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marylin monroe
Showing posts with label creatine. Show all posts
Showing posts with label creatine. Show all posts

Fit Kids = Smart Kids, Creatine & Muscle Repair, Epigenetic Transfer From one Leg to Another. Plus: Fat Effects of Anti-Psychotics, Larger Muscle = Greater CNS Impact, Rhodiola a Natural Opiate, Hawthorn for More & Thicker Hair

It's never too early for your first push-up ;-)
"10" is this week's SuppVersity figure of the week. Ten as in "ten push-ups" which is the mean number of push-ups the 12 year-old boys and girls from the Coe study you can read about in one of the items of today's news mash-up aka "On Short Notice". I am honestly not yet sure what to make of it, it's not as bad as what I had expected based on a couple of observations I have made as of late, but it still goes to show you that you cannot take the most fundamental feats of physical fitness for granted, when it comes to pre-/peri-pubertal kids in today's sedentary society.

Now, while I am still trying to make up my mind I would suggest we take a look at the actual outcomes of the study. The 10 push-ups were after all only part of the subject characteristics and not the reason Coe et al. actually conducted their study.

Fit Kids are smart kids - Strength and cardio both matter!

You can hardly start your career as a physical culturist too early, there are simply way too many benefits from giving your body the nutrients and the exercise it needs and therefore it is actually not surprising that conclusion of a recently published paper in the Journal of Sports Medicine and Physical Fitness reads:
"Students with the highest fitness level performed better on standardized tests and students with the lowest fitness level performed lower in class grades" (Coe. 2012)
Interestingly enough, this effect was associated with both cardiorespiratory fitness and strength, which brings us back to yesterday's news about the PGC-1 alpha isoforms (read the comments as well) and the detailed follow up I just decided to post on the whole matter, tomorrow.
Figure 1: Spearman rank correlations and achievements cores in terms of grades (0:min, 80:max), test scores (% of max) and combined (% of mean of all kids; data based on Coe. 2012)
Since this is the first study of its kind to investigate all five established parameters of health-related fitness (HFR), it should also be mentioned that body composition, flexibility and muscular endurance did not show the same statistically significant correlations the scientists observed for cardiorespiratory endurance and muscle strength in the kids (52% boy, 48% girls; all from the same age group ~12 years). Now, it would be nice if the people who design the curricula would keep that in mind, when they add junk after junk to the syllabus and regard sports and being active as an unnecessary diversion from the constant intellectual drills.

Creatine can do much, but it can't accelerate skeletal muscle repair after a workout 

The results of a recent study from the Department of Kinesiology and Physical Education at the Wilfrid Laurier University in Canada (McKinnon. 2012) , in the course of which  a total of 27 male (n = 15) and female (n = 12) participants between the ages of 18-24 completed an experimental training protocol with either
  • 2x creatine monohydrate (20g) and a carbohydrate supplement (20g) in order to blend consistency and taste (CREA),
  • 2x 40 g of maltodextrin only in 500mL of water (MALTO), or
  • no supplementation at all (control)  
The supplement was consumed over a 5-day period (check out the "Pharmacokinetics of Creatine" posts and you will learn that this dosage regimen is an unnecessary overkill - even if you insist on "loading") after which the participants participated in a baseline strength test that was followed by a muscle-damaging protocol that consisted of maximal force eccentric contractions:
Suggested read: "Creatine a Proven Non-Anabolic Agent: It's the Increase in Training Intensity that Will Give You the Hypertrophic Edge (read full story)
"Subjects performed 60 maximal eccentric contractions that were divided into 6 sets of 10 repetitions, with a 45 second rest period between repetitions.  The velocity of eccentric contractions was varied between sets (2 at 75°/sec, 2 at 90°/sec, and 2 at 120°/sec). This protocol has been used in previous studies and has been shown to be an effective means of inducing skeletal muscle damage (Cooke et al., 2009). The researchers also provided verbal encouragement to the subjects to help maintain maximal effort throughout the protocol." (McKinnon. 2012)
After adequate rest, the first of 5 post-tests was conducted. The results (figure 2) clearly show that despite the overall greater force recovery in the creatine group, the relative rebound after an allegedly higher drop was seen in the MALTO group while it was minimal in the no-supplement group.
Figure 2: Force recovery and muscle soreness at 0h, 24h, 48h, 72h, 96h in the control, maltodextrin and creatine groups subsequent to a 5-day suppelemtation regimen (nothing,  2x 20g crea + 2x20g malto, or 2x40g malto (McKinnon. 2012)
Overall the scientists are yet still right, when they say that "creatine supplementation failed to significantly influence indices elbow flexor muscle damage or rate of muscle recovery following eccentric muscle contractions." After all, there were no statistically significant differences between either the muscle force loss and rate of recovery or muscle soreness (small figure in figure 2) between the groups - and it is unlikely that this would change after the initial 96h of recovery.

Additional suggested reads:
  • DHEA Blunts Muscle Damage During 5 Days of Combined Endurance, Strength and HIIT Training in Young Men (read more)
  • Speed Up Your Regeneration and Propel Your Gains by Taking a HOT Bath Bath 2-Days Before Arduous Workouts (read more)
  • Overtraining, Inflammation, Insufficient Repair: Scientists Shed Some More Light on the Counterproductive Triad of Ups & Downs in Testosterone, IL-6, IL-10, COX II & Co (read more)
Ah, I almost forget to mention, you see that the mean isometric peak torque is not even back up to 100% after 96h, right? Remember that whenever you decide that it would be a good idea to do "yet another set of forced reps". It is possible that the seasoned strength training veteran you are, you recover faster than the subjects in the study at hand who had not trained for at least 4 months, but it stands out of question that eccentric forced reps will increase the time you need to regenerate, let alone to see what we are all striving for, i.e. super-compensation effects (see suggested links on the right for more on "doing too much" and faster recuperation after workouts).

Working out one leg changes genes in the other leg as well 

The progress research in the area of epigenetics, i.e. the changes of gene methylation and thus activity in response to nutrition, exercise and other variables you can easily control is actually amazing. With the recent publication of a study into what you may call epi-genetic cross-reactivity further contributing to our insights into the relations of the local and system epigenetic effects of exercise and their respective metabolic downstream effect (Catoire. 2012).
Figure 3: Graphical summary of the study design and selected results (Catoire. 2012)
As you can see in my graphical mini-summary of the study design (top) and outcomes (middle + bottom) in figure 3 there was a whole lot going on... and that despite the fact that I did already spare you a complete page with font 10 lists of genes that changed (you do have the numbers, I guess that shall suffice) and paired them in groups. What's funny is that, when it's all said and done, this does yet again tie in to yesterday's news on PGC-1 alpha 4 - how? Well, let's hear (or read), what the scientists have to say in the discussion of their results:
"Many of the observed exercise-induced changes in gene expression are likely part of an acute stress response related to disturbances in homeostasis elicited by exercise. The most highly induced genes in the exercising leg were all members of the NR4A family, a subgroup of orphan receptors within the nuclear receptor superfamily. NR4A1 and NR4A3 have been reported to be upregulated shortly after acute exercise and during recovery in rat, pig, and human [24], and this upregulation likely occurs locally by contractile stimuli. This finding was confirmed by our study in which we observed an upregulation of NR4As in the exercising, but not in the non-exercising leg. NR4A transcription factors are also known to be induced by adrenaline and noradrenaline. Circulating adrenalin and noradrenalin levels were increased in our study but must exert only a minor effect as NR4As were exclusively induced in the exercising leg,. [...] NR4A1 and 3 are thought to play a key role in regulating energy metabolism and early adaptation. [...] The results may imply that NR4A family might play an important role in the regulation of metabolic responses after exercise." (Catoire. 2012)
The study at hand does thus add yet another puzzle piece to the image of the crossroads of the endocrine (from one tissue to the other) and intracrine (in this case in the exercised muscle) effects of energy and metabolic changes on the one hand and muscular contraction and local stress, on the other hand. As closely interwoven as they are, we are now - thanks to the novel gene essays - able to see through the complex network, understand what exercise does to our physiology and can then, in the next step, come up with ways to modulate these effects for our own benefit.

