Exhaustive Aerobic Exercise Increases Serum Calcium Levels and Dietary Requirements

You probably have heard of the fundamental importance of calcium as a structural component of bones. Yet, calcium is way more than the building block of our bone structure and the concrete the of the hopefully non-existent plaque in your arteries. It is also one of the major players in muscle contraction. Thus, it is not very surprising that a group of Iranian Scientists (Pourvaghar. 2011) found major effects of pro-longed (15min) high intensity aerobic exercise on serum calcium levels of 12 randomly selected student athletes (22.36y; 75kg @ 1.76m):

[…] the participants' mean of serum calcium concentration in the first stage and before Balke exhausting aerobic exercise was measured 98.38 ng/mic L. In the second stage, i.e. after the exhausting aerobic activity, it increased to 114.96 ng/mic L. Research results indicated that the difference in serum calcium concentration between the first and second stages is significant (P= 0.0001).

With the calcium that is appearing in the blood of the athletes being leeched from bones, organs to fulfill the increased calcium needs of active muscle tissue. Due to calcium “consumption” and urinary losses, the scientists speculate, the overall result to be a negative calcium balance.

Figure 1: Serum Calcium levels of athletes before, immediately after and 24h after exhaustive aerobic exercise. (Pourvaghar. 2011)

In view of the fact that, in the 24h after exercise, there is no sudden falloff (only -9.13%) of blood calcium, I would yet advice against extensive calcium supplementation. Previous works from other researchers have conclusively shown that a nutritionally dense, calorically adequate, diverse, calcium-rich diet satisfies the needs of both, the average gymrat and the hard training endurance athletes.

For athletes on a weight-reduction diet, or active gym-goers who – due to whatever other reasons – consume a diet that is low (<1.000mg/d) in calcium supplementing with a bio-available form of calcium, like calcium citrate, could yet be a viable strategy to prevent bone loss and sustain exercise performance.

An Old Dog Learns New Tricks: "Fatloss Fat" Tetradecylthioacetic Acid (TTA) Cardioprotective in Diabetic Rats

Do you remember the acronym TTA? Tetradecylthioacetic Acid? No. Well, I guess then you were not into fat burners in the early 2000s. TTA, a thia-fatty acid, was all the rage back in the day: Supplement producers claimed it would literally melt fat away and it actually turned out that some users had outstanding results megadosing respective supplements. Others, however, got bloated and/or started cramping. In view of these nasty side effects, most companies decided to reformulate their products and - with the exception of a few so-called "non-thermogenic" fat burners - TTA has almost disappeared from the market.

An international team of scientists from Norway and Canada (Khalid. 2011) has now discovered that the artificial fatty acid tetradecylthioacetic acid, which was originally intended as a drug for the treatment of the metabolic syndrome, might have the potential to protect type II diabetics from heart attacks.
In a previous study (Hafstad. 2009) the scientists had already shown that TTA does increase myocardial fatty acid oxidation in normal mice, a finding that would generally suggest impaired cardiac efficiency and thus be considered detrimental. In the current study on hyperlipidemic [high blood lipid levels] type 2 diabetic mice, however, TTA-treatment (0.5%, 8 days) had almost opposite effects on on cardiac metabolism and function

We found that TTA treatment increased myocardial FA oxidation, not only in non-diabetic (db/+) mice, but also in diabetic (db/db) mice, despite a clear lipid-lowering effect. While TTA had deleterious effects in hearts from non-diabetic mice (decreased efficiency and impaired mitochondrial respiratory capacity), these effects were not observed in db/db hearts. In db/db hearts TTA improved ischemic tolerance, an effect that is most likely related to TTA's antioxidant property.

Being a specifically designed (Pan-)PPAR-ligand [TTA seems to activate all PPAR-receptors] the lipid lowering effect of TTA was to be expected. The differential effect on heart function in healthy and diabetic rats, however, comes as a surprise and reminds us, again, that not all that has been shown to help sick people is beneficial - and sometimes its not even safe! - for the healthy part of the population.

Figure 1: Myocardial fatty acid and glucose oxidation in hearts of db/+ (white  545
bars) and db/db (gray bars) mice. Results are mean of 8-9 hearts in each group. (Khalid. 2011)

So, regardless how promising the shift in substrate metabolism from carbohydrates to fats, as it is visualized in figure 1 may appear, if you just want to shed a few pounds of unaesthetic, but healthy subcutaneous body fat, stay away from tetradecylthioacetic acid - for your heart's sake!

More on Putting Carbs to Good Use: Scott Connelly's BodyRX Show - Tune in Live at 12:00pm PDT

Who listened to my interview on Super Human Radio, yesterday, may have heard my advice to tune in to today's BodyRX Show with Dr. Scott Connelly, Vince Andrich, Layne Norton, Patrick Arnold and (this is new) me, ProfDrAndro, being the brains behind a completely overhauled show concept, I promise you won't be disappointed.

BodyRx Radio Show #017

Tune in Live @ 12pm PDT

Here is a short glimpse onto what is waiting for you:

On our last BodyRx Radio show (#016) we learned that by reducing carb intake from levels at the top of the food pyramid (>60% of energy) to a modest 35-40% of energy, you can effectively “teach” your body to preferentially store the carbs you eat into muscle cells and NOT your fat cells [cf. Effect of Macronutrient Composition]. But, when does reducing carb intake negatively impact your performance in the gym, where the work to build muscle takes place? More importantly, does that number change if you alter your training program? We take this age old question head on with:

• A revealing interview with renowned researcher Dr. Kevin Tipton by our very own Dr. Scott Connelly.
  
• Next, Vince Andrich taps into the minds of two of the industries top physique competitors and personal trainer/coaches; Pete Ciccone and his wife Meriza Deguzman––listen for their practical advice that men and women can use right NOW!
  
• Lastly,  renowned chemist Patrick Arnold will take on a list of hard hitting questions that will give listeners an inside look at the popular diet and energy compound; geranium. We know you’ll agree this is a one-of-a-kind interview since it was Patrick Arnold himself who brought this compound to the market several years ago, and is now the darling of the supplement world.

The prominent line-up alone makes it worth listening - no doubts about that, folks!

ProfDrAndro @ Super Human Radio: Set to Be Obese? Of Set & Settle Points on Your Way to a Super Human Physique

Just in case you got nothing else to do: Tune in live and listen to some more (probably Carl) or less (probably me ;-) intelligent Supp-Talk on Carl Lenore's Super Human Radio!

Topic: Set & settle points and how contemporary science
may contribute & explain your personal weight loss success

Update: available for Download now

Listen live @ 9:00AM AM/12:00PM ET

Putting Carbs to Good Use: Meta-Review Reports Ergogenic Effect of Carbohydrates in Endurance Athletes

One of the leitmotifs, many of my posts here at the SuppVersity share, is the idea that (almost) everything works for someone. From the feedback I am receiving, from the crowd this blog is attracting, I gather that my general advice against high carbohydrate intake is (as human as that may be) often misinterpreted as "carbs are evil, beware of all carbs"! For the average pizza eating fast-food junkie, this certainly is an adequate message, because even if he believes that carbs are the root of all disease, without a MAJOR change in his dietary habits (I am not talking of ordering the normal, instead of the super size menu at McDonalds, here) he will probably still get way more carbs out of his diet than it would fit his sedentary lifestyle.
If, however you are an athlete or avid gym-goer you may probably already start to notice that following what you took to be a one-solution-fits-it-all recommendation lead to performance decreases, laziness, brainfog, lack of sexual desire, bad sleep and many of the other symptoms you would find, when you googled one of the ambiguous terms "adrenal fatigue" or "general fatigue syndrome"... Carbs are more than just insulin triggers, and fatteners. Glucose is the gasoline in your fuel tank and - most importantly - its the substrate your nervous system thrives on. And while it might not be necessary to eat them, very active (and lean) individuals may derive similar benefits from a moderate carb consumption as the athletes from the 50 studies included in a meta-review by Themesi et al. (Themesi. 2011).

