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. 2013)

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. 2013)

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. 2013) , 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. 2013)

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. 2013)

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. 2013).

Figure 3: Graphical summary of the study design and selected results (Catoire. 2013)

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. 2013)

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. 2013).

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. 2013)
• The greater the muscle group you work, the larger the impact on the central nervous system will be (Rossmann. 2013) -- 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. 2013).-- 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. 2013) -- 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. 2013 [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. 2013; 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. 2013 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. 2013 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). 2013 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. 2013 Nov 12.
• Skrede J, Steen VM, Ferno J. Antipsychotic-induced increase in lipid biosynthesis: activation through inhibition? Journal of Lipid Research. December 7, 2013 [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. 2013 Mar 14;3:CD008449.

Aspartame's Anti-Insulinogenic Effects During a Workout; Optimal Protein Intake on a Diet is Relative. Plus: Folate Fortification, Spirulia, Succinate, Sucrose, Pork Brain & the Low Cholesterol-Suicide Connection Reviewed!

Unbelievable: The results of the latest study from the University of Western Sidney appear to suggest that you could keep your insulin levels at bay, if you mixed your sugary intra-workout supplement with aspartame-laden diet coke instead of water! The mechanism that's behind this phenomenon does yet still have to be elucidated.

You may be surprised to see a long headline, a long post and a couple of bullet points: "Looks like On Short Notice, reads like On Short Notice, but is not published on Saturday? What's that?" The answer to this question is easy. Lot's of interesting stuff I have come across as of late! And while some of them, like the study on the marginal utility of higher protein intakes on a diet would actually deserve their own post, I decided to give you the "long(er) version of a short notice" in order not to miss any of them... and yes, this means there is going to be more than today's news on the unexpected anti-insulinogenic effects of aspartame, the only partly expected outcomes of the US folic acid fortification program, the aforementioned protein study, the usefulness of spirulina, succinate and sucrose supplements for athletes and physical culturists and some brainy insights into a possible connection between low cholesterol, depression and suicide risk in men and women... ah, ok I see, you are already reading the aspartame item - well, go for it!

• The astonishing anti-insulin effects of intra-workout aspartame consumption Meanwhile even bodybuilders who are injecting and "supplementing" with all sorts of unquestionably unhealthy stuff are so afraid of the hitherto still rather vaguely established pro-carcinogenic effects of aspartame that supplement companies place huge stickers on the boxes of their products saying "ASPARTAME FREE!" Now, I am pretty sure that a recently published study that was conducted by scientists from the School of Science and Health at the University of Western Sydney in Campbelltown, Australia (Siegler. 2013), won't do much about that, but you will probably have to agree that it is still remarkable, to say the least, that the co-administration of an artificial sweetener which has not produced any glucose, insulin or whatever response in previous trials (cf. "Sweeter than your tongue allows") would do that!?

  

  Figure 1: While the mechanism is still unknown and the results need to be repeated in a second experiment, there is no question that the drop in insulin during the workout (see arrow(s)) which occurred during the carbohydrate + aspartame trial in the presence of identical glucose ingestion and blood glucose levels warrants further investigations (based on Siegler. 2013)

  During the four trials, which were separated by 7-10 days of rest, the 9 healthy, recreationally active males (age: 22±2 years; height: 180±9 cm; weight: 78.6±8.5 kg; participating in regular physical exercise at least twice per week) who had volunteered for this (in the eyes of some aspartame extremists, probably unethical undertaking ;-) cycled fasted for 60 minutes in a climate controlled laboratory. The only difference between the four sessions was the "intra-workout nutrition" the participants were fed, with...
  

  1. carbohydrate - 2% maltodextrin and 5% sucrose (figure 1, C),
  2. carbs + aspartame - 0.04% aspartame with 2% maltodextrin and 5% sucrose (figure 1, CA),
  3. water - plain water, only (figure 1, W), and
  4. aspartame + malto - 0.04% aspartame with 2% maltodextrin (figure 1, A)

  As it is common practice in studies like this, "all participants were instructed to follow the same diet and training schedule for the three days prior to each experimental trial." (Siegler. 2013, my emphasis)
  The respective intra-workout beverages were to be consumed in boluses of 4ml/kg body weight before and at 15-minute intervals throughout the trial. For the CHO groups this summed up to a total carbohydrate intake of 104.4±11.3g per participant and did - probably not to your surprise - cause a corresponding increase in insulin levels... with one exception, however: the intraworkout period in the CHO + Aspartame group (figure 1, red), when the insulin level dropped, during the exercise sessions and bumped back up to the same level as in the carbs only control afterwards (see figure 1).
  As the researchers point out, we do not yet have a mechanistic explanation for this phenomenon... nor can we even be sure that this was not some sort of strange artifact, so that
  

  "the disparity between insulin levels [does not only] warrant further investigation with a larger cohort of clinically relevant subject populations (e.g. metabolic syndrome, diabetes, etc.) [, but must also] be considered when designing nutrition-based, exercise intervention studies [in the future]" (Siegler. 2013