It is clear that this is not going to be easy and the presence of two "mutants" among the 12 relatively old  study participants (52 year; "old" only for studies like this, of course!) suggests that any cookie cuter solutions are probably about to fail. I mean, if you have got two guys out of twelve where the overall magnitude of gene expression changes in the exercising and non-exercising leg were very similar, it is more than likely that you would see these and other anomalies very frequently; and each of them would have to be considered if you wanted to design he optimal workout (nutrition and supplementation) regimen for an individual (good news for personal trainers, if you know what you are doing, no sciency compendium is ever going to replace you ;-)

In rehab, doctors and therapists use the neurological stimulation a stiff leg receives, when you move the other while looking into a mirror that fools you into believing that the stiff leg would be moving as well.
In that it does not even really matter, whether the observed anomalies were actually due to genetic differences or, as the scientists suspect simply the result of unconsciously performed isometric contractions in of the non-exercising leg. The ensuing neuronal activation could have brought about similar effects as they are observed (and intended) during mirror therapy (see image on the right), where an involuntary neural stimulation of the muscles in a stiff leg occurs, when the mirror fools you into believing that you actually just moved your stiff leg, or other body part, when it was in fact only the counter-lateral limb that moved (note: one of the latest reviews of the literature says about its efficacy in stroke rehab would facilitate the recovery of "motor function, activities of daily living and pain" and could be recommended "at least as an adjunct to normal rehabilitation for patients after stroke"; cf. Thieme. 2012).

With the effects of neural stimulation, which has already been shown to induce gene expression changes via increased calcium concentrations in the skeletal muscle as well as via other mechanisms (Long. 2007; Kanzleiter. 2009; Chin. 2010, we do thus have a third player in the epigenetic / protein regulatory exercise orchestrate that does now consist of a metabolic, a contractile / stress mediated and a neuronal component. As far as skeletal muscle hypertrophy is concerned, the local expression does still appear to be the major determinant of adaptation and thus growth - to train your left leg only expecting that the other will grow due to "bystander effects" is therefore almost as hilarious as skipping leg day with the lame excuse that your legs would grow from training your biceps ;-)

On ultra short notice

With that I'll call it a day as far as the detailed posts are concerned and invite you to come back tomorrow, when I am going to pick up on this discussion in a detailed post on the Roa study on PGC-1 alpha 4, muscle growth, myofiber composition, strength development, workouts and the whole megillah. For the time being here is a bunch of unsorted other things I considered newsworthy:
  • Anti-psychotics increase lipid synthesis by depressing it!? What sounds totally counterintuitive, is actually the main message of an editorial to the latest issue of the Journal of Lipid Research, in which Skreede, Steen & Ferno argue that a paper by Canfrán-Duque et al. clearly suggests that the obesity and hypercholesterolemic effects of 2nd generation anti-psychotics such as clozapine, risperidone, and ziprasidone are brought about by the counter-regulatory upregulation of cellular lipogenesis in response to their suppressive effect on cholesterol synthesis. (Skreede. 2012)
  • The greater the muscle group you work, the larger the impact on the central nervous system will be (Rossmann. 2012) -- In the end everybody will know that intuitive, back and leg days are the hardest and most taxing to the whole system. Based on a trial involving eight young men who performed exhaustive large (cycling – BIKE) and small (knee extensor – KE) muscle mass dynamic exercises at 85% of the modality-specific maximal workload, scientists from Salt Lake City did now provide further experimental evidence that supports the notion that the CNS tolerates a greater magnitude of peripheral fatigue and likely a greater intramuscular metabolic disturbance when the pertinent afferent signaling comes from small vs. large muscle groups . 
  • Rhodiola Rosea turns out to be an opiate (Lee. 2012).-- In a recent study scientists from the Chi-Mei Medical Center in Yong Kang, Tainan City, Taiwan were able to show that the popular but questionable (as far as the significance of its effects are concerned) adaptogen rhodiala decreased the systolic blood pressure of spontaneously hypertensive rats. Intriguingly the effect was blunted by the administration of the selective opioid μ-receptor antagonist, cyprodime, but not by naloxonazine, an antagonist specific to opioid μ1-receptor, which suggests that a direct effect on the opiate receptor. Moreover, the level of mood enhancing and relaxing beta-endorphins rose in both wild type and hypertensive rodents (with the effect being more pronounced in the latter)
  • Chinese hawthorn for the hair, not the heart (Shin. 2012) -- I guess if you hear hawthorn or Crataegus you will probably think of its purported beneficial effects on heart health. Now if the results from a recent rodent study are applicable to humans, as well, you will soon have to establish a novel neuronal connection between (Chinese) hawthorn and your scalp, or rather the hair on your scalp . With its beneficial effects on the initiation of the anagen phase in mice in teloge and the ensuing increase in skin color, thickness of the hair shafts, and density (number and size) of the hair. Oral C. pinnatifida extract (at a human equivalent dose of ~320mg/day) could soon be all the rage among men and women who fear for their superb head of hair.
I think this is enough for today. There is a life beyond the SuppVersity not for you, of course, but for me - so while you head over to the SuppVersity facebook page for even more news, I am going to enjoy Saturday night ;-)

    References:
    • Canfrán-Duque, A., M. Casado, Ó. Pastor, J. Sánchez-Wandelmer, G. Peña, M. Lerma, P. Mariscal, P. Bracher, M. Lasunción, and R. Busto. Atypical antipsychotics alter cholesterol and fatty acid metabolism in vitro. J Lipid Res. 2012 [in press]
    • Catoire M, Mensink M, Boekschoten MV, Hangelbroek R, Müller M, et al.  Pronounced Effects of Acute Endurance Exercise on Gene Expression in Resting and Exercising Human Skeletal Muscle. PLoS ONE 7. 2012; 11: e51066.
    • Chin ER. Intracellular Ca2+ signaling in skeletal muscle: decoding a complex message. Exerc Sport Sci Rev. 2010 Apr;38(2):76-85. 
    • Coe DP, Pivarnik JM, Womack CJ, Reeves MJ, Malina RM. Health-related fitness and academic achievement in middle school students. J Sports Med Phys Fitness. 2012 Dec;52(6):654-60. 
    • Kanzleiter T, Wilks D, Preston E, Ye J, Frangioudakis G, Cooney GJ. Regulation of the nuclear hormone receptor nur77 in muscle: influence of exercise-activated pathways in vitro and obesity in vivo. Biochim Biophys Acta. 2009 Aug;1792(8):777-82. 
    • Lee WJ, Chung HH, Cheng YZ, Lin HJ, Cheng JT. Rhodiola-Water Extract Induces β-endorphin Secretion to Lower Blood Pressure in Spontaneously Hypertensive Rats. Phytother Res. 2012 Nov 28.
    • Long YC, Glund S, Garcia-Roves PM, Zierath JR. Calcineurin regulates skeletal muscle metabolism via coordinated changes in gene expression. J Biol Chem. 2007 Jan 19;282(3):1607-14.
    • Rossman MJ, Venturelli M, McDaniel J, Amann M, Richardson RS. Muscle mass and peripheral fatigue: a potential role for afferent feedback? Acta Physiol (Oxf). 2012 Dec;206(4):242-50. 
    • Shin HS, Lee JM, Park SY, Yang JE, Kim JH, Yi TH. Hair Growth Activity of Crataegus pinnatifida on C57BL/6 Mouse Model. Phytother Res. 2012 Nov 12.
    • Skrede J, Steen VM, Ferno J. Antipsychotic-induced increase in lipid biosynthesis: activation through inhibition? Journal of Lipid Research. December 7, 2012 [Epub ahead of print] 
    • Thieme H, Mehrholz J, Pohl M, Behrens J, Dohle C. Mirror therapy for improving motor function after stroke. Cochrane Database Syst Rev. 2012 Mar 14;3:CD008449.

    3.2g of Beta Alanine Reduce Rate of Perceived Exertion, Increase Time to Exhaustion and Ventilatory Threshold. Vegetarians, Older People and Diabetics May Benefit Most.

    Image 1: If you are into running, ladies, beta alanine is for you ;-)
    Those of you who make sure that they are getting their highly educative daily dose of the SuppVersity *rofl* will be aware that today's blogpost is, once again, dealing with beta alanine. Contrary to yesterday's post, which dealt with its pharmacokinetics, we are today going to have another look at what kind of real world performance outcomes the average (female!) physical culturist can expect from taking at least 3.2g of the beta amino acid per day - a dosage that has been shown in previous studies to increase intra-muscular carnosine levels by 27–39% in fast- and slow-twitch muscle fibers, respectively (Baguet. 2009). And though I do not want to spoil things, I can already tell you that the results make it quite clear why beta alanine is not the next creatine.