The scientists' results suggest that intake of a <8% carbohydrate beverage (~50-80g) [TT] in the course of an endurance event (≥1 h) significantly "enhances endurance exercise performance in adults" as measured by submaximal exercise performance and time to exhaustion [TTE]:

The ES [effect size] for submaximal exercise followed by TT was significant (ES = 0.53; 95% CI = 0.37–0.69; P < 0.001) as was the ES for TT (ES = 0.30; 95% CI = 0.07–0.53; P = 0.011). The weighted mean improvement in exercise performance favored CHO ingestion (7.5 and 2.0%, respectively). TTE (ES = 0.47; 95% CI = 0.32–0.62; P < 0.001) and submaximal exercise followed by TTE (ES = 0.44; 95% CI = 0.08–0.80; P = 0.017) also showed significant effects, with weighted mean improvements of 15.1 and 54.2%, respectively, with CHO ingestion. Similar trends were evident for subanalyses of studies using only male or trained participants, for exercise of 1–3 h duration, and where CHO and PLA beverages were matched for electrolyte content.

Against this background, can the relevant question really be: "To carb or not to carb?" Probably not. You better follow Vince Andrich's recent advice and ask yourself "Are you working your sugar-bags (muscles) hard enough to earn your fair share of carb intake?" in order to make sure that you use just as much carbs as it takes to optimize performance without compromising health and body composition.

Epidemiological Study Shows Correlation Between Anti-Oxidant Intake and C-Reactive Protein & Homocystein

After a sudden onset of discussions around the beneficial or even detrimental effects of vitamin supplements in general and antioxidants in particular in the mid to late 2000s, vitamins and, even more, other anti-oxidants have been put back on the map, lately.

A recent epidemiological study from the University of Connecticut (Floegel. 2011) provides further evidence for the hypothesis that, after all, consumption of adequate amounts of vitamins C and E, beta carotene, flavonoids and selenium would be beneficial to your overall health

Intakes of vitamins C and E and carotene were inversely associated with the probability of having serum CRP concentrations >3 mg/l in multivariate logistic regression models. Flavonoid and Se intakes were not associated with the odds of elevated serum CRP concentrations. The mean plasma Hcy concentration was 8·61 (95 % CI 8·48, 8·74) μmol/l. Intakes of vitamins C, E, carotenes and Se were inversely associated with the odds of plasma Hcy [Homocysteine] concentrations >13 μmol/l after adjusting for covariates

While all these results appear to be quite unambiguous, you still have to keep in mind that they support the interpretation "antioxidants are healthy" only, if we assume that the relation between high C-Reactive Protein [CRP], inflammation and the metabolic syndrome, as well as the relation between homocysteine and heart disease is more than just a correlative one; and, to my best knowledge, no study has yet been able to show that injection of homocysteine caused heart disease or an increase in CRP increases inflammation or causes tissue damage. In this context, for example, the hitherto hardly understood involvement of "positive inflammation", such as an exercise induced rise in IL-6 levels, come to mind. In this context, studies such as Ristow et al. (2009) that found the positive effects of exercise being blocked by antioxidant supplementation would warrant further research into what - irrespective of reductions in purported markers of inflammation and cardiac disease - the actual health outcome of higher antioxidant intakes are.


Note: Don't get me wrong. I do not want to argue against a diet rich in natural antioxidants. I just want YOU to be aware that the proven health benefits from eating healthy, antioxidant-rich foods cannot be extrapolated to high (or even mega-dose) vitamin & flavonoid supplements and that taking megadoses of isolated antioxidants such as alpha-tocopherol (especially in its synthetic form and without the complementary tocopherols and -trienols), which is the most commonly sold form of vitamin E, may in fact do more harm than good.

Now Its Official: Propecia Drug Finasteride Kills Male Libido Permanently

Image 1: Chemical structure of finasteride

Other than the FDA some European medicine and health care agencies, such as the Swedish Medical Products Agency and the Medicines and Healthcare Products Regulatory Agency of the United Kingdom already had the guts to declare in their patient informations that "persistence of erectile dysfunction after discontinuation of treatment with Propecia has been reported in post-marketing use." While this was obviously no reason for the all-mighty FDA to correct or re-evaluate their own documents, two it did intrigue Michael S. Irwig and Swapna Kolukula, two US scientists from Washington and Baltimore, respectively.

In their study (Irwig. 2011), the scientists conducted standardized interviews with 71 otherwise healthy men (age: 21–46y), who experienced permanent (>3 months) sexual side effects after temporary use of Finasteride. Their reports are staggering:

94% developed low libido, 92% developed erectile dysfunction, 92% developed decreased arousal, and 69% developed problems with orgasm. The mean number of sexual episodes per month dropped and the total sexual dysfunction score increased for before and after finasteride use according to the Arizona Sexual Experience Scale (P < 0.0001 for both).

These sexual side effects occurred after a "mean duration of finasteride use [of] 28 months" and they were persistent up to the interview date. For the study population this meant that they had already been suffering 40 months, on average, when the interviews took place; and chances are that many of them will suffer the consequences of an insufficient (or should I say incompetent or corrupted?) drug approval process and consequent indoctrination of medical practitioners for the rest of their lives.

Note: After receiving some critical feedback via facebook, I feel that it is necessary to point out that the result of the study may not be misinterpreted as "Every Finasteride user will experience persistent decreases in libido, erectile disfunction etc.", but as "In those percentage of Finasteride users, where such side effects occur, they can potentially be permanent." So the news is neither that Finasteride will cause these effects in each and every user, nor that it may cause such side effects (that is in fact mentioned in the package insert, I suppose), but that IF side effects occur, it is possible that they are persistent.

Fat or Fire, What Comes First? Scientists Answer: Obesity Alone Triggers Inflammatory Signaling in Mice

The metabolic syndrome, i.e. the combination of obesity, inflammation and insulin resistance, is at the center of contemporary medical research. In my appearance on Carl Lenore's Super Human Radio, I already mentioned that from a logical perspective the mainstream belief, inflammation was the root of all evil, must be flawed. How should the reaction to a problem be the cause of the very problem itself? A recent study coming from a group of Korean scientists strengthens my conviction that out of the triad that not inflammation, but rather obesity or - one step further up in the genesis of the pathology - the combination of an unhealthy diet and a sedentary lifestyle is at the heart of the triad we now call the "metabolic syndrome".

Kim et al. investigated the pro-inflammatory signaling cascade in either diet-induced (DIO) or leptin gene deficient (ob/ob) obese mice and found that obesity alone ...

[...] up-regulated the expression of TLR1–9 and TLR11–13 in murine adipose tissues, a phenomenon linked with downstream nuclear factor κB [inflammatory protein linked to linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development], interferon regulatory factors, and STAT-1 activation, and up-regulated the expression of cytokines and chemokines via MyD88-dependent and MyD88-independent cascades [activate NF-κB].

Thus, obesity sets the scene for inflammation and inflammation in turn triggers a cascade of unfavorable metabolic and hormonal changes which in and out of themselves result in further weight gain...

Here, we have a self-enhancing pathologic circle, which - and this is probably an even more important result of the study - was especially "effective" in the group of diet-induced obese mice:

The magnitudes of the obesity-induced up-regulation of the TLR1, TLR4, TLR5, TLR8, TLR9 and TLR12 genes in the visceral adipose tissue were greater in the DIO mice than in the ob/ob mice. Similarly, the expression of the IFNα and IFNβ genes significantly increased in the adipose tissues of the DIO mice but did not change in the adipose tissues of the ob/ob mice.

