behind. Read more about how he is going to tackle this problem area, this week.

Time is flying by, only 2 weeks and Adelfo will start the hot phase of his contest preparation for the Wheelchair Nationals 2012 in Palm Beach Gardens, FL. From the last installment of the series, you will probably remember that he is using this time to streamline his raw-foods intermittent fasting diet regimen, which - he hinted at that in the last installment already, has not hampered his training progress the least. Currently at 149.5lbs with a body fat percentage of 13.4% he is hitting the gym more motivated than anytime before, as you will read and see in today's installment of Adelfo's exclusive contest-prep log, here at the SuppVersity.

If you want success, you have to constantly reinvent your diet

I already mentioned in the last installment of this series that I felt like the introduction of more and more raw foods into my diet had really helped with both strength as well as size gains in the gym. So, before I delve a little into my current training modalities, I thought I'd share a few additional thoughts on my current nutritional regimen with you.

Image 2: Adelfo's latest preworkout goodness for you to copy: Raw Kiwi Strawberry PreWorkout Shake - 20g protein, 44g carbs, 5g fiber, 28g; 508kcal of muscle building all natural foods, free of artificial flavors and sweeteners, yet 100% delicious!

Although everything seems to be working just fine at the moment, I am already planning ahead. When I start my prep, I will add a protein shake (50g) right after my workout, and then have the rest of my PWO meal when I get home... I just weighed myself today. 149.5 pounds, that's what the scale is telling me and what my current calculations are based on. I estimate my initial caloric needs at about 2,250 calories per day and given the amount of food I am slamming down at the moment, the addition of a protein shake immediately after my workout will help me to get up to those 2,250 calories as a reasonable starting point for my contest prep. While this may be my first prep on an intermittent fast, I figure that  

... whether you fast intermittently or not, you got to start a every diet with a reasonably high caloric intake...

If you do not lose weight as fast as you want to you can still cut back on calories. If, on the other hand, you are losing weight much to fast, chances are your will already have lost valuable muscle tissue, when you realize that you need to add in that additional protein shake that preserves lean tissue and revitalizes your metabolism. The occasional hunger pangs, I have been experiencing in the course of the last week are an early warning sign, I am not going to ignore.

Building a huge back sometimes forces you back to the drawing board

Image 3: Trying to build a killer back like the "Governator", but no clue which exercises will work? Then you better check out the SuppVersity EMG Serie with The Best Back Exercises of Witdh and Thickness.

I already mentioned in the SuppVersity Student Spotlight that I like it fast and heavy (I am speaking of training here, guys ;-) Currently, however, I am experimenting with some sort of heavy/light alternating training pattern, which looks like that:

• Monday: Chest/Triceps (heavy day)
  5 chest exercises & 2 Triceps exercises
• Tuesday: Back/Biceps (heavy day)
  5 back exercises & 2 biceps exercises
• Wednesday: Rest (not so heavy day ;-)
• Thursday: Triceps/Chest (volume / higher reps)
  5 triceps exercises & 2 chest exercises
• Friday: Biceps/ Back (volume / higher reps)
  5 biceps exercises & 2 back exercises
• Saturday: Shoulders (volume / higher reps)
  the only exercise I go really heavy on are shoulder presses

I consider my back one of my weakest body parts, so I've expanded my back training exercises. I used to do different variation of lat pulldowns, in the past, mainly because I was limited due to my mobility. Similarly, many gyms have machines I could not use until, after a lot of hard work, my core and trunk muscles got stronger and I began to feel a lot more confident to just try and experiment with new exercises, machines, grips, etc.

Video 1: Adelfo training back 2 weeks before the hot phase of his contest preparation is about to begin.

I guess, if you have not already been, Adelfo did now get you interested in "How on earth can you train in a wheelchair, at all?"... if you want to see a part of his current routine, i.e.

• seated rows - underhand grip
• wheelchair pullups
• seated rows - overhand grip

I suggest you click on the video to the left and enjoy a lesson in "how to train your back properly" - if the expression picture perfect form had not been out there for quite some time, someone probably would have come up with it after seeing this video ;-)

Currently, I do most of my back exercises on cables and machines, especially the hammer strength machines - those are my favorites. I also do body weight exercises for my back, such as pull ups and chin ups (see video 1). I use machines and cables because I am not able to transfer onto a T-bar row or do any type of standing or bent-over rows, so I try to just mimic those exercises as much as I can through machines. I train my back twice a week usually on Tuesdays and Fridays. I combine my back exercises with biceps.