    Somehow ergogenic, yet not really antioxidant

    For the study that was conducted at the Applied Physiology Laboratory at the University of North Carolina, study that was conducted by A.E. Smith recruited 24 "recreationally active" women, of which the authors state that they "engag[ed] in 3–7 days per week of aerobic, resistance or recreational activities, but were not highly trained competitive athletes". With a mean age of 21.8 years, a height of 165cm and a body weight of 61.5kg the subjects are thusly representative of the average young woman who goes to the gym to either get or keep in shape. I am specifically emphasizing this, because - at least in the early days - beta alanine was heavily marketed as "the creatine for women" who fear the water retention people still claim was an inevitable side effect of creatine supplementation.
    Image 2: If you retain water, this is not due to creatine monohydrate. Either you are taking to much (creatine loading is a thing of the past) or you have bought a product with shitloads of carbs in it - in that case, chances are its not only water you are gaining ;-)
    Does creatine supplementation inevitably lead to water retention and weight gain? Just because this myth is still perpetuated, especially among female figure competitors, I thought it may be worth addressing this again: Pure creatine monohydrate without the sugar and the other bullshit you will find in many creatine supplements does not necessarily lead to increases in either total body or water weight. A study by Rawson et al. showed only recently that the consumption of 0.03g/kg creatine for six weeks did not result in statistically significant changes in body weight or water in men or women, despite significantly increased plasma creatine concentration and enhanced resistance to fatigue during repeated bouts of high-intensity contractions (Rawson. 2011).
    The women were advised to simply stick to their usual routine and to refrain from taking any supplements and medications except from their 2x800mg beta alanine tablets. The latter were to be taken 3x a day... so according to Cocker, they should have consumed 2x0.8g x3/day = 4.8g/day and not, as the scientists state "3.2 g daily". Now, according to Smith et al. this was the "required dosage" all participants met. I can however not say, whether this means that the third dose was optional... and this is not the only oddity in this study, where it is well worth to look beyond the assessments and conclusions of the authors.

    At the beginning and the end of the 28-day supplementation period, the women had to perform a graded oxygen consumption test (VO2max) to evaluate VO2max, time to exhaustion, ventilatory threshold and establish peak velocity (PV), as well as a "non-damaging treadmill run (oxidative stress run) for 40 min at 70% PV [peak velocity]". Before, immediately after and in the 2-6h post running window total antioxidant capacity (TAC), superoxide dismutase (SOD), 8-isoprostane (8ISO) and reduced glutathione (GSH) were measured. In addition to that, heart rate and ratings of perceived exertion were recorded during the 40 min run. The two main metrics of the study were thusly the potential anti-oxidant effects (TAC, SOD, 8ISO, GSH) and the anticipated immediate ergogenic effects (VO2Max, time to exhaustion, heart rate and perceived exertion) of beta alanine supplementation.
    Figure 1: Effect of 28 days of beta alanine supplementation on maximal oxygen consumption (VO2max), time to exhaustion during a graded exercise test (VO2TTE) and ventilatory threshold (VT) and qualitative practical significance (data and caption adapted from Smith. 2011)
    If you now have a look at the my graphical rehash of the scientists own evaluation of the effect beta alanine supplementation had on VO2Max, the time to exhaustion (VO2TTE) and the ventilatory threshold (VT), you will have to concede that mean improvements of 0.28%, 6.6% and 3.7%, respectively, as well as the large discrepancies among the subjects (from beneficial over negligible to harmful) do not actually speak for beta alanine.
    Figure 2: Effect of beta alanine supplementation on oxidative stress markers measured as total
    antioxidant capacity (TAC) and glutathione (GSH) and the qualitative practical significance
    for women (data and caption adapted from Smith. 2011)
    Things get even more confusing when we take a look at the antioxidant effects of beta alanine. Not only were the levels of superoxide dismutase (SOD) and 8-isoprostane (8ISO) not different between groups, and the effect of beta alanine on the total antioxidant capacity (TOC) of the subjects negligible, the scientists' summary of the effects does even suggest that, after an initial amelioration of the negative effect of treadmill running on GSH, there was some sort of a "likely harmful" rebound 6h after the 40 min exercise bout. Before you do now flush your beta alanine stores down the toilette, I suggest you first take a look at the actual (absolute) effects beta alanine supplementation had on the exercise induced changes in GSH levels:
    Figure 3: Absolute GSH levels (in µM) immediately before (pre), post, 2h and 4h after treadmill running in the placebo and beta alanine supplemented women before (pre) and after (post) the 28-day supplementation period (compiled based on data from Smith. 2011)
    As you can see in figure 3, there was an (unexplained) increase in GSH in the course of the 28-day supplementation period in both groups. With 2%, the latter was statistically non-significantly greater in the beta alanine group, and the "likely harmful" effect of beta alanine supplementation 6h after the end of the treadmill-run is simply the result of a smaller increase in GSH, when you compare the pre- to post-supplementation levels at the 6h mark - and I guess, you would agree that a +27% increase in GSH is not exactly something that deserves to be called "likely harmful", wouldn't you?

    All-clear: Beta alanine is not ergolytic ;-)

    Now that we have gotten that straight, let's get to the last (and most) significant benefit the women in the beta alanine group had from taking the supplement: a statistically significant reduction in the rate of perceived exertion during treadmill running (cf. figure 4).
    Figure 4: Rates of perceived exertion during 40 min treadmill running before (pre) and after (post) 28 days of supplementation with beta alanine or placebo; small graph: relative difference post supplementation in women receiving BA vs. placebo (data calculated based on Smith. 2011)
    It goes without saying that being 18% less fatigued is something that could well be worth spending the roughly 7$ for a 28-day supply on (calculation based on a dose of 3.2g per day taken over 28 days and assuming you buy your beta alanine in bulk at one of the major suppliers). This, by the way, could be particularly true if you belong to one of the following groups, who have been found to have low intra-muscular carnosine levels, to begin with:
      Image 3: Older people are only one of the three groups who are "at risk" of low carnosine levels and are thusly most likely to benefit from beta alanine supplementation.
    1. vegetarians - a 2011 study by Evaraert et al. found that "Vegetarians have a lower carnosine content of 26% in gastrocnemius compared to omnivores" (Everaert. 2011); and according to another recent study, the soleus carnosine content of vegetarians was "non-significantly" reduced by -9% after 5 weeks of sprint training, while the same protocol elicited increases of +11% in omnivores (Baguet. 2011)
    2. older people - Evaraert et al. found a linear decline (ca. -10% in 20 years) in carnosine levels with age (correlation r=-0.26; Everaert. 2011); and Stout et al. report a highly significant +29% increase in physical working capacity at the fatigue threshold in twenty-six men (n = 9) and women (n = 17) (age ± SD = 72.8 ± 11.1 yrs) who  had been supplementing with 800 mg three times per day for 90 days (Stout. 2008)
    3. type-2 diabetics - according to Gualano et al. type-2 diabetics have "significantly lower carnosine content (−45%) in gastrocnemius muscle", a relative deficiency of which the scientists argue that it "may be partially associated with defective mechanisms against oxidative, glycative and carbonyl stress in muscle." (Gualano. 2011)
    After all, it does yet not really matter whether you are a type-2 diabetic, a vegetarian or simply getting older, compared to many (if not most) of the other overpriced ergogenics that are advertised all over the web, beta alanine is certainly not only one of the cheapest, but also one of the most promising candidates for the 3rd place on your list of staples, where (whey) protein and creatine should nevertheless still occupy position 1 and 2, respectively. And the fact that it did not prove to be a potent antioxidant in this study need not really be a disadvantage, after all, we still do not know whether the exercise-induced oxidative "damage" is not what actually triggers the highly desirable adaptive responses (cf. previous posts on "hormesis"), we are all looking for, when we are hitting the gym.