So, its not in your genes, but in your hands, feet and mouth to ward off the plague of the 21st century: Exercise and eat healthy to get lean and/or stay lean and stave off inflammation and diabetes.

Effects of Macronutrient Composition on Metabolic Signaling: Higher Protein Diet Favors Glycogen Storage in Muscle Over Adipose Tissue

Those of you who have already listened to the latest, revamped (and improved) episode of Dr Scott Connelly's BodyRx Show will already have heard of Suzanne Devkota's and Donald K Layman's study (Devkota. 2011) on the effects of different meal compositions on the postprandial glucose disposal. For the rest of you who have missed the episode and those of you who like their info white-on-black, here are the main results...

For 10 days, Devkota and Layman fed 60 rats a diet containing either 60% of energy from carbohydrates, 12% protein, 28% fat (CHO) or 35% carbohydrate, 35% protein, 30% fat (PRO) and evaluated plasma levels of insulin, glucose and C-peptide, as well as muscle and adipose tissue Akt, p70S6K and Erk 1/2 (markers of glucose and protein metabolism and cellular growth, respectively).

The graphs in figure 1 illustrate their most significant finding quite nicely. Other than in the case of the protein-fed rats, blood glucose is preferentially stored in fat tissue in the 30-90 min time window upon the ingestion of a meal in the high carb (CHO) group

Figure 1: Muscle and adipose tissue Akt expression (marker of glucose metabolism) after "high" protein (PRO) and high carbohydrate (CHO) meal, respectively (Devkota. 2011

The authors summarize this effect of macronutrient partitioning on metabolic signaling that is supported by the rest of their data as follows:

Animals chronically consuming the CHO diet produced greater metabolic signaling in adipose tissue to handle excess glucose and blunted signaling in skeletal muscle consistent with interpretation of insulin resistance. Conversely, animals consuming the PRO diet produced greater metabolic signaling in skeletal muscle with little signaling in adipose.

To fuel your workouts, it thus seems not only unnecessary, but even detrimental, to consume high amounts of carbohydrates. A "lower"  [note: even the high protein diet that was matched to the USDA's acceptable macronutrient distribution ranges (AMDR) had a carbohydrate content of 35% and thus a 1:1 protein to carb ratio!] carbohydrate intake, on the other hand, appears to prime your body to store glycogen primarily in muscle tissue. On a "high" protein, "lower" carb diet, you thus get the performance benefit without the unwanted fat gain and isn't this what we all are looking for?

Got a Pot Belly? Stubborn Belly Fat? Unhandy Love Handles? Massage Them Away!

"Massage away your pot belly!" Sounds hillarious, doesn't it. Well, a small study (Rahimi. 2011) coming from scientists from the University of Mashhad in Iran suggests that massaging your love handles could actually facilitate localized fatloss.

In their study, Rahimi and Javahery put 16 healthy - I quote - "non-sportsperson male students"  ;-), aged 20-27y on a 5x a week massage regimen (15-20 min) that had, if not outstanding, then at least statistically significant results:

The results of correlated t test show that the mean values of skin fold fat of the stomach are of the participants before and after the massage program was 36.81 and 36.12 respectively, which shows a significant decrease after 30 sessions of massage (p=0.036).

- 2% skin fold: You are not impressed? Well, me neither. Although the increased blood flow to the subcutaneous fat pads may, as the scientists speculate, have a beneficial effect on local fat mobilization, I would suggest you better spend the time in the gym or doing sprints on the track to not only mobilize, but also oxidize these stubborn and unaesthetic fat pads and simultaneously improve your cardiac and metabolic health.

On a side note: If there is anything significant to learn from this study, it is that sometimes, even scientists try to trick you into believing that what they found (similar to what supplement companies sell) is a great thing. Look at the following graph from the study:

Figure 1: pretest (1) and posttest (2) mean values of the subcutaneous fat of the stomach area of the participants (Rahimi. 2011)

Just by selecting a very narrow scaling on the Y-axis of the graph, the scientist create the impression that their massage therapy was a huge success. If, however, you take a closer look, you inevitably notice the figures and the bluff is exposed. Remember tricks like that, when you look at the colorful graphs in supplement ads all over the Internet. Or as Churchill is said to have put it (in fact this is another myth) “Never trust any statistics that you didn’t forge yourself.”

NAC + Zinc + Selen = Silver Bullett Against Mercury Poisoning

Mercury certainly is among the most dangerous and, at the same time, most ubiquitous heavy metals, we are exposed to. In a recent article (thanks to Dominique for raising my awareness of its publication) strength coach Charles Poliquin references a 2010 study from Michigan State (Wirth. 2010) :

Looking at several well-designed studies, they determined that even low exposures from cadmium, lead and mercury had an impact on semen quality and reproductive hormone levels in men.

As far as solutions to this problem are concerned, Polliquin refers somewhat dubiously to "a specific herbal combination" of "andrographis paniculata, zinc citrate, humulus lupulus, and curcuma longa" without providing scientific evidence for why he thinks this specific formula would work (guess what, Charles sells it ;-). Chances would have it, though, that Joshi et al., in a very recent study (Joshi. 2011, still ahead of print) report the beneficial effects of another, from my perspective, probably even more potent combination of nutrients/antioxidants in experimentally induced mercury poisoning:

Exposure to DMM [dimethylmercury] caused significant alterations in cytochrome P450 (CYP) activity, microsomal lipid peroxidation, and proteins [in rats]. Activities of transaminases (aspartate aminotransferase/alanine aminotransferase), alkaline phosphatase, and lactate dehydrogenase in serum, as well as activities of CYP enzymes aniline hydroxylase (AH), amidopyrine-N-demethylase (AND) in liver microsomes and activities of acid phosphatase, alkaline phosphatase, glucose-6-phophatase, and succinic dehydrogenase in the liver and kidney, were significantly altered after DMM administration. DMM exposure also induced severe hepato-renal alterations at the histopathological level. NAC, along with Zn and Se, dramatically reversed the alterations in all of the variables more toward control.

Actually these results do not come as a surprise, as all three of these nutrients/antioxidants are well-known for their beneficial effects on (liver) enzyme activity and thus heavy metal clearance. Those of you, who read Tim Ferris' book The 4 Hour Body may also remember that his Brazil nut consumption (he ate them for their high selenium content, 1 ounce contains 544µg, i.e. 780% DV) along with other nutritional changes tripled his testosterone levels from low normal levels to the upper quartile of the range. In that, it is of secondary importance whether this was a mercury related effect, or not, since an increase in the detoxification abilities of the liver, as it was achieved in the study by twice a week supplementation with NAC (360mg/kg; human equivalent dose [HED] ~ 52mg/kg)  + Zn (130mg(kg; HED ~ 26mg/kg) + Se 0.5mg/kg; HED ~0.08mg/kg), will benefit the hormonal millieu via multiple pathways (increased estrogen clearance being one of them).

A word of caution: I advice against using the dosing scheme applied in the study, i.e. twice a week mega-dosing of supplements. Spread across a whole week, the human equivalent doses (for an 80kg human being) would equal roughly 600mg NAC, 300mg Zinc and 1mg* Selenium per day, which - apart from the exorbitant amount of zinc (I would not take more than 100-150mg/day even for short term interventions) - constitutes a quite reasonable nutrient stack for shorter detox protocols (4-6 weeks) for mercury, cadmium (cf. eg. Said. 2010) and other heavy metals with an increase in testosterone being one of the possible positive "side effects".