  That this observation could actually have very practical implications, both, in view of its potentially compromising effects on blood glucose levels in diabetics, where any insulin blocking effect of aspartame would probably reduce the already compromised glucose uptake even more, as well as in view of the anti-lipolytic (=blocks the release of fat from the cells) of insulin during a workout, which could actually be blocked with a minuscule amount of aspartame ... but alas, until the results have been confirmed and the mechanism behind this effect has been elucidated, what we are doing here is more or less intellectual masturbation - nothing to feel bad about, but still not the real deal ;-)

• 

  Figure 2: This is what the USDA expected to happen - more folic acid in food = higher intake (here in the elderly) = lower homocysteine levels; the reality looked pretty different, though, at least in adolescents the folic acid intake went up, but the homocysteine levels did not go down; moreover the B12 levels have declined as well... how much of this is related to confounding factors still has to be elucidated, but as of now it does not seem as if the fortification program was the success the USDA wanted it to be (Mc Bride. 2007).

  US adolescents and their "healthy grains" are now folic acid fortified, but are they also healthier? According to a study that has just been published in the Journal of Public Health, the great idea to put another artificial vitamin into our the food chain and fortify "healthy" cereal-grain products with folic acid, was so "successful" that the average US teen (14y at the time the fortification program began, 18y now) does now have 16% higher folate and 14% higher B6 concentrations.
  Instead of the expected decrease in homocysteine levels, of which scientists still believe that it plays in imminently important role in the development of heart disease, its serum levels did likewise increase by 17%, while the serum concentrations of vitamin B₁₂ decreased by 11 % post-fortification. The additional ~118 μg folate/d the subjects ingested from the fortified food products, appeared to be particularly useless (or even detrimental?) for boys / young men whose total homocysteine (tHcy) levels increased by 24%  to a much greater extent than in the girls / young women.
  Honestly, I don't really know what to make of these results at the moment, ... at least nothing better than to shake my head over the hilariousness of trying to turn junk(-food) into (good) food by simply enriching it with artificial vitamins. On the other hand, I am happy that even Daniel A. Enquobahrie and his colleagues feel that it is "warranted to investigate the significance of these improvements in folate status on clinical outcomes, in the post-fortification era." (Enquobahrie. 2013) - and that not just because the fortification program did not produce the desired results, but also because the folic acid intake already started to exceed the RDA in many of the subjects. This, and the alarming decrease in B12 levels of which Katherine L. Tucker had cautioned in the 2007 interview with Judy Mc Bride, already, that "better diagnosis for B12 deficiency should be given high priority"(Mc Bride. 2007) do not "warrant", imho, they rather make it imperative to follow the effect of this "nationwide health program" very closely.

• 

  Figure 3: The principle of relativity for protein based body recompositioning diets - When it comes to weight los, the word "high" in high protein diets must always be seen in the context of habitual protein intake and to whom we are comparing our dieters; or put simply: The average SAD dieter benefits from every gram, the average bodybuilder will hardly benefit from the 7th whey shake.

  Effectiveness of high(er) protein diets for weight loss depends on spread / change vs. baseline not on total protein intake That's basically how you could summarize the conclusion of the latest review of the existing data on the influnece of (high) protein intakes on changes in body composition by John D. Bosse and his colleagues from the University of Utah. To find out whether either the protein change (=high protein diets are only effective when the change in protein intake from baseline to intervention is large enough) or the protein spread theory (=those dieters within a cohort with the highest protein intake will see the most beneficial changes in body comosition) could explain the different outcomes of previous studies best, the researches collected an impressive dataset comprising 51 peer-review studies the analysis of which yielded the following two main results (Bosse. 2013):
  1. The 35 successful dietary interventions had on average 58.4% higher average protein intakes than those trials in which the authors had not been able to observe an additional beneficial of going high protein over the standard calorical restriction approach
  2. The 17 successful (=greater anthropomorphic changes than with calorie restriction alone) of the 25 studies, where the baseline protein intake of the subjects was available, the increase in protein intake was 28.6% (if you ate 100g protein per day before, that would mean you would eat 128.6g while you are dieting), minimal increases in 4.7% range, on the other hand, did not provide any additional benefit over energy reduction, alone.
  Overall, the review does therefore support the original hypothesis of the researchers that there are certain thresholds which have to be surpassed before dieters will see any benefits from an increase in protein intake. This does yet also mean, that for someone who is already eating 200g of protein on a daily basis, the addition of a protein shake with 20g of protein is probably not going to make so much of a difference as it would be way below the 28.6% change in protein intake, the protein change theory would prescribe (see [2] in the list above). As a matter of fact going higher and higher (e.g. like eating 300g of protein per day), will, if anything stall, not propel your progress, after all, there will be too little room for other nutrients, when you are already getting the lions share of your daily energy intake from protein... and NO you cannot lose weight without being in a caloric deficit, even if that is not readily calculable by the idiotic "calories-in-vs-calories-out" equation.
• The BMJ Supplement Review says: Thumbs up for sucrose, thumbs down for succinate and undecided  for spirulina In installment #36 of the A-Z of Nutritional Supplement Supplements, a series dedicated to review the pros and cons of purported ergogenic aids, the authors conclude that ...