      Disappointing Results in 28-Day Creatine + β-Alanine Study: No Performance Benefits, No Muscle Gain, No Fat Loss, No Increase in Phosphocreatine & Carnosine in 32 Women

      Let's take a closer look at the study and find how it was possible that two proven ergogenics "failed".
      Creatine and beta-alanine belong to the few "proven ergogenics", but according to the latest study from the University of Pittsburg, the Texas Christian University, the University of Wisconsin – La Crosse and the Texas A&M University they are not as effective as some of us may think. Specifically the effects of beta-alanine which was tested in what you may call its "comfort zone", i.e. a graded exercise test on the cycle ergometer for VO2peak with lactate threshold determination, and multiple Wingate anaerobic capacity tests. And still, the overall results of the study is that there a "no consistent additive benefits of BA [beta alanine] and CRE [creatine] supplementation in recreationally active women.
      If you are using creatine already try adding bicarbonate as extra-cellular pH-buffer

      The Hazards of Acidosis

      Build Bigger Legs W/ Bicarbonate

      HIIT it Hard W/ NaCHO3

      Creatine + BA = Perfect Match

      Bicarb Buffers Creatine

      Beta Alanine Fails to HIIT Back
      In today's SuppVersity article, we are going to have a closer look at the study design, its outcomes and potential explanations for the absence of the highly desirable performance enhancing effects of these two (alleged) ergogenic powerhouses.

      As you may know I am not a fan of beta alanine, anyway. Yet despite my alleged bias, I have to admit that the wingate tests the scientists used to determine the effects of the supplementation protocol may have been too short for BA to work. In the most comprehensive meta-analysis of the research to-date, Hobson et al. (2012) found that there are no ergogenic effects to beta alanine on exercises lasting less than 60s or more than 240s; and in the "ergogenic" 60-240s zone, the performance benefit is only 2.85%.
      Figure 1: In view of the short study duration it's no wonder that there were no significant effects on body fat and lean mass, but the fact that the beta alanine only group actually gained fat after an initial high loss of body fat is still awkward - still, statistically significant was only the time effect, which tells you that exercise works (Kresta. 2014).
      And as far as the absence of benefits of creatine are concerned. The results of the study are in line with previous experimental evidence like that presented by Green et al. who report in their 2001 article in the The Journal of Strength & Conditioning Research that...
      "[...] short-term Cr supplementation does not enhance MP and PP during repeated upper-and lower-body Wingate tests when not accompanied by an increase in body weight." (Kresta. 2001)
      Similarly, Hoffman et al. (2008) could not find perfomance benefits of short-duration beta alanine supplementation in college football players, what the scientists from the College of New Jersey did find, though was an increases training volume and reduces subjective feelings of fatigue in their highly trained subjects in response to the ingestion of 4.5g/day of beta alanine (Hoffman. 2008).

      All in all, the results are thus less surprising than they appear to be...

      ... at least for those of you who don't believe in the unsustainable promises of the supplement industry, but rely on experimental evidence, only. For creatine, the scientists tested the wrong type of exercise. For beta alanine the exercise duration (60s) on the wingate tests was not long enough to show significant performance increases.
      Figure 2: Non-significant (!) changes in carnosine (should increase with BA supplementation) and phosphocreatine (should increase with creatine supplementation) in the BA, BAC, CRE and placebo group (Kresta. 2014).
      What the previous brief review of selected experimental evidence does not explain, though, are (a) neither the beta alanine, nor the creatine or combined supplementation lead to statistically significant increases in carnosine (via beta alanine) or phosphocreatine (via creatine), (b) the levels of phosphocreatine the high energy resource, that is believed to be responsible for most of the beneficial effects of creatine actually dropped after 2 weeks on maintenance dose of 0.1g/kg creatine, when it was administered after a 0.3g/kg creatine pre-load. These results stand in contrast to previous studies, like...
      • Harris and colleagues (2001) who reported that β-ALA supplementation (3.2 g/day) resulted in a 42% increase in muscle carnosine levels after four weeks of supplementation not due to the fact that the carnosine levels didn't increase, but rather due to the fact that the scientists did not find statistically significant interactions among groups in muscle carnosine levels.

        As Kresta et al. (2014) point out, "the lack of statistical significance was apparently due to the large variability in muscle carnosine levels observed in response to β-ALA supplementation, assay variability, and/or inadequate sample size", so that "[m]ore research is needed to determine the effects of β-ALA supplementation on muscle carnosine levels in recreationally-active women" (Kresta. 2014).
      • Greenhaff et al. (1994) or Harris et al. (1992) who found significant increases in phosphocreatine with similar preloading + maintenance creatine supplementation schemes as the one used in the study at hand, but yielded significantly higher and above all consistent increases in creatine of up to 40% . Results from the present study found non-significant increases in muscle PCr of up to 40%

        Again, Kresta et al. suspect that "the lack of significance may have simply been a result of the small sample size", but add that "it is also known that there is individual variability in response to creatine supplementation" (Kresta. 2014) - a fact that is imho unlikely to be a likely cause of the lack of effect in all subjects, though.
      Overall it is thus difficult to determine the lack of consistence improvements in carnosine and phosphocreatine levels in the study at hand, it may yet, as Kresta et al. suggest also be possible...
      A study by Everaert, et al. indicates that women have naturally lower carnosine levels (Evaerart. 2011 | see figure abvove). Previous studies, e.g. Tallon (2006), however, found no such difference which is interpreted by Harris et al. in their 2012 review as evidence that "that the apparent gender difference reported by Everaert et al. (2011) may have been simply due to a higher type I:II ratio in females in the voxel sampled." (Harris. 2012)
      "[...]that sex may have played a role in response to creatine and/or β-ALA supplementation. In this regard, most studies on creatine and β-ALA supplementation have been conducted on males and there is some evidence that females may respond differently to creatine and/or β-ALA supplementation. For example, Fosberg and colleagues (Forsberg. 1991) reported that females had greater total creatine amounts relative to tissue weight; however, other studies show there is no difference between males and females (Forsberg. 1991; Stegen. 2014).

      There are also some data suggesting that men may have greater muscle carnosine levels than women (Derave. 2002; Harris. 2012); however, a recent study showed sex did not have an effect on increasing carnosine levels with supplementation (Stegen. 2014). Additionally, Bex and coworkers (2014) reported that carnosine loading is more pronounced in trained versus untrained individuals" (Kresta. 2014).
      It is thus possible, but imho again not very likely that the fact that the subjects in the study at hand were women and or their individual training status may have had and impact on the hardly existing response to creatine and/or β-ALA supplementation.
      Creatine + bicarbonate appears to offer a superior synergism | learn why
      In the end, it's yet not the increase in carnosine or phosphocreatine that's important for us. What we are looking for are performance increases, which were probably absent due to the selected tests, on which previous studies have already shown that creatine and beta alanine have failed before to produce significant performance increases (see previous elaborations on the non-existent effects of BA on 60s and >240s exercise and the issue with creatine and wingate tests), plus changes in body composition for which the four-week study period may simply have been too short.

      Against that background I would like to point out that the study at hand does not indicate that either beta alanine or creatine are useful. What it does, thought, is to remind us of the fact that (a) you won't see results over night and (b) even beta alanine and creatine are exercise-specific ergogenics and won't boost your performance an each and every type of exercise to the same extent. Or what do you think are the implications? Comment on Facebook!
      References:
      • Bex, Tine, et al. "Muscle carnosine loading by beta-alanine supplementation is more pronounced in trained vs. untrained muscles." Journal of Applied Physiology 116.2 (2014): 204-209.
      • Derave, Wim, et al. "Muscle carnosine metabolism and β-alanine supplementation in relation to exercise and training." Sports medicine 40.3 (2010): 247-263.
      • Everaert, Inge, et al. "Vegetarianism, female gender and increasing age, but not CNDP1 genotype, are associated with reduced muscle carnosine levels in humans." Amino acids 40.4 (2011): 1221-1229.
      • Green, J. Matt, et al. "The effects of creatine supplementation on repeated upper-and lower-body Wingate performance." The Journal of Strength & Conditioning Research 15.1 (2001): 36-41.
      • Harris, Roger C., et al. "The absorption of orally supplied β-alanine and its effect on muscle carnosine synthesis in human vastus lateralis." Amino acids 30.3 (2006): 279-289. 
      • Harris, R. C., et al. "Determinants of muscle carnosine content." Amino acids 43.1 (2012): 5-12.
      • Hobson, Ruth M., et al. "Effects of β-alanine supplementation on exercise performance: a meta-analysis." Amino acids 43.1 (2012): 25-37.
      • Hoffman, Jay R., et al. "Short-duration< i> β</i>-alanine supplementation increases training volume and reduces subjective feelings of fatigue in college football players." Nutrition Research 28.1 (2008): 31-35. 
      • Kresta, Julie Y., et al. "Effects of 28 days of beta-alanine and creatine monohydrate supplementation on muscle carnosine, body composition and exercise performance in recreationally active females." Journal of the International Society of Sports Nutrition 9.Suppl 1 (2012): P17.
      • Stegen, Sanne, et al. "The Beta-Alanine Dose for Maintaining Moderately Elevated Muscle Carnosine Levels." Medicine and science in sports and exercise (2014).
      • Tallon, Mark J., et al. "Carnosine, taurine and enzyme activities of human skeletal muscle fibres from elderly subjects with osteoarthritis and young moderately active subjects." Biogerontology 8.2 (2007): 129-137.