*Note on selenium toxicity: Rumors have it that selenium is toxic even at doses of >400µg. Most of these reports yet turned out to be based on anecdotal evidence from people who poisoned themselves with supplements that contained up to 200x the labeled dose (e.g. >40mg! selenium in MacFarquhar. 2010). It is thus very unfortunate that current data on the ‘Lowest Adverse Effect Level’ (LOAEL) is lacking. A 1989 study by Yang et al. give1.5mg/day as a threshold beyond which longterm supplementation may produce adverse side effects. And though this is below the 1g derived from the results of the rat study, I recommend to better err on the side of caution and to stick to max. 200-400µg supplemental selenium + a handfull of Brazil nuts from time to time as part of a safe antioxidant supplement stack.

Protein's Effects on Gene Expression: Higher Protein Lower Carbohydrate Diet Spares Gylcogen, Lowers Insulin and Reduces Lipogenesis

High protein diets have become the "gold standard" within the fitness community. On the countless bodybuilding, fitness and weight loss related bulletin boards on the Internet, athletes, gymrats and even overweight house-wives report outstanding benefits of a higher than normal protein intake on weight gain and/or fat loss. French scientists (Stepien. 2011) have now taken a closer look at the mechanism behind these success stories and found a strong (epi)genetic component (for an introduction to epigenetics, I recommend listening to Dr Rouse's interview series on Carl Lenore's Super Human Radio).

 Figure 1: Effect of high protein diet on genes regulating lipogenesis [lipo = fat; genesis = production] in the liver (Stepien. 2011)

Stepien et al. fed 80 male winstar rats either a normal or a high protein (50% protein) diet for 1,3,6 or 14 days and evaluated the mRNA levels [indicators of how active these genes are] of genes "involved in carbohydrate and lipid metabolism", energy expenditure (EE) and substrate oxidation, as well as liver glycogen, plasma glucose and hormones. What they observed stands in line with the positive anecdotal evidence you will find if you google muscle gain or fat loss "success stories":

    In liver, HP feeding 1) decreased mRNA encoding glycolysis enzymes (GK, L-PK) and lipogenesis enzymes(ACC, FAS), 2) increased mRNA encoding gluconeogenesis enzymes (PEPCK), 3) first lowered, then restored mRNA encoding glycogen synthesis enzyme (GS), 4) did not change mRNA encoding b-oxidation enzymes (CPT1, ACOX1, bHAD).

So, interestingly, with the exception of the 1st day of the experiment (where the increase in protein intake resulted in a short-term increase in fat oxidation), fat oxidation was stable (cf. 4) The "fat burning" effect, which is often ascribed to high protein diets, thus is not existent - or let's say its not a direct one, but a result of the synergy of other genetic and metabolic adaptations and the calorie restriction all weight loss regimens have in common.

Figure 2: Postprandial macronutrient balance as assessed during a 4 h period after the intake of a calibrated meal consisting of 4 g of an adequate diet.  (Stepien. 2011)

Here is where the insulin lowering effect, the reduced hepatic glucose uptake and the reduction in lipogenesis (cf. fig. 1) come into play. Combined with an overall increase in postprandial energy expenditure (observed only under long term high protein feeding conditions, cf. fig 2, HP14) and a slight but significant increase in the percentage of fat (LOX, fig. 2) that is used to fuel these demands, these genetic and metabolic adaption (most prominently the lower insulin levels and the reduction in lipogenesis) are the most probable mechanisms to explain the reduced fat gains and increases in fat loss on high protein weight gain and weight loss diets, respectively.

Muscle Building Takes Time. Less in Newbies, Though: 9.6% More Muscle in 8 Weeks

"Patience is a virtue!" Many bodybuilders and fitness enthusiasts have to learn this the hard way - even on drugs, muscles won't grow (hypertrophy) within days and visible gains in lean muscle mass will take years or month. Although the results of a recent study (DeFreitas. 2011) done by scientists from the University of Oklahoma won't help to overcome the delay between training induced muscle stimulus and physiological hypertrophy response, the observations of DeFraitas et al. are nevertheless interesting.

By the means of weekly testing the scientists wanted to determine the "precise time course of skeletal muscle hypertrophy" in response to 8 weeks on a specifically designed high intensity resistance training program in 25 healthy, sedentary men. The measured outcomes were whole muscle cross-sectional area (CSA) of the dominant thigh (via computer tomography) and isometric maximum voluntary contractions (MVC). 

After only two training sessions (W1) [=week 1], the mean thigh muscle CSA increased by 5.0 cm² (3.46%; p < 0.05) from the pre-testing (P1) and continued to increase with each testing session. It is possible that muscular edema may have inXuenced the early CSA results. To adjust for this possibility, with edema assumedly at its highest at W1, the next significant increase from W1 was at W3. W4 was the Wrst signiWcant increase of MVC over P1. Therefore, signifcant skeletal muscle hypertrophy likely occurred around weeks 3–4.

While edema, unquestionably, are one possible reason for the sudden increase in "muscle mass" being a 'sedentary newbie' to strength training may well be another factor contributing to the immediacy of the muscle gains (do not expect to see similar results as an experienced athlete!). The scientists reliance on sedentary subjects compromises the significance of the whole study (in view of what athletes and gymrats may expect), thus the measured overall gains, impressive +13.9 cm² (9.60%) CSA, appear hardly transferable to a "reasonably" trained group of subjects, as well.

Figure 1: Development of muscle size (measured as CSA of thigh muscle) and force (measured as MCV) in 25 formerly sedentary subjects on an 8 week high intensity strength training program (DeFreitas. 2011)

Comment: Its really a pitty that out of monetary and organizational reasons all these studies are done on newbies, whom you could send work on a construction site for 8 weeks and see immense gains in strength and muscles, when they do not get hit by a block of concrete. So, do not feel discouraged if - in the course of the whole last year, you did not gain +13.9 cm² in your tigh muscle. You are probably just to athletic already ;-)

Supplemental (!) Coconut Diet Reduces Waist Circumference in Men more Than in Women While Leaving Lipid Profiles Unchanged

I take the recent New York Times Article on coconut oil as clear evidence of the fact that the health benefit of tropical oils is getting more and more public attention. Studies that establish the many anecdotal reports you can find all over the Internet may even speed up this process and thus I am happy to report the findings of a Malasian study (Liau. 2011) that clearly underlines that the "bad" saturated fat cannot be so "bad" after all.

The scientists had a group of 20 healthy, but obese Malay volunteers consume an additional 30 mL of coconut oil (approx 2 tablespoons) per day taken in three divided doses, half an hour before each meal (as far as digestive side effects are concerned, this was the best tolerated dose as assessed before the actual study) and found...

that only waist circumference [WC] was significantly reduced after one month of VCO with a mean reduction of 2.87 +/-4.95 cm.

The high standard deviation of this data may well be attributed to the fact that there was no additional control of the dietary habits of the volunteers. The study says subjects "continued their weight loss efforts", but you probably know these "efforts" often turn out to be hardly comparable. I also feel that the real-world significance of the scientists statistical assessment "WC reduction was only seen in males" must be reevaluated, especially in view of the fact that "the reduction [meaning in cm WC] was larger in females" and the reduction in females with BMI <30 (4.8 +/-6.1 cm), other than in females with BMI >30 2.61 +/-2.17) was statistically significant (for more data cf. figure 1).

Figure 1: Comparison of mean differences in anthropometric measurements and lipid profile values in 7 males and 13 females after VCO consumption. (Liau. 2011)

I refrain from commenting on the reasons and invite readers to come up with their own theories, why someone who has gotten to a BMI of >30 (!!) may have problems losing weight on an uncontrolled intervention. What this should tell you, however, is that you may safely assume that 2 x tablespoons of coconut oil (~30ml) à day may be a worthwhile addition to your well-planned diet & exercise regimen.