Image 4: Next time he will be posing in front of the American flag, it will be with a procard in his hands ;-)

I usually like to train real heavy on Mondays and Tuesdays, because that's when I feel the strongest after my Sunday refeeds, so I end up training back real heavy once and with a higher volume and/or higher reps, the other day. That being said, I still try to lift as heavy as I can even within the higher rep-ranges.

On heavy days my set/ rep range are 4-5 sets of 5 reps (not including warmup sets) I try to increase the weight on every set whether it be just a 5 pound increase each set, just as long as I am trying to better my last set. On my volume/ higher rep days, my rep ranges are 4-5 sets of 8-12 reps.

I usually start off with exercises for thickness, so I always do row exercises first...

• seated row machine - I use this to mimic the T-bar rows
• seated row machine - this is a different variation that has a lower under hand grip and I use this to mimic some what of a bent over row where you have an under hand grip
• seated high rows on the hammer strength machine - one of my favorites, I can go real heavy and get a real good squeeze on my back
• single arm cable rows  - on a cable machine, I tie myself to the opposite end, while I have somebody pull the cable for me, and with a under hand grip I can do single arm rows, I know its hard to explain but I will eventually get video of it, couldn't do it today because there were a lot of people occupying "my" machines ;-)

Image 4: Leaning back slightly
(135° vs. 180°) on lat pull-downs
increases the activation.

The exercises I feel contribute more to the width of my back are

• wide grip lat pulldowns - I tie a weight belt around my chair so that I can lift heavy without getting lifted off my chair
• under hand grip lat pulldowns and wide grip behind the neck lat pulldowns
• close grip pulldowns - I use the V-bar
• wheelchair pull ups and wheelchair chin ups

As any reasonable trainee would do, I obviously don't do every exercise in every workout. For me it depends on how I feel the very day and which exercises I actually can do - as I mentioned I need a helping hand on some of the moves ;-)

I guess that's it for this weeks, folks. I am already looking forward to next Thursday, where - I can guarantee that - Dr. Andro and I will have some more interesting stuff for you to read, watch and think about. Until then, those of you interested in more information on diet and exercise science should check out both, the SuppVersity EMG Series and Dr. Andro's latest "baby", his Intermittent Thoughts on Intermittent Fasting... but, with all that reading, don't forget to hit the gym! 

Demonized N-6 Pufas Surprisingly Ergogenic: Safflower Oil More Than Doubles Swimming Endurance of Aging Mice.

Image 1: Unexpectedly ergogenic - Carthamus tinctorius L., better known as "safflower", a highly branched, herbaceous, thistle-like annual.

As a regular visitor of the SuppVersity and/or listener of SuperHumanRadio, you will be familiar with my skepticism towards fish oil supplementation as the "good for all" wonder-supplement in an athletic population. You will also be familiar with studies such as Filaire et al. (2010) which showed increased MDA (malondyaldehide) levels (and thus more, not less toxic waste) in athletes receiving 600mg of EPA and 400mg of DHA for 6 weeks. Thusly, it may not come as a total surprise that Guihua Zhang and his colleagues the National Food Research Institute and the National Institute of Vegetable and Tea Sciences in Japan found that 12 weeks on a diet containing 6% fish oil reduced endurance performance in aged mice by -20%. What may be more surprising, though, is that the vilified n6-pufas from safflower oil more than doubled the rodents' endurance performance.

Video 1: Not the swimming test performed in the study, but maybe an explanation why mouse-oil might be good for fish, but not vice versa - or have you ever seen a mouse eating a fish?

In view of the fact that the mice in the lard group suffered a similar loss in endurance performance, it should be said that the overall effect of fish oil, as well as lard, could in fact have been a null-effect. In other words, contrary to safflower oil, fish oil and lard had no beneficial effect on swimming endurance, so that an age-related decline in swimming endurance would have become obvious. After all, the average mouse-life is no longer than ~100-150 weeks, so that another 12 weeks are quite a time-span for 52 weeks old mice. On the other hand, previous studies such as Shimomura et al. (Shimomura. 1990) and Rustan (Rustan. 1993) would point toward an overall negative effect of high SFA+MUFA (lard) and high N3-PUFA (fish oil) on fatty acid oxidation in skeletal muscle and subsequently (endurance) exercise performance.

In the study, 40 male Crlj:CD-1 (ICR) mice had been randomly assigned to one out of three groups with the 6% of fatty acids of their experimental diet coming from either lard (n=13), safflower oil (n=13) or fish oil (n = 14) for 12 weeks.

Figure 1: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on swimming endurance of aged mice (data calculated based on Zhang. 2011).