      Adelfo Cerame - Road to The Wheelchair Nationals '12: My Five Simple Tricks for Guilt Free Thanksgiving Celebrations. Plus: Four Dietary Supplements You Should not Miss!

      Image 1: Adelfo on Wednesday before the feast began. We will see how he looks next week ;-)
      I guess, this blogpost should actually begin with the words "Happy Thanksgiving" in big, bold letters, but for us Europeans - and me as a German, in particular - today is a regular working day. Nevertheless, it is a day to celebrate, because THIS is actually post #600 here at the SuppVersity and I am in fact grateful (and thusly giving thanks) that you, my dear students, readers, followers or however else you want to refer to yourselves, are still interested in my perspective(s) on what is going on in the world of fitness, bodybuilding, sports and exercise science.

      That being said, I do still hope that all of you (who actually have a holiday) are having a good time with your friends and family, just like my friend Adelfo, who has sent me his weekly contest-prep update and his best wishes to all of you last night, already ....

      Turkey, pie, ... pie, turkey, ... turkey ... and some supplements!

      Ok guys, I’m going to try and make this real brief because I actually started my Thanksgiving Day Feast a day early, so that I’ve been falling in and out of sleep from all the turkey and pie and still have to prepare for another day of furious eating again tomorrow, in order to "peak" (just to stick to the bodybuilding terminology) right on Thanksgiving!

      Image 2: I like protein blends and Lean Supreme is one of my favorites. I gets it for $32 for 4.2lbs at my local Nutrition Zone.

      As you know from the previous installments of this series, I have planned these 2 cheat / refeed days long ahead. In fact, being able to go somewhat overboard on Thanksgiving, Christmas, New Years Eve and my birthday was part of the reasoning behind starting my contest preparation so early.  But before I give you guys some pointers on how to approach these holiday feasts, I thought it was about time to address the subject of supplements. I know I've hinted at being on a budget and cutting back on my usage of protein powder in a previous episode; luckily I have recently been able to stock back up on my four staples, i.e. those supplements, I think are really worth spending your money on.

      For me the "basic four" are
      • a high quality protein powder
      • a bag of bulk BCAAs
      • a quality multi-vitamin, and 
      • the good old creatine monohydrate
      Protein powder, BCAAs, a mulit and creatine are what I would call the "foundation" of my supplementation regimen. If I cannot afford all of these, I am not going to buy any other  supplement - "prioritizing" is the name of the game. If my budget allows that I am yet planning on experimenting with a few other products in the weeks to come. What I currently have on my mind are a decent fat burner, some bulk D-Aspartic Acid and a test booster if I can find one that actually works...
      Image 3: Protein powder, multi-vitamins, creatine monohydrate, and BCAA’s, combined with good training + nutrition, and that’s all you need to build your physique… well at least for me it is ;-)
      Remember, all four, the protein powder, the BCAAs, the multi-vitamin and the creatine are add-ons; they are not part of what I call my "nutritional regimen". They do not replace any nutrients (as Dr. Andro would say: "They are called supplements not replacements" ;-) and I am well aware that I won't get anything out of them, if my diet and training are not 100% in check. Never fool yourself into the false security that you are taking supplements, X,Y and Z and could thusly let your nutritional protocol slide. No supplement gives you the excuse to eat like shit or skip a training session! You can do without quality supplements but you can’t do without quality foods - although the colorful adverts in some of the muscle mags, try to make you believe otherwise.
      Image 4: Huge thanks to Jack Gurlekian and Dr. Andro for helping me out on the supplement side.
      Before I get started on Holiday feasting, I’d like to give a shout out to Jack Gurlekian and thank him for hooking me up with some of the supplements that he distributes and makes himself… I’d also like to thank Dr. Andro himself for helping me out with finances to help me purchase some supplements that should hold me off for a couple months : Creapure(TM), glutamine peptides & ZMA from True Protein. Inner Armour supplements and Jack’s very own amino acid blends! [A note by Dr. Andro: Additional sponsors are always welcome ;-]
      My holiday season feasts 101!

      The holiday season is approaching and you all know what that means? Epic holiday feasts and it starts with Thanksgiving, continues on Christmas and ends with New Years Eve. And when it’s all said and done, all you’re left with is a GUT full of regret! In order to help you to keep both the gut, as well as the regret at bay, I want to share with you how I like to prepare myself for the holiday food gauntlet…

      Image 5: This thanks giving plate looks way better than the government's MyPlate
      Actually it all begins with keeping myself in good physical shape and keeping my physique as lean as I can year round. If you read the last installment of Dr. Andro's Intermittent Thoughts Series on "Why to cut before bulking" you will be aware of the hormonal and metabolic advantages which come with being lean. That being said, there is actually little reason, why I could not enjoy occasions like this without any regret, if it's not just a few days out on the next contest, which obviously isn't yet the case... and if you have been following the whole series since September, you will also be aware that I am exactly on schedule - a schedule that allows for a long consistent cut, precisely because I knew that Thanksgiving, Christmas and New Years Eve were coming and being in decent shape by then would allow me do some serious and more importantly guilt free eating ;-)

      5 simple rules to survive the feast without too much damage

      Being on an intermittent fasting protocol does help here as well, I have already touched on that in a previous installment - when you pack your complete caloric intake into a small feeding window "overeating" (no, not eating like shit!) is part of the game, anyway. Ok, the foods are probably different on Thanksgiving, but the caloric intake may in fact not vary too much. Moreover, the muscle specific improvements in insulin sensitivity that come with training fasting make it less likely that you store all the good and not so good nutrients you are about to eat today in the form of glycogen or even new muscle tissue, rather than as triglyceride droplets in your love handles.

      Personally I do adhere to the the following 5 principles for intermittently fasted holiday celebrations in order to keep any potential damage to my physique at a minimum:
      1. I give myself a caloric buffer throughout the week before the big day. I don’t starve myself but I don’t eat as much. I try to be like around 200-300 calories shy of my daily caloric intake (1800 kcal). And being on IF, I do not even notice this 200-300 calorie reduction as far as my appetite is concerned.
      2. I stick to proteins and moderate fats throughout the week before the big feast. Just sticking to proteins, moderate fats, veggies and fruits, will help you with making that caloric buffer, simply because they are satiating. I still had my PWO chocolate milk, and PWO carbs with my meal.
      3. I fast before the big feast. You may want to even throw in an intense and heavy weight training session before, so you can get more bang for your buck when you eat! (Though I wont be doing that because it’s my rest day)
      4. Once I get to the party and begin my feast, I focus first on filling up on protein like turkey, chicken, roasts, fish and BBQ meats. This way I’m sure to hit my protein macros and to fill up with some good protein, then I’ll have my desserts like cakes and pies … and a couple shots of liquor and a couple glasses of wine ;-) But once I’m full… That’s it! I wont force myself to eat more just because there’s a lot of food. I’ll wait a couple of hours like I would normally do (on regular days), until I’m hungry again before I’ll eat again. I try to get in the same amounts of meals that I usually would during my feeding hours (3-4 meals) but obviously the meals will be much bigger... yeah, and with a little bit more junk ;-)
      5. I push away the remote thoughts of guilt and enjoy the day! I mean, you train hard and eat smart year round to keep yourself lean & mean. One day is not going to reverse all your efforts, maybe some bloat and a little water retention, but that will subsides in a couple days. Other than that… Enjoy your Thanksgiving, because I know I will!
      Happy Thanksgiving Everyone! Eat responsibly and don’t eat & drive full ;-)

      VPX Pre- & Post-Workout Nutrition Gets "Sponsored" Scientific Approval: +4% Lean Mass, -6% Body Fat, +13% Upper and +21% Lower Body Strength in 29 Days

      Image 1: Supplemental double-whammy. VPX' now
      "scientifically proven" pre- & postworkout products
      This is one of those cases, where I cannot decide whether I should applaud VPX or just shake my head... the scientist in me says: "Hey, you know how that is - with a research grant from the government cutting edge science is impossible, especially if you want to investigate something as 'profane' as building muscle". The cynic skeptic, on the other hand, whispers: "Come on, what results would you expect, if the study was financed by the producer of the supplement under scrutiny?" I guess I will applaud skeptically and exercise special caution in my analysis of the latest study from the Department of Health and Performance at Baylor University (Willoughby. 2011).