On a side note: Who knows how much centimeters the volunteers had lost if the had just replaced some of the "good" seed oils in their diets? Well, I guess in view of the fact that the scientists seemed surprised that the bad saturated fats in coconut oil did not ruin their volunteers fatty acid profiles, they probably considered it unethical to ask their participants to completely replace corn with coconut oil ;-)

Energy Restriction + Whey = Dieting Success, BUT the Magic is not in the Alpha-Lactalbumin

Ever since the first studies showed the beneficial effect of dairy in general and whey in particular on weight loss induced by caloric restriction, scientists have been arguing for alpha-lactalbumin being the key, or at least one of the key factors that contribute to the anti-obesity effects of milk products.

A group of scientists from Finland (Shi. 2011) did now investigate the exact contribution of alpha-lactalbumin to the dairy / whey induced anti-obesity effects. For 50 days Shi et al. fed mice on one out of three isocaloric, energy restricted diets containing either casein (calcium 0.8%) or two different high-calcium (1.8%) whey protein-based (α-lac + Ca and AA + Ca) amino acid mixes, which differed only in the amount of a-lactalbumin they contained. The results contradict the hypothesis that alpha-lactalbumin is the/a major driving force behind dairy induced weight loss outcomes:

The mice on α-lac and AA lost significantly more weight and body fat than mice on casein diet (P < 0.05). There was no difference between α-lac and AA diets. Ad libitum feeding after weight loss resulted in weight regain and fat accumulation in all groups

So, in the end, it obviously all comes down to the amino acid composition of whey protein that makes it superior to casein, but not to a similarly composed amino acid mixture without the addition of the alpha-lactalbumin fraction. The fact that none of the tested proteins had an advantage over the other in a non-dieting (i.e. calorically not restricted) environment, also indicates that it is the improved provision of essential amino acids from whey, which makes the difference.

Figure 1: Body fat percentage of mice after 50 days on different calorically restricted dietary regimens (Shi. 2011)

Yet, other than the ever-growing leucine fan-group on the web may now be led to believe, a further in-group differentiation  (cf. figure 1) into mice receiving additional amino acids (+100% aspartic acid & tryptophan, or +100% leucine) shows that additional leucine does not improve, but in fact blunt fat loss. In this otherwise isocaloric environment, this is probably due to the reduced percentage of other (essential and conditionally essential) amino acids in the chow, the consequences of which may be impaired fatty acid oxidation and suboptimal metabolic function in general.

One last thing, though: Before you completely discard the value of casein or even alpha-lactalbumin in your diet, I better told you that, compared to the amino acid group (without alpha-lactalbumin), all four, the whey + alpha-lactalbumin (all three groups), as well as the casein group retained a higher amount of muscle mass than the amino acid group (cf. figure 2) - with the results for the +100% asp + trp and the +100% leucine being statistically significant.

Bottom line: To cut body fat use pure whey with natural alpha-lactalbumine to optimize fat loss and retain muscle mass. Since, the difference in muscle retention to the other whey + alpha lactalbumine groups is not significant, the addition of supplemental amino acids including the "holy" (you may recognize I cannot stand the way it is currently hyped by the industry) leucine could make sense if you want to gain muscle; according to the data from this study, it is yet superfluous if your intention is to cut body fat.

Chrysine: 5,7-dihydroxyflavone for Bigger Balls and Higher Serum Testosterone

Polyphenols in general and flavonoids in particular are every supplement producer's favorite. Its so easy to pick up some exotic plant from somewhere deep down in the jungle, extract an exotic flavonoid, give it a fancy chemical looking name and provide some in-vitro data on his anti-oxidant omnipotence or whatever. In most cases the compounds disappear from the market within weeks, yet chrysine which is extracted from the Common Passion Flower, has been around for years. A recent study (Ciftcy. 2011) by Ciftci et al. provides further evidence that its market persistence may not be without a reason.

Over the time course of the scientists fed a group of lab rats 50 mg/kg chrysin (human equivalent ~8mg/kg) or placebo for 60 days and found:

that chrysin significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels, but did not change the formation of TBARS significantly. In addition, sperm motility, sperm concentration and serum testosterone levels significantly increased, whereas abnormal sperm rate significantly decreased with chrysin treatment.

In essence the improvement in antioxidant markers (vs. placebo) went hand in hand with a measurable increase in sperm health and serum testosterone.

Figure 1: Testosterone levels of rats after 60 day intervention with 50mg/kg chrysin. (Ciftcy. 2011)

 "Great", well, maybe not so... although this is an almost 50% increase in testosterone, we do not know how other important hormonal parameters such as SHBG (binds testosterone and thus renders it basically useless), estrogen or cortisol looked like. An estimation of the "muscle building effects", the producers of respective supplements are advertising, is thus futile. And, if you asked my opinion, even if SHBG did not budge and we have an appropriate increase in free testosterone, the latter is probably too little to induce noticeable changes in strength and/or body composition.

ALA + Vitamin E Make Up for Fructose Induced Cardiovascular and Metabolic Changes

Alpha Lipoic Acid (ALA) and vitamin E are among the most investigated and best-known natural antioxidants. And, despite the fact that scientists came to realize, that both, ALA as well as alpha-tocopherol, are far from being the saviors of the metabolically deranged, they were once hailed as, a recent study from the University of Queensland (Patel. 2011) demonstrates their therapeutic potential in an animal model that (unfortunately) is not far from the high fructose corn syrup fed morbidly obese man/woman in a western(-ized) society.

Patel et al. found that supplementation with vitamin E (either α-tocopherol or tocotrienol-rich fraction, 0.84 g/kg food) and α-lipoic acid (1.6 g/kg food) could prevent (high fructose diet + Vit E + ALA) and even reverse (Vit E + ALA after high fructose diet for 8 weeks; reversal protocol) "glucose intolerance, hypertension, and increased collagen deposition in the heart together with an increased ventricular stiffness" in rats fed a high fructose diet over a course of 16 (prevention) / 8 + 8 (reversal) weeks.

Figure 1: (a): Plasma glucose concentrations following oral gavage of glucose (2 g/kg) recorded after 16 weeks for rats fed with corn starch (⬤), fructose (⚪), or fructose with α-tocopherol and α-lipoic acid as either prevention (FTPP) (▲) or reversal (FTPR) (▾) protocols. (Patel. 2011)

As a faithful visitor of the SuppVersity, you probably won't be surprised to read that supplementation with a tocotrienol enriched vitamin E source produced even more favorable outcomes in terms of blood glucose (5.0 vs. 6.4mmol/L in the prevention groups) and the other markers of metabolic health. It should not astonish you, anyway. It's no coincidence that nature provides us with certain nutrients in certain ratios and isolated alpha-tocopherol is something you won't find in nature...

8 Weeks of 5mg/kg Zinc-Sulfate Fire Up Immune System of Turkish Wrestlers

Regular readers of this blog will have noticed that I am generally opposed to mega-dose supplementation with isolated nutrients and so I do not really know what to make of the results of a recent investigation (Kara. 2011) into the effects of 5mg/kg bodyweight zinc-sulfate on cytokine response in 15–17 year-old male subjects.

At the beginning of the study, there were no significant differences of the measured parameters between the four study groups. At the end of the study, the levels of TNF-α, IL-2, and IFN-γ were significantly higher in the two zinc-supplemented groups compared to those that did not receive supplementation, regardless of the activity status (p < 0.01).

Most interestingly, mega-dose (I do not really get, why the authors call 350mg zinc, which would be the dose for a 70kg subject still "physiological") zinc-sulfate supplementation elevated TNF-alpha, IL-2 and IFN-Gamma by >90% regardless of whether the subjects were active sportsmen or sedentary.