As the data in figure 1 goes to show, the fat content of the diet, i.e. low PUFA (lard), high N3-PUFA (fish oil) and high N6-PUFA (safflower oil) had a profound impact on the swimming performance of the animals. In view of the fact that we cannot completely rule out that the "negative effect" of lard and fish oil were simply due to an age-induced decline in swimming performance (cf. red box above), the most important finding of this study is however the +113% endurance increase in the safflower group, and not so much the -20% performance decreases in the other groups in swimming endurance [if you asked me, it's a pitty that there is no control group on a mixed diet]

Figure 2: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on lactate levels pre and post endurance exercise in aged mice (data calculated based on Zhang. 2011).

As Zhang et al. point out, this increase in endurance performance cannot be explained based on increases in muscle or liver glycogen stores, because scientists measured "[s]imilar glycogen storage and plasma glucose levels in sedentary mice in the three diet groups suggest". A better explanation relates to the significant differences in the accumulation of plasma lactate following swimming (cf. figure 2), where lactate levels were "significantly lower" in the safflower oil group than in the lard (+57%) and non-significantly higher in the fish oil (+14%) group.

These results imply that the improved endurance associated with dietary safflower oil may be due, at least in part, to glycogen sparing. The working skeletal muscle is not only the major site of lactate production but is also important for utilization of lactate, which is mainly removed by oxidation. The decreased accumulation of lactate observed in aged mice fed safflower oil could be due to increased lactate oxidation and subsequent utilization as an additional energy source during swimming.

Yet the effect on accumulation or utilization of lactate was not the only difference that may have contributed to the increase in swimming performance that was observed in the safflower oil group. As the researchers point out,

the significant increase in muscle and liver CPT activities and decrease in plasma NEFA levels observed following exhaustive swimming in mice fed safflower oil implies an upregulation of fatty acid metabolism in these mice.

The absence of these effect in the lard or fish oil fed animals suggest that "the safflower oil group may have increased fatty acid utilization for energy than the other diet groups". In that, it is particularly noteworthy that we are talking about a localized increase in CPT activity and consequent fatty acid oxidation in muscle tissue. The increased liver CPT in the fish oil group, on the other hand could have contributed to an overall negative effect of fish oil consumption on endurance performance that would have been corroborated by the established suppressive effect of N3PUFAs on fatty acid synthesis (Kim. 1999; Nakatani. 2004)  and lipid oxidation (Rustan. 1993), against the backdrop of which less fatty acids became available for and subsequently oxidized in skeletal muscle.

Image 2: Biological activities of IL-6 (illustration by Prof. Dr. Heinrich)

Not directly relevant to the endurance aspect, but nevertheless interesting is another result of the study, which is the absence, respectively statistically insignificant elevation of elevations in the inflammatory maker IL-6 in the exercised (non-existent) and sedentary (non-significant) mice on the safflower oil diet. A result the anti-n6-faction in the diet-guru camp will probably find surprising and which goes against previous findings by Moon et al. (Moon. 2003) and Garcia-Escobar (Garcia-Escobar. 2010) - on the other hand, this also means that it was not the increase in IL6, which has in human studies been shown to selectively stimulate lipolysis in skeletal muscle (Wolsk. 2010), that facilitated the increase in endurance performance.

If and in what extent the reduction in plasma ferritin (fe) levels in the fish oil group (-13% sedentary; -24% exercised; both compared to lard, with slightly greater reductions compared to safflower oil) could have been an additional factor in a complex equation of substrate availability, usage and enzyme activity which could eventually explain the perfomance increases and decreases in the different groups is questionable. After all, the fe levels in the lard and safflower oil groups were virtually identical.

So, what would be the overall lesson, we can learn from the results of this study? Fish oil is poison, safflower oil liquid gold? Probably not. Yet, while it may still be questionable in how far the mouse metabolism is a good model for the human one, the inhibition of fatty acid synthesis and the increased fatty acid oxidation observed in mice as a consequence of fish oil feeding is present in humans, as well. Moreover, I assume you would agree that not everything that would be beneficial for the average sedentary borderline to morbidly obese inhabitant of the Western Hemisphere, is equally beneficial for performance-oriented athletes - or would you suggest 200 meter sprinters start swallowing statins and blood pressure medications? So, wouldn't it be remotely possible, then that a physical culturist (as I hope you would consider yourself to be one) would be much better off with a reasonable amount of those "nasty" n6-PUFAs in his/her diet to keep the fire in the mitochondrial furnace of his/her muscles in full blast? If you want to, ask your guru about it ;-)

Arms Don't Grow Faster With Leg Training: Stuart M. Phillips Busts Ronnestad's "Hormonal Ghosts"

Image 1: Although Tom Platz had massive
arms, as well, there is little conclusive scientific
evidence that this was a result of leg training.