      As in previous studies (Willoughby. 2007; Willoughby. 2009), Darryn S. Willoughby and his colleagues availed themselves of a buckload of VPX supplements and recruited 19 previously recreationally active, yet untrained (*) men with an average age of 22.8 +/-4.67 years, a height of 179.5 +/-6.38 cm and a total body mass of 79.1 +/-16.13 kg for another study into the effects of two supplements, which are supposed to "advance you to the next level of fitness" (VPX. 2011). Strength and body composition (body fat measured reliably by DEXA, not body-impedance), venous blood sampling and muscle biopsies were performed on day 0 and day 29 of the 4-week study period, in the course of which the participants underwent a standardized resistance training protocol (upper-/lower-body split, 4x à week), which mirrored the one that had been used in Willoughby. 2009 already (*).
      Figure 1: Illustration of the training regimen (based on Willoughby. 2011)
      The bodybuilding-type beginner 2x split training regimen is unquestionably a huge plus of the study (cf. figure 1). Performed twice a weak, this is what real world training would look like and so that it stands out of question that the results of the study will translate into practice - at least for everyone who has not touched a dumbbell more than thrice a week within the last 12 and abstained from all sorts of performance enhancing supplements and drugs within the last 3 months (*).

      The NO Shotgun approach to protein NO SyntheSize??? 

      Figure 2: Ingredient profiles of
      No Shotgun and No SyntheSize
      More important than the identical training regimen was yet obviously the supplementation protocol, to which the participants were assigned in a double-blind randomization process (on a side note: "double-blind" means that not only the subjects, but the scientists, as well, did not know which participants received the placebo and which ones the VPX products). While half of the subjects consumed a maltodextrose placebo (27g pre, 27g post workout), the subjects in the "NOSS" group consumed the same amount of NO Shotgun and NO SyntheSize as their pre- and posworkout supplement, respectively. Now, as the names imply, both supplements are intended to increase nitric oxide production and protein synthesis, yet with a focus on the former in NO Shotgun that is loaden with arginine and a heap of stimulants and a focus on the latter in NO SyntheSize, the composition of which is pretty similar (cf. figure 2), yet without the "Redline Energy & Meltdown Fat Burning Technology" ;-)

      Although there were no specifically dietary guidelines, the research did at least collect some nutritional data based on a 4-day questionnaire all participants had to answer at the beginning and end of the study. While there was a slight reduction in the total caloric intake in the carb group (interestingly mainly from carbohydates), neither the intra-group changes, nor the inter-group differences reached statistical significance.

      More muscle, less fat! Trainee, what more can you ask for?

      That there were no differences is yet something you cannot say of the changes in body composition the study participants underwent in the course of this 28-day intervention.
      Figure 3: Relative changes (compared to baseline) in body composition after 16 strength training sessions in 28 days with either 54g of maltodextrin or 27g of NO Shotgun and 27g NO Synthesize pre- and postworkout (Willoughby. 2011)
      As a passing view of the relative changes (compared to baseline) in figure 3 show, the NOSS group (receiving NO Shotgun prior and NO SyntheSize post workout) registered significantly more pronounced elevations in fat free mass (p<.023 indicates that the chances that this was sheer coincidence are 23%) and - contrary to the carbohydrate group - lost -6% of their body fat, while the carb eaters added another 2% of adipose tissue to their love-handles.
      Figure 4: Changes in upper and lower body strength (in kg/kg body weight during bench press and leg press at 1RM) after 16 strength training sessions in 28 days with either 54g of maltodextrin or 27g of NO Shotgun and 27g of NO Synthesize pre- and postworkout (Willoughby. 2011)
      Interestingly, the lean mass increase went hand in hand with likewise (statistically) significantly greater (p-values see figure 4) increases in both upper (+13% vs. +1%) and lower (+21% vs. +11%) strength in the subjects in the NO Shotgun + NO SyntheSize groups.
      * you may have wondered what all the asterisks in the previous paragraphs meant... well, they indicate specificities in the study design detractors may call "precautions that ensure that the VPX supplements are sitting pretty" ... I mean the exact same supplementation protocol performed on a bunch of veteran bodybuilders would probably not have elicited any measurable effects on body composition - keep that in mind when you interpret the results.
      Now, it obviously should not surprise you that the protein (and leucine) loaden and creatine, beta-alanine spiked workout supplements outperform simple sugar water. It is thus more interesting to take another look at the data from the 2009 "NO Shotgun only"-study, Willoughby et al. have done (Willoughby. 2009). On the exact same training protocol, yet with only 27g of NO Shotgun or placebo 30min preworkout, the participants lost less body fat (-1.21%), but gained the exact same ~4% of lean mass and comparable increases in bench press and leg press 1RM (+8.82% and +18.4%, respectively).

      Scientifically proven ingredients make scientifically proven products

      I leave it up to you whether or not the results of this study will influence your next supplement purchase - after all, even the VPX guys will be aware that their supplements are not so unique that intelligent people like you would not be able to identify the key ingredients in their products (EAAs, hydrolized protein, creatine, beta alanine, some workout-boosting stimulants, etc.) and realize that there are way more than those two products which would probably have produced identically (within statistical margins) results, if, and here we've come full circle, if their respective manufacturers had the money and the balls to do scientific studies on their products.

      Combinations that Work: HMB & Isometric Training for Lean Mass, Creatine & Powerlifting for Leaning Out and Carnitine & Bodybuilding for Powerlifting?

      Image 1: Jacek Spychala - I must admit, I don't know if he was one of the subjects, but 38 of his colleagues from the Polish National Powerlifting Team were (powerlifting.pl)
      As an athlete and even as a regular fitness enthusiast, you got to chose your training and supplementation modalities according to your professional or personal goals (in fact, the failure to do so is, in my mind, one of the main causes why so many trainees do not get the desired results at the gym). A very recent study from the Department of Combat Sports and Weightlifting at the Józef Pilsudski University School of Physical Education (I wish every University had such a department ;-) in Warsaw, Poland, sheds some light onto combinations which work, and combinations which don't... and trust me you will be surprised by the results of Dr. Marek Kruszewski's controlled intervention study (Kruszewski. 2011).

      Kruszewski recruited recruited a total of 170 (! that alone is noteworthy !) subjects who participated in a three-tier placebo-controlled study on the effects dietary supplementation of l-carnitine, creatine and HMB combined with different modes of strength training (bodybuilding type circuit training, powerlifting and isometric training) had on muscle strength, lifting performance and body composition (for a graphical overview of the study design see figure 1).
      Figure 1: Graphical illustration of the three tiers (l-carnitine, creatine, HMB), general information and detailed information on the exact exercise protocol of the isometric workout of the HMB group
      Not only the sheer size of the study with active and placebo groups of ~30 previously untrained subjects, each, in the l-carnitine and HMB tier of the study are impressive, the participation of 38 powerlifters from the Polish National Team (cf. video of Daniel Grabowski, with a 2254lbs total) is, as well. If each group had received all three of the supplements subsequently and body composition had not been measured with an expensive but still not 100% accurate body impedance device, this study would have been the equivalent of the egg-laying-wool-milk-sow of the Natural Rythmicity for Maximum Fat & Minimal Muscle Loss episode of the Intermittent Thoughts, but I guess we cannot have it all ;-)

      2g HMB + isometric training for lean muscle gains!