Figure 1: Serum IL-2 levels in the study groups (pg/ml) (Kara. 2011)

Other than one might expect zinc supplementation did thus not only blunt exercise induced reductions in immunity, but provoked an overall increase in cytokines which are associated to leukocyte (IL-2) and macrophage (IFN-Gamma) or both (TNF-alpha) activation. In view of the not yet fully understood involvement of these cytokines in metabolic and autoimmune diseases, the authors' conclusion that this "Physiological dose of zinc supplementation to athletes may be useful for sport health and nutrition" does yet appear to be premature.

Energy Drinks Increase Resting Metabolic Rate, But Do Not Influence Energy Expenditure During Exercise

Ever wondered, whether the drink that was once rumored to contain "taurine from bull sperm" and similar fashionable "energy drinks" are of any use? Well, a recent study (Nienhuesser. 2011) coming from an international team of scientists showed that the consumption of each and every of the three energy drinks used in this study lead to a statistically significant increase in resting metabolic rate (RMR).

[...] in a randomly assigned cross-over design, the subjects consumed 473 ml of one of three commercially available energy drinks or a placebo and then RMR and RER [respiratory exchange ratio; i.e. a measure of the relative amount of fat/carbs that is used as fuel] were measured 1 hour later.  The subjects then engaged in 15 minutes of treadmill exercise at 50% of V02max, during which RER and oxygen consumption (VO2) were measured. RMR was not changed by placebo, but increased (P<0.05, means ± se) above baseline by 10 ± 2.5%, 15.0 ± 2.9%, and 15.3 ± 2.9%, following Energy Drink One, Energy Drink Two, and Energy Drink Three (respectively) [...]

In view of the stimulating effect, some of the ingredients (cf. Table 1) of these chemical containing beverages exhibit, these results do not come as a surprise.

Table 1: Listing of ingredients according to Nienhuesser. 2011

What may be surprising, however, is that the study results suggest that - at least from a "calorie expenditure" point of view - the consumption of an energy drink before exercise appears to be less effective than drinking it after exercise or at your desk at the office...

Gadgetry & Caffeine a Dynamic Duo for Sleep Deprivation and, Consequently, Obesity in School-Aged Children

Ever wondered what your children do, when you send them to bed in the evening? According to the results of a study from the Department of Family and Community Health at the University of Maryland School of Nursing, they probably drink Coke and watch TV or play video-games. Does not sound too bad? Well, Calamaro et al. found that children who

drank caffeinated beverages had 15 fewer minutes of sleep per night than did children who did not drink such beverages (b = –0.27, P = .002). Children with three technology items in their bedroom received 45 fewer minutes of sleep than did children without these items in their bedroom (b = –0.75, P = .010).

Still not impressed? What if I told you that these kids missed out on 15 to 60 minutes of what - to my mind - is the most healthiest, most anabolic and most lipolytic time of the day (sleep), and that the study provides evidence for the hypothesis that the immediate consequence of caffeine induced sleep deprivation is obesity? If you do now reconsider whether your 7 year old really needs his own TV-set and whether plain water ain't no viable alternative for Red Bull and Coca Cola, you've already taken the first step to make a change that could - in the years to come - save your children from turning from the "fat guy / girl" in elementary school into the fat and diabetic guy / girl at high school.

Arginine + Glycine a Synergistic Duo for Gut Health

Lately, "gut health" has become a topic of interest way beyond colonics and irritable bowel syndrome. Scientists begin to understand more and more how important an intact intestinal system is for nutrient absorption, infection defense and general health. The results of a very recent study published in the Journal of Colerectal Disease (Picano. 2011) are thus relevant for all of us.

In an experiment with rats Picano et al. found that a combination therapy of l-arginine and glycine inhibited irradiation induced damage to the colon walls of the animals:

Stereologic analysis showed that irradiation induced a reduction of the total volume of the colon wall of group II and III animals compared to healthy controls, but not of group IV animals supplemented with glycine. The mucosal layer of the irradiated animals of all groups was reduced compared to healthy group I animals, but supplementation with L-arginine and glycine was effective in maintaining the epithelial surface of the mucosal layer.

Although I hope none of you is treated (or otherwise exposed) to similar doses of ionizing radiation, it certainly won't hurt your gut health to have an eye on your dietary intake of these two amino acids, in order to maintain optimal gut health.

Caramel Coloring, E150D, or Coca Cola Brown: Not So Carcinogenic as Some People Would Have It

You probably have read it in the NEWS: "Caramel Coloring in Cola carcinogenic!" Well, after yesterday's post on aspartame, I thought it might be advisable to have a closer look at this one, as well. After all, it suddenly appeared more likely that the sulfite ammonia caramel in your diet coke would kill you than the overly dreaded artificial sweetener aspartame.

Although almost none of the webpages, which covered the carcinogenicity of caramel coloring cites the original source of this information, it is yet not difficult to find the respective study (Moon. 2001) on PubMed. It was published in the Journal of Agriculture and Food Chemistry and contains the following small table with data about the amount of 4(5)-Methylimidazole (a byproduct of the production process) in five commercially available cola softdrinks:

cola soft-drink	amount (μg/mL)	in one bottle (μg/591 mL)
brand 1	0.36±0.02	212.76
brand 2	0.32±0.01	189.12
brand 3	0.30±0.01	177.30
brand 4	0.32±0.02	189.12
brand 5	0.36±0.00	212.76

Now, on their own, this figures are hardly significant. Put into the context of the findings of a previous study (NTP. 2007) on the toxicity of this particular chemical, however, they may be disquieting, yet far less alarming than the media would have it:

[...] carcinogenic incidences were observed in experimental mice when they were fed diets containing 0, 312, 625, or 1250 ppm 4-methylimidazole for 2 years. The amounts of 4-methylimidazole in these diets were equivalent to average daily doses of approximately 4, 80, and 170 mg/kg of body weight to mice. If a person weighing 60 kg consumes one bottle of cola soft drink, only 3.3 μg/kg 4-methylimidazole is ingested. Therefore, the amounts ingested from these beverages may not be significant.

As with my previous blogpost on aspartame. I do by no means want to trivialize the toxic potential of these chemicals; nor is it my intention to encourage the use of any chemical substances in foodstuff, BUT I want YOU not to fall victim to each and every fear monger, trying to tell you that XYZ will kill you instantly, when the very science he references tells otherwise. In fact, if you are a man you probably would not have to worry at all, since the NTP study showed "no evidence of carcinogenic activity of 4-methylimidazole in male F344/N rats" at either of the injected dosages over a 2 year period. And in case you are a women, you better open another bottle of coke immediately, because you still have 999x0.5l bottles of Coca Cola to drink today (and for the next 2 years) to "feed" the cancer ;-)

Carbohydrate Restriction Reduces Liver Triglycerides More Effectively Than Calorie Restriction - With Equal Weight Loss Outcomes.

A calorie is not a calorie, I hope you knew that even before Garry Taubes published his famous NY Times best-seller. Yet, in case you are still looking for respective studies to show to medially indoctrinated family members or friends, who still believe that - even if fat is not the enemy - half ratios would be the key to health & longevity, you might be interested in the results of a very recent investigation by Browning et al. (Browning. 2011).

The scientists put a group 18 non-alcoholic-fatty-liver patients on either a carbohydrate-restricted (<20g/day) or a calorie restricted (1200-1500kcal/day) diet - just to make sure you get this right: the carb-restricted group ate as much calories as they wanted! - and measured hepatic triglyceride levels before and after the 2 week dietary intervention. Probably to the surprise of many members of the medical orthodoxy, both groups lost about the same amount of weight (in fact the low-carb group lost -4.6kg, while the low-calorie group lost only -4.0kg!), yet the low-carb group had a much greater reduction in hepatic triglyceride levels:

Liver triglycerides decreased significantly with weight loss (P , 0.001) but decreased significantly more (P = 0.008) in carbohydrate-restricted subjects (-55.6%) than in calorie-restricted subjects (-28.6%).