Usually I am offering you my thoughts and comments on the results of the studies I am presenting here at the SuppVersity. In this case however, I am going to rely on the insightful analysis of Stuart M. Phillips, head of the Department of Kinesiology, Exercise Metabolism Research Group at the McMaster University, who spotted some interesting inconsistencies in a recently published paper by Ronnestad et al. who had reported that (contrary to conclusive findings from dozens of study by Phillips and others) endogenous hormone release from leg training had a major impact on the anabolic response in the arm flexors (cf. news from March, 2nd / I plead guilty of not having seen these inconsistencies, though I must say in mitigation that back in March I only reported, not commented on studies).

As Phillips points out, Ronnestad's conclusion that training legs+arms results in bigger guns or, rather, that without training legs, your arms won't grow at all is funded in

selective reporting (considering only the site of the largest CSA), incomplete statistical analysis (not comparing the changes (in CSA between arms), and questionable MR practices (Phillips. 2011)

In his analysis of the Ronnestad study, Phillips shows conclusively that, according to Ronnestad's own figures (Phillips refers to figure 6 of the paper, in particular), the authors' statement that

only L + A [leg plus arm training—a high ‘anabolic’ hormonal exposure condition] achieved increase in the CSA at the part of the arm flexors with the largest cross-sectional area (p \ 0.001), while no changes occurred in A [arm only training—a low ‘anabolic’ hormonal exposure condition]. (Ronnestad. 2011)

is not sustainable, since "examination of Fig. 6 in their paper reveals that significant hypertrophy did occur at two sites (of 4 measured) in the A arm", i.e. the non-leg-trained arm. By means as simple as drawing a few vertical lines (cf. figure 1) Phillips is able to show that the hypertrophic response to the training stimulus was in fact identical in three out of the four measured cross sections.

Figure 1: Four horizontal lines are all it took Phillips to show that there must be something wrong with Ronnestad's data; after all, it is unlikely that section 8 of the biceps had atrophied in the course of the stud (illustration taken from Phillip's letter to the editor of the European Journal of Applied Physiology)

Phillips makes a point that, unless one assumes that - for whatever reasons - there has been a strictly localized atrophy in section 8 of the arm (cf. mismatch of pre-values in left and right graph of figure 1), the most likely explanation for the mismatch would be that "the pre- and post-training scans were not aligned at the same point along the arm". Smart-witted as Phillips is, he also observed that with the purportedly greater changes in muscle cross-sectional-area in the leg+arm condition it is strictly impossible for the muscle volume to be identical, unless "the authors believe that the A arm got longer". I would assume that you agree with me that even with eccentric muscle training this would be a rather surprising event. Consequently, this is another argument in favor of the obvious absence of measurable effects of an overall more anabolic milieu in the "arm + leg training"-condition on the hypertrophy response to strength training - or, in short, we still have no conclusive evidence that training legs before arms would make the latter grow faster.

Image 2: Make your biceps grow with the SuppVersity EMG series!

Now, if the hypertophy response was identical, it is even more surprising that the "leg+arm" group exhibited "through some inexplicable mechanism" (Phillips. 2011) an overall greater 1RM strength than the control group. Phillips, who does not refrain from pointing out that "this [was] a surprising observation that was not even alluded to in the paper", argues that this result stands in stark contrast to the "central fatigue" hypothesis Ronnestad et al. cite as an explanation for the "dampened" (Ronnestad. 2011) training loads in the "leg+arm" training group. Phillips, on the other hand, speculates that it could be a direct result of a "a superior neuromuscular adaptation" (Phillips. 2011, my emphasis), which would be the exact opposite of what Ronnestad et al. had in mind.

Even if one neglects the questionable measuring practice of Ronnestad et al., in the course of which the "scanned arm [was] stretched behind the head and centered in the middle of the machine" (Ronnestad. 2011), the absence of an "estimate of variability of the procedure they used in their lab" and the questionable reference to "similarities" to magneto resonance scans (note that Ronnestad et al. used CT scans ;-) carried out by Moss et al. (Moss. 1997), the Ronnestad study is a particularly good example for the way research hypotheses can interfere with the "objective results" of scientific studies by establishing a (often unconscious) bias towards "desired" results. Selective reporting, incomplete statistical analysis and ad-hoc explanations for differences to the findings of previous studies are the undesirable, yet completely human manifestations of this phenomenon, I want everyone of you to be aware of - even if this means that my own thoughts and conclusions, which are almost always produced under time-pressure, are about to get more critical comments in the future ;-)