      Image 2: HMB is getting
      cheaper, lately
      I thought, I'd give the most "exotic" training variety (isometric training) the advantage and tell you about the effects 2g of HMB per day (4 servings of 500mg; one with breakfast, one before, one after the workout and one in the evening; for 5 weeks = 20 training sessions) had on the strength performance and body composition of 69 previously untrained, strength trainees -  not only to raise the awareness that isometric contractions could be a valuable addition to everyones regime (something my friend Rob Regish also advocates in his Blueprint), but also because the effects observed in this tier of the study were, as Kruszewski points out, "[t]he most distinctive and desirable" ones:
      Although this type of supplementation [HMB] was used in the group of subjects who trained using the isometric method, regarded as a training system not associated with increases in lean body mass (LBM), the obtained results indicate that HMB may also affect LBM. In view of the fact that LBM involves mainly muscles containing about 70% water, the demonstrated significant elevation of LBM accompanied by the reduced water content in the bodies of the examined competitors is difficult to explain.
      Now, I've got you listening my iron-friends, don't I? Increased lean mass (+1.31kg), decreased (as the author points out, later) "presumably extracellular" water - sounds like it was coming from a competitive bodybuilder's "dry dreams", doesn't it? Well, the one thing that would be missing now, is a way to get rid of the fat - but wait, weren't there other supplements in the study, as well?

      10g Creatine (+10g dextrose) + powerlifting for fat loss!

      Image 3: Creatine monohydrate
      for fat loss? That's a surprise.
      Yes, there were, and believe it or not, not l-carnitine and circuit training, but creatine and powerlifting will shed the fat - even in elite level powerlifters! By continuing their regular (pyramid style, cf. figure 1) powerlifting training, the 16 power lifters from the Polish National Team, who received the 20g/day creatine + dextrose combination did not only improve their powerlifting performance by a statistically significant +15.6kg over the placebo group, they also and, as Kruszewski points out, "surprisingly" lost a significant amount of body fat in the course of the 20 training sessions they completed within the 5 week study period:

      [...] the present results indicate that supplementation with this compound [creatine] led to a significant reduction in the fat content and increase in the water content of the organisms of powerlifters from the Polish National Team.
      In view of the results, the author observed in the last group, the one which did a bodybuilding-type circuit training that was supplemented with 900mg of l-carnitine l-tartrate per day (cf. figure 1), I find it pretty amusing that according to Kruszwski the "effect of creatine may be much more far-reaching than that indicated in the manufacturers’ leaflets", which is something, he certainly would not say of l-carnitine.

      900mg l-carnitine l-tartrate + "bodybuilding-type" circuit training for powerlifting? 

      Image 4: L-carnitine alone will not transform your physique like this magic mirror - no matter what the advertisement leaflet in the latest muscle mag says ;-)
      The results in the l-carnitine supplemented group (3x300mg l-carnitine l-tartrate) were mixed. While the previously untrained subjects obviously gained strength in the course of the 15 workouts they performed in the 5 week study period, there were huge intergroup differences - meaning that a few subjects appeared to benefit from carnitine, while the majority didn't. Moreover, fat loss or beneficial changes of body composition, which is what l-carnitine is marketed for, were completely absent in the l-carnitine group. And while the training intensity was pretty low (although the trainees had to perform the 3rd of their three training circles to complete failure) this does not really surprise me, as the "fat burning" effect of oral carnitine supplementation has been debunked by more than a dozen well-designed studies, so that you better follow Kruszewski's advice and "treat advertisements of this compound [l-carnitine] with reserve" ;-) He goes on to explain that...
      [...i]t is possible that individuals with inherited or acquired L-carnitine deficiency manifested by increased deposition of fat in the body may benefit from such supplementation and improve their body composition by consuming appropriate amounts of this substance accompanied by proper (predominantly aerobic) exercising. However, additional L-carnitine supplementation in individuals with normal production and concentration of this substance in the body is superfluous.
      On the other hand, Kruszewski admits that despite the absence of significant improvements in muscle torque, the powerlifting performance of the subjects in the l-carnitine group increased statistically significantly more than the one in the placebo group (+13.7kg) which is ...
      surprising in view of the fact that such an effect [increase in powerlifting performance] of L-carnitine has very rarely been reported and emphasized.
      He goes on to suggest that these improvements may be related to l-carnitines impact "on the general physical fitness of the organism". Yet, whatever the reasons may be - out of this triumvirate, l-carnitine would certainly be the least effective addition to your regimen - whatever your goals may be.

      Isometric training and HMB supplementation, on the other hand, emerge as as surprise winner. With statistically significant (+17.7kg) increases in power-lifting performance, significant increases in muscle torque, and a +1,31kg increase in body mass (predominantly lean muscle) that was accompanied by a likewise significant reduction in extracellular water, it may be a good idea to take advantage of the falling HMB prices (buy in bulk!) and to incorporate some isometric exercises into your workout regimen ... what do you say?

      Creatine, DHT, Hair Loss & Prostate Cancer - Bro-Scientific Old Wives' Tales or Possible Side Effect? Plus: (Non-)Sense Creatine Loading, Exercise Induced 5-α Reduction & More

      Poor guy! Must have taken too much creatine and treated his hair for muscle ;-) Ok, seriously, creatine may have helped a little that he was able to build this impressive physique, but the hair? Come on, seriously!?
      If you have been around the bulletin boards of the fitness and bodybuilding community, I am pretty sure you will have heard about creatine induced increases in dehydrotestosterone (DHT). Probably you will also have had someone chime in who claimed that his hair started to fall out, when he started to use creatine supplements - right? Well, I guess in that case you will probably also remember how another guy chimed in and said: "Hold on does that mean that creatine will cause prostate cancer?"

      Never heard something like that? I suggest you trust my word, then; and in case you want "scientific evidence" head over to www.pubmed.com and type in "creatine D" it will offer you "creatine DHT" as one of the typical search phrases people are looking for.

      Cock-and-bull - right?

      It is true that there is a study that supports the concept of increased DHT levels in athletes (20 collegiate rugby players to be precise) in response to 21 days of creatine supplementation. The athletes who participated in the said trial came from a Rugby Institute situated near Stellenbosch University in South Africa. None of the subjects had taken any supplements with their normal diet for 6 weeks before the trial in the course of which all had been randomized to one of the following groups:
      • creatine: 25g creatine + 25g glucose for 7 days; 5g crea + 25g glucose for 14 days
      • placebo: 50g glucose for 7 days; 30g glucose for 14 days
      The subjects underwent standardized training, albeit for different player positions, during the whole study period. All subjects were residents at the institute and the ate the same food at the cafeteria. Moreover, all 20 were just coming back from a winter break and were "in similar condition as the start of the study and not fatigued from consecutive weeks of match play" (van der Merwe. 2009).
      Instead of simply taking more you may rather want to "Super Charge Creatine W/ Baking Soda" | learn more
      Creatine loading is neither necessary nor useful for the majority of athletes. Unless you have a meet close ahead there is no need to gobble down 25g+ doses of creatine - specifically not in one sitting. While the typical creatine supplementation protocol consists of a loading phase of 20 g creatine/d or 0.3 g creatine/kg/d that's followed by a 3-5 g/day (or 0.03g/kg) maintenance phase (Buford. 2007), it is also possible to use daily doses of ~3–6 g or between 0.03 to 0.1 g/kg per day (Willoughby. 2001; Hickner. 2010).
      All subjects were lean (13-14% body fat and muscular 75kg muscle of 86-87kg total body weight) and thus way more representative of the average creatine guzzling gymrat than untrained average Joes whose beer bellies may well have messed up their endocrine system to an extend that could explain the DHT increases from 0.98 nmol/L to 1.53 nmol/L. The fact that the DHT levels in the control group did not change significantly in the course of the 7-day loading phase (in fact they dropped, but due to the high standard deviation the drop from 1.26 nmol/L to 1.09 nmol/L was non-significant), lends further support that the changes, the researchers observed must have been the result of the 25g of creatine the 10 subjects in the active arm of the trial had to swallow on during the first seven days of the study period.
      Figure 1: Serum DHT levels total (left) and expressed relative to baseline levels in control group (right); data calculated based on van der Merwe et al. 2009
      As you will probably already have read in-between the lines, I am not exactly impressed - let alone scared - by these results. Why? Well, the initial 56% increase in DHT was not only followed by a -10% decline during the maintenance phase, but this decline brought the DHT levels of the young men in the creatine group pretty close to where they had been in the placebo group at T0 (1.38nmol/L vs. 1.26 nmol/L for creatine vs. placebo, respectively).