So, even if you are not particularly interested in your liver health, the fact that by eating to satiety and just dropping your carb intake to <20g/day you can lose the same ~4.5kg you would lose if you starved yourself for 14 days should prick your ears.

Diet Coke & Liver Damage? Long Term Very High Dose Aspartame Consumption Impairs Antioxidant Defense of Rat Livers.

The ever-growing group of health conscious costumers is rightly very skeptical of artificial sweeteners in general and Aspartame in particular. A recent study (Abhilash. 2011) done by scientists from the Mahatma Gandhi University in Kottayam, Kerala, India, seems to rectify this attitude.

The scientists fed rats drinking water that contained either no, i.e. 0mg, 500mg or 1.000mg aspartame per kg body weight day for a period of 160days. The rats from the 1.000mg/kg group showed...

[...] a significant increase in activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and γ- glutamyl transferase (GGT). The concentration of reduced glutathione (GSH) and the activity of glutathione peroxidase (GPx), and glutathione reductase (GR) were significantly reduced in the liver of rats that had received aspartame (1000mg/kg.b.wt).

The presence of "leukocyte infiltration in aspartame-treated rats (1000mg/kg.b.wt)" further underlines that high dose aspartame consumption over a period of 160 days induced "hepatocellular injury and alterations in liver antioxidant status" by increasing the detoxification burden on the liver to supra-physiological levels.

Yet, what does that mean for the average consumer? Let us put the figures into perspective: 1 liter of diet coke contains about 390mg of aspartame. The rats in the high dose aspartame group in the study (which is the only one where anti-oxidant status fell enough to induce histological side effects) received 1.000mg/kg of aspartame per day. In human equivalent dosages (HED), this is 162mg/kg, which would be 11.35g of aspartame or 29 l diet coke for a 70kg adult. Not that I want to trivialize the possible liver toxicity due to aspartame consumption, but let's be honest: you would probably long have died from hyperhydration before you would notice any of the toxic effects induced by the consumption of an artificial sweetener, which - far from being healthy - is yet not as toxic as some health-fetishists would have it.

In spite of the fact that a diet coke here and there won't kill you, you should still ask yourselves, whether or not you really need this "spawn" of a society where we want all the convenience and (unnaturally sweet) taste of unhealthy foods without the negative consequences for our health? I mean, you obviously chose the "diet" version because you want to avoid sugar; but do you still want the sweet taste, which (at least for some artificial sweeteners, eg. Nakagawa. 2009) has been shown to increase insulin secretion even in the absence of direct beta cell stimulation!? If you are willing to accept this compromise and do not care about the other chemicals your average can of diet coke "nourishes" you with, fine! But do not tell me later on, I had told you that diet coke was good for you ;-)

Review of Intervention Studies Shows: Weight Loss Success Independent of Meal Frequency

"Eat 3 large meals à day!", "Eat smaller meals every 2 hours!", "Eat a single meal and fast the rest of the day!" If you have been trying to find information on how to lose weight effectively, you probably heard all these "expert" advises. What if I told you that a recent review of 25 weight loss interventions shows that it simply does not matter!

In an extensive review of the literature, Palmer et al. (Palmer. 2011) conclude:

Manipulating the EF [eating frequency] of a client seeking weight management is unlikely to provide any additional benefits to weight, body composition or health. The theoretical benefits of manipulating EF may not be sustained in the real life clinical setting as a change to EF may be difficult to maintain over the longer term. Current evidence does not support many of the theories that encourage manipulating EF for weight management. Focus needs to be placed on dietary weight management strategies that are achievable and sustainable over the longer term.

Better body composition? Only inconclusive evidence. Better glucose tolerance in non-diabetics? Definitely not. Decreased risk of heart disease? Unlikely. Less hunger? At least not with three vs. six meals. Bottom line: Another myth debunked!

Want to Burn More Fat During Your Cardio Training? Eat Low Carb Before Workout!

Modulation of substrate utilization is the key to effective weight loss. For years we have been told that "training in the zone" (referring to a specific heart rate) would do the trick - recent research does yet suggest otherwise: High Intensity Interval Training (HIIT) has been shown to be at least as effective in burning off unwanted body fat, as the longstanding "gold standard", Low Intensity Steady State (LISS) in the "fat burning zone".

Researchers from the Department of Exercise Science and Sports Studies at Springfield College, Springfield, MA, USA, have now found that apart from the type of exercise you chose to perform, the nutrition, especially in the hours before working out, determines whether you will predominantly burn fat or carbs to sustain the workout.

In their study (Gregory. 2011), Gregory et al. compared the metabolic responses of a group of 8 "active, pre-menopausal" women to a 30 minute exercise regimen performed after either a low carbohydrate (LC: 392 kcal @ 15% carbohydrate, 68% fat, and 18% protein) or a low fat (LF: 396 kcal @ 78% carbohydrate, 7% fat, and 15% protein) meal. Respiratory gas exchange (RER), blood glucose (G), insulin (IN), triglycerides (TG), and free fatty acids (FFA) were measured. While "no significant differences existed between test meals for fasting blood measurements", the post-exercise results showed significant differences:

Postexercise (PE) FFA (mEq·L-1) levels were significantly greater following LC [1.1 (0.3) vs. 0.5 (0.3)]. PE TG (mg·dL-1) levels were significantly greater following LC [152.0 (53.1) vs. 114.4 (40.9)]. RER was significantly lower at all time points following LC compared to LF.

With the respiratory gas exchange being a measure of the relative contribution of fatty acids to fulfill the exercise-induced energy demand (Chessex. 1995), the researchers rightly conclude "ingestion of a single LC meal resulted in greater lipid oxidation at rest and during exercise as compared to a single LF meal." But, let's be honest - did you expect anything else?

More Conflicting Evidence on Leucine Metabolite: HMB Makes Volleyballers Stronger.

The leucine metabolite HMB, i.e. β-Hydroxy-β-Methylbutyric acid, is unquestionable the comeback kid of the supplement industry. "It works!", "It's useless!", ... every now and then a new study supports one side of the debate. A group of international scientists does now present a study, which would support the use of the expensive, yet readily available amino acid.

Portal et al. (Portal. 2011) investigated the effect of 3g HMB/day "on body composition, muscle strength, anaerobic and aerobic capacity, anabolic/catabolic hormones and inflammatory mediators in elite, national team level adolescent volleyball players (13.5–18 years, 14 males, 14 females, Tanner stage 4–5) during the first 7 weeks of the training season". The results were unequivocal, yet not overtly impressive:

HMB led to a significant greater increase in FFM by skinfold thickness (56.4 ± 10.2 to 56.3 ± 8.6 vs. 59.3 ±  11.3 to 61.6 ± 11.3 kg in the control and HMB group, respectively, p < 0.001). HMB led to a significant greater increase in both dominant and non-dominant knee flexion isokinetic force/FFM, measured at fast (180°/sec) and slow (60°/sec) angle speeds, but had no significant effect on knee extension and elbow flexion and extension. HMB led to a significant greater increase in peak and mean anaerobic power determined by the Wingate anaerobic test (peak power: 15.5 ± 1.6 to 16.2 ± 1.2 vs. 15.4 ± 1.6 to 17.2 ± 1.2 watts/FFM, mean power: 10.6 ± 0.9 to 10.8 ± 1.1 vs. 10.7 ± 0.8 to 11.8 ± 1.0 watts/FFM in control and HMB group, respectively, p < 0.01), with no effect on fatigue index.

With no measurable effect on aerobic fitness, anabolic hormone levels or inflammatory mediators, the use of HMB appears to be advisable only in power and strength athletes.

