LED Therapy: 30% Increase in Max. # of Reps in New Study, Increased Stamina and More Recent LLLT / LEDT Data

LED Therapy: 30% Increase in Max. # of Reps in New Study, Increased Stamina and More Recent LLLT / LEDT Data

laser therapy LED LEDT leg training LLLT low level laser therapy performance quadriceps recovery

The scientists used an LEDT device from Thor on two points on the distal portion of the vastus lateralis, two points on the distal portion of the vastus medialis and two centered points along the rectus femoris (see Figure 1, right).

It may be partly my fault that most of you ask me for supplements to take to increase their performance and do not expect often not even consider the possibility of being told about technological items like a low-level laser diode device to up their gains or boost their fat loss...

When I started this blog a few years ago, I was guilty of believing that supplements would be the most relevant ergogenics for anyone who trains, myself. Today, ~2,300 articles later, this has changed: don't get me wrong - supplements can be useful, but diet, training and - at least in a few cases - even things like using light emitting diode therapy (LEDT) or low-level laser therapy (LLLT), as it is also called, are much higher on the "things that really work"-list.

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In that, it is important to point out that a recent study from the Georgia Southern University (Hemmings. 2016) is neither the first study to show significant performance / recovery benefits from LEDT, nor is it the first study I wrote about (read previous articles). The experiment Hemmings et al. conducted is yet the first to evaluate the effects of different dosages of LEDT (30 vs. 60 vs. 120 seconds on each irradiation point, see Figure 1, right) that was applied by the means of a low-level laser (THOR, London, UK) on muscular fatigue of the quadriceps after two sets of three maximal voluntary isometric contractions (MVIC).

Figure 1: Comparison of repetitions and blood lactate concentrations between all four trials; illustration of the irradiation