      The high DHT levels observed in the study at hand, were only midrange

      If that does not comfort you, maybe it will help, if I tell you that the reference range for adult men ranges from 0.8-3.4 nmol/L (NHS Pathology. 2013 - please note that these reference ranges vary from lab to lab, in ng/dL the upper limit usually is 85ng/dL, which is 2.93nmol/L). Accordingly, the total DHT level of the subjects in the van der Merwe study did not even scratch the 50% mark on the reference range, when they maxed out at the end of the 7-day loading phase.

      With a meager 9% difference to the baseline levels in the control group and a total DHT level of 1.38nmol/L in the "low DHT" zone of the reference range, I wouldn't say it is necessary (from a mere safety perspective) to investigate, as Green suggested it in a 2010 letter to the editor, whether the creatine supplement that has been used in the study may have been contaminated with androgenic compounds (Green. 2010). To answer the question about the why, i.e. "Why did the DHT levels in the creatine group go up, while those in the control group remained the same?",  it would yet in fact be nice to know if we were dealing with the side effects of androgenic compounds in the creatine supplement or the physiological effects of exercise, which has repeatedly been shown to be able to increase both intra-muscular and systemic DHT levels in men and rodent models (see the bottom line for selected references).

      Want to learn how to modulate your DHT levels naturally? Rice, safflower, sorghum & Co. can help! learn more
      In view of the fact that these increases are intensity dependent, but limited by the androgen suppressive effects of overtraining, The increased DHT levels may eventually have been a secondary response to increased training loads and the ameliorative effect creatine exerts on the androgen suppressive effects of overreaching (Volek. 2004).

      And while I cannot tell you if this actually was the reason for the increase in DHT, I can tell you that the scientists assertion that what they observed was a "large increase in DHT rather than a marginal (possibly physiologically insignificant)"  (van de Merwe. 2009) is (at best) warranted if we look at the intra-group effect. In view of the broad "normal" range and the low baseline DHT levels in the creatine group, this relevance of this relative increase is yet more than questionable.

      And the increasing DHT:Testosterone ratio?

      Even at the risk of sounding like a smart ass, I do not want to forgot to mention that the "oh so dangerous" increase in DHT/T levels the scientists emphasize in their conclusion was found to be associated with a reduced risk of hair loss (-35% risk reduction) in 315 male subjects who were stratified with regard to age, race, and case-control (Demark-Wahnefried. 1997).

      This and similar observations which have been made by Nomura et al. (1988), Hsing (1993) Shaneyfelt (2000) with respect to the non-significant impact of high(er) serum DHT levels on the occurance of prostate cancer and, more importantly, the increased risk that comes with higher T:DHT ratios, I seriously doubt that you have to be concerned about either your superb head of hair or your hitherto still pain and cancer free prostate when you are downing your daily dose of 3-5g creatine monohydrate.
      No! Physical activity does not cause prostate cancer. I guess you will be surprised that I even address this issue, but due to several major shortcomings in previous prospective and epidemiological studies, you will easily find studies such as the one by Cerhan et al. which claims that men with a high physical activity have a 90%(!) increased risk of prostate cancer. What the abstract does not tell you, though, is that the researchers "forgot" to conduct a time lagged analysis to overcome the "I started to exercise yesterday, so I exercise vigorously every day" effect and did thus fail to measure consistent physical activity. Edward et al. did just that over a 4 year period and observed a -53% risk reduction for men aged 65+ to develop advanced prostate cancer.
      Take home message: Despite being statistically relevant the absolute changes in the DHT levels van der Merwe et al. observed in the study at hand were neither physiologically relevant (DHT remained well within the reference range), nor totally inexplicable. Being afraid of hair loss, let alone prostate cancer, in response to the consumption of (untainted) creatine supplements is thus totally unwarranted.

      And just in case you still want to freak out, I suggest you keep sitting on your ass for the rest of your life and refrain from ever playing football or any other sport again... why? Well according to Lupo et al., your DHT levels will double during a single football match. This and similar observations by Hawkins in a middle aged men on a 12-months aerobic exercise program (14.5% increase with moderate intensity cardio 6x per week; cf. Hawkins. 2008), as well as the results from Aizawa et al. who were able to demonstrate "that acute exercise enhances the local bioactive androgen metabolism in the skeletal muscle of both sexes" and not just men, do as bro-logic dictates suggest that any kind of physical activity will make you hair fall out and your prostate grow... now tell me how realistic is that?
      References:
      • Aizawa K, Iemitsu M, Maeda S, Otsuki T, Sato K, Ushida T, Mesaki N, Akimoto T. Acute exercise activates local bioactive androgen metabolism in skeletal muscle. Steroids. 2010 Mar;75(3):219-23.
      • Buford T, Kreider R, Stout J, Greenwood M, Campbell B, Spano M, Ziegenfuss T, Lopez H, Landis J, Antonio J:International Society of Sports Nutrition position stand: creatine supplementation and exercise.J Int Soc Sports Nutr. 2007;4.
      • Cerhan JR, Torner JC, Lynch CF, Rubenstein LM, Lemke JH, Cohen MB, Lubaroff DM, Wallace RB. Association of smoking, body mass, and physical activity with risk of prostate cancer in the Iowa 65+ Rural Health Study (United States). Cancer Causes Control. 1997 Mar;8(2):229-38. 
      • Demark-Wahnefried W, Lesko SM, Conaway MR, Robertson CN, Clark RV, Lobaugh B,
        Mathias BJ, Strigo TS, Paulson DF. Serum androgens: associations with prostate
        cancer risk and hair patterning. J Androl. 1997 Sep-Oct;18(5):495-500. 
      • Giovannucci EL, Liu Y, Leitzmann MF, Stampfer MJ, Willett WC. A prospective study of physical activity and incident and fatal prostate cancer. Arch Intern Med. 2005 May 9;165(9):1005-10.
      • Hawkins VN, Foster-Schubert K, Chubak J, Sorensen B, Ulrich CM, Stancyzk FZ, Plymate S, Stanford J, White E, Potter JD, McTiernan A. Effect of exercise on serum sex hormones in men: a 12-month randomized clinical trial. Med Sci Sports Exerc. 2008 Feb;40(2):223-33
      • Hickner R, Dyck D, Sklar J, Hatley H, Byrd P:Effect of 28 days of creatine ingestion on muscle metabolism and performance of a simulated cycling road race.J Int Soc Sports Nutr 2010;7:26.
      • Hsing AW, Comstock GW. Serological precursors of cancer: serum hormones and risk of subsequent prostate cancer. Cancer Epidemiol Biomarkers Prev. 1993 Jan-Feb;2(1):27-32.
      • van der Merwe J, Brooks NE, Myburgh KH. Three weeks of creatine monohydrate supplementation affects dihydrotestosterone to testosterone ratio in college-aged rugby players. Clin J Sport Med. 2009 Sep;19(5):399-404.
      • Nomura A, Heilbrun LK, Stemmermann GN, Judd HL. Prediagnostic serum hormones and the risk of prostate cancer. Cancer Res. 1988 Jun 15;48(12):3515-7.
      • Shaneyfelt T, Husein R, Bubley G, Mantzoros CS. Hormonal predictors of prostate cancer: a meta-analysis. J Clin Oncol. 2000 Feb;18(4):847-53.
      • Van der Merwe J, Brooks NE, Myburgh KH. Three weeks of creatine monohydrate supplementation affects DHT to testosterone ratio in college-aged rugby players.Clin J Sports Med. 2009;19:399–404.
      • Volek JS, Ratamess NA, Rubin MR, Gómez AL, French DN, McGuigan MM, Scheett TP, Sharman MJ, Häkkinen K, Kraemer WJ. The effects of creatine supplementation on muscular performance and body composition responses to short-term resistance training overreaching. Eur J Appl Physiol. 2004 May;91(5-6):628-37.
      • Willoughby DS, Rosene J:Effects of oral creatine and resistance training on myosin heavy chain expression.Med Sci Sports Exerc2001,33:1674–1681.