If you are a bodybuilder on a high protein diet, I would however doubt that you would see any benefits from additional HMB. A diet rich in quality protein (high BCAA and particularly leucine content) should provide you with adequate amounts of leucine to keep endogenous HMB levels elevated.

Low Dose Caffeine Ameliorates Catabolic Effects and Increases AMPK and PPAR Expression During Reduced Food Intake in Mice

Caffeine, "the mother of all stimulants", has lately developed a bad reputation. Stress, Cortisol, Adrenal Fatique, Insulin Resistance etc. are only the most recognized buzzwords occurring within the context of caffeine consumption. A very recent paper (Shermann. 2011) coming from scientists from the University of Jerusalem draws a wholly different picture.

Shermann et al. investigated the effect of caffeine consumption (3.5 mg/kg/day or 7 mg/kg/day) on circadian rhythms and expression of disease and metabolic markers in mice under two distinct dietary conditions over a period of sixteen weeks. When the rats were fed an ad libitum diet (meaning they could consume as much food as they wanted), ...

caffeine reduced the average daily mRNA levels of certain disease and inflammatory markers, such as liver alpha fetoprotein (Afp), C-reactive protein (Crp), jejunum alanine aminotransferase (Alt), growth arrest and DNA damage 45β (Gadd45β), Interleukin 1α (Il-1α), Il-1β mRNA and serum plasminogen activator inhibitor 1 (PAI-1).

For those of you who still want to shed some pounds of fat, it may yet be even more interesting to read that "caffeine supplementation led to decreased expression of catabolic factors under RF". With the RF = restricted feeding condition being comparable to what is known as "intermittent fasting" in the fitness community, this finding is highly significant.

Figure 1: Metabolic markers PPAR-Gamma (above) and PPAR-Alpha (below) in mice fed an ad libitum (AL) or a restricted diet (RF) (Shermann. 2011)

This is particularly valid given the fact that there was a highly significant increase in PPAR-Gamma, PPAR-Alpha (cf. figure 1) and AMPK (not shown) activities in the group receiving "high dose" (7mg/kg; for humans this would equal a pretty low dose of about 0.6mg/kg) caffeine. Both, peroxisome proliferator activated receptor (PPAR), as well as AMPK are regarded as master metabolic regulators that have been implicated in the physiology of fat loss. A moderate caffeine consumption, i.e. about one cup of coffee, in the course of an intermittent fast, may thus well spare muscle protein and burn body fat, at the same time.

Omega 3 Attenuates Exercise Induced Rise in Inflammatory Markers, BUT is This Necessarily a Good Thing?

I want to take the results of a recent study (Bakhtyar. 2011) published in the Clinical Journal of Sport Medicine as an opportunity to readdress the question of whether or not the Omega 3 induced suppression of inflammation must be considered a good or a bad thing, both in view of athletic performance, as well from a health and longevity perspective.

Those of you, who listened to my interview on Carl Lenore's Super Human Radio show, will know that my understanding of "inflammation" is somewhat different from the mass market "explanation" of "a fire that causes damage". To be precise inflammation, or what scientists generally measure, is the release of signals (inflammatory markers) that tell immune cells to do their jobs. So, saying that inflammation is the root of all disease would be like saying that someone who calls the firefighters is to blame for the fire - but I am digressing from the topic at hand...

After administering 1.5g/day of an omega 3 supplement (experimental group) to every third of 45 previously untrained volunteers, Bakhtyar et al. found the subjects' "inflammatory" response to eccentric exercise to be modified:

The experimental group showed less elevation in TNF-α and PGE₂ immediately, 24, and 48 hours after exercise, when compared with the other groups. Significantly less elevation was shown in the concentration of IL-6, CK, and Mb for the experimental group at 24 and 48 hours after exercise. The experimental group also demonstrated a significant trend toward reduction in the plasma concentration of LDH immediately, 24, and 48 hours after the exercise program.

Now, what does this tell us about the training effect and health outcomes of the exercise regimen?

• With inflammation being a not yet fully understood prerequisite for muscular repair and hypertrophy, it would warrant further investigations like muscle biopsies and consistent training regimens with continuously monitored strength and muscle gains to conclude that omega 3 supplementation is beneficial in terms of physical performance.
• In view of the conclusions Pedersen draws in a recent review (Pedersen. 2011) of the role of exercise induced myokines, i.e. inflammatory markers released by muscles (myo- = muscle-), in chronic disease, blunting of muscular IL-6 release, which has been linked to muscular AMPK activation, increased glucose uptake and fat oxidation, omega 3 supplementation is probably counter-indicated in a health oriented exercise regimen, anyway.

I hope more scientists such as Pedersen will begin to question the current "anti-inflammatory" paradigm, so that major players in the medial landscape will be forced to take on their findings and stop portraying long chain polyunsaturated fatty acids in general and fish oil in particular as the savior of the fat and diabetic. Instead they should encourage people to finally get their asses off their sofas to induce exactly that amount of healthy, exercise-induced inflammation omega 3 supplementation appeared to suppress in the aforementioned study.

Flavanol-Rich Lychee Fruit Extract Displays Potent Antioxidant Activity in Trained Long-Distance Runners

If I told you about each and every "new" antioxidant that produced some marvelous effects in the petri-dishes of some scientists somewhere on a random university campus, there would hardly be any space left for interesting information on this blog. In the case of the particular lychee fruit extract (FRLFE), Nishizawa et al. (Nishizawa. 2011) selected for their study, we do not only have a human study, but also direct information on how supplementation with 50mg of Oligonol (brand name of the extract) influenced inflammatory markers and performance of 20 university level marathon runners over the course of 2 months:

Some parameters, including the white blood cell count, were significantly modified by FRLFE supplementation [46.3 FRLFE vs. 57.6 control]. Compared with the placebo group, the change in the serum interleukin-6 level between pre- and mid-training were significantly lower in the FRLFE group, while the change in the transforming growth factor-β level between pre- and post-training was significantly greater in the FRLFE group.

This increase in TGF-Beta is significant, because...

...TGF-β controls cell growth and proliferation (Massagué, 1998), and may be secreted in response to strenuous physical training and cell damage during training.

TGF-beta is thus another case, where an "inflammatory marker" indicates repair and (possibly) hypertrophy rather than damage and catabolism. Consequently, it is unlikely that the consumption of a highly anti-oxidant flavanol-rich lychee fruit extract hampers muscle growth. Who knows, maybe we are going to see respective supplements in the near future - meanwhile, I suggest you get yourself some of these Chinese soapberries at your local fruit store ;-)

Heart Protective Effect of Red Wine not Exclusively Due to Resveratrol. Melatonin Potentially the Major Player!

Resveratrol, the red wine polephynol still is in everyone's mouth (literally, as well as metaphorically), yet a recent (Lamont. 2011) study published in the Journal of Pineal Research indicates that another hitherto overlooked constituent of the fermented grape juice factors into its protective value: Melatonin.

Lamont et al. found that, at the doses which can be found in red wine, naturally, individually, as well as in combination resveratrol and/or melatonin ...

... significantly reduced infarct size compared with control hearts in wild-type mouse hearts (25 ± 3% and 25 ± 3% respectively versus control 69 ± 3%, P < 0.001) [...] Furthermore, perfusion with either melatonin or resveratrol increased STAT3 phosphorylation prior to ischemia by 79% and 50%, respectively (P < 0.001 versus control).

Both, melatonin, as well as resveratrol, appear to work via the "survivor activating factor enhancement" [SAFE]. What I consider more important, yet is the scientists' finding that

 [...] melatonin confers a comparable protective effect to resveratrol but at a concentration 30,000 times lower.

And their conclusion that "melatonin may be considered as a primary antioxidant in red wine". So what else could be healthier than a glas of good wine right before a good night's sleep?