  

  Figure 4: In view of the fact that the TCA or citric acid cycle is one of the #1 aerobic source of cellular energy (APT) and succinate is one of its intermediates it makes sense that supplementation could improve exercise performance, but hitherto this has not been confirmed.

  • ...the studies on spirulina fail to "study well-trained individuals", to use appropriate standardization regimen with relevance for physical culturists and athletes, identify the active ingredients and their effect on the antioxidant status, of which the respective scientists speculate that it would be the underlying mechanism of the observed ergogenic effects on chronic low-intensity exercise regimen
  • ...the research on succinate (only) supplementation is basically non-existent and claims with respect to its permanence enhancing effects is mostly based on theoretical considerations about its role in the TCA cycle 
  • ...despite the general trend within our society, where the overconsumption of sucrose (table sugar) is one of the major offenders to public health, "there may be value in, or at least room for, its inclusion in sports products targeting the provision of carbohydrate fuel during exercise"
  Nothing exciting, but a realistic and educative analysis, which has all the classic elements you should keep in mind, whenever you try to find out whether a product is worth its money: What research is there? What are the results? Are the positive results significant for me as a person? And... in the case of succrose: Could the use of this ergogenic aid be an obstacle for another goal of mine? I mean, you can benefit from guzzling tons of sugary drinks during your workouts, but if "looking good naked" is your primary goal and your performance only a means to an end - it is probably not wise to do so ;-)

• 

  Figure 5: Suicide risk in psychiatric patients /w (SA) or w/out (PS) prev. suicide attempt and surgical control (SC) in lowest, 2nd and 3rd cmp. to highest quartiles (Olié. 2011)

  Can pork brain in milk tell us something about suicide? Those of you who are on the SuppVersity Facebook news RSS channel will already know the image on the right. I only saw it today, but as Mark mentioned on my Facebook wall, he has used it (the image not the brain) in lectures before... be that as it may, that reminded me of an older study on the highly significant correlation between cholesterol levels and suicide attempts Emilie Olié and her colleagues observed in a 2010 study on the reliability of serum cholesterol levels as a predictor of the suicide risk in 3207 subjects [510 patients with a history of suicidal attempts (SA), 275 patients with no history of suicidal attempts (PC), and 2422 surgical controls (SC); Olié. 2011].
  The exact mechanism for the highly significant increase in suicide risk, esp. among women with previous suicide attempts in the lowest (1st quartile) is still not fully elucidated, Olié et al reference previous studies which suggest that low serum cholesterol levels, a "potentialmarker of central nervous systemcholesterol", impair the serotoninergic activity and" increase impulsivity" and thus precipitate to severe depression and the tendency and ability to pot a premature end to your life.
  In view of the fact that this and similar results were derived exclusively from analysis of psychiatric patients and considering that the cholesterol levels in the SA group were already significantly lower that in the PC and SC control (178±36 mg/dL vs. 217±43 mg/dL and 219±52 mg/dL, respectively) we should be very wary of transferring these results 1:1 to the "normal" people. 

I guess this is enough for today. After all, news are not so different than protein, it's the relative intake that makes all the difference - in other words: If I keep flooding you with those awesome posts, you won't appreciate each and every of them the same way you do now... and we don't want that to happen, do we? 

References:

• Bosse JD, Dixon BM. Dietary protein in weight management: a review proposing protein spread and change theories. Nutr Metab (Lond). 2013 Sep 12;9(1):81.
• Enquobahrie DA, Feldman HA, Hoelscher DH, Steffen LM, Webber LS, Zive MM, Rimm EB, Stampfer MJ, Osganian SK. Serum homocysteine and folate concentrations among a US cohort of adolescents before and after folic acid fortification. Public Health Nutrition. 2013; 15: 1818-1826.
• Mc Bride. Foods To Be Fortified With Folic Acid. USDA ARS. News. February 7, 2007. < http://www.ars.usda.gov/is/ar/archive/jun97/folate0697.htm > retrieved on September 14, 2013.
• Olié E, Picot MC, Guillaume S, Abbar M, Courtet P. Measurement of total serum cholesterol in the evaluation of suicidal risk. J Affect Disord. 2011 Sep;133(1-2):234-8.
• Siegler J, Howell K, Vince R, Bray J, Towlson C, Peart D, Mellor D, Atkin S. Aspartame in conjunction with carbohydrate reduces insulin levels during endurance exercise. J Int Soc Sports Nutr. 2013 Aug 1;9(1):36.
• Zemski AJ, Quinlivan RM, Gibala M, Burke LM, Stear SJ, Castell LM. A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: Part 36. Br J Sports Med. 2013 Sep;46(12):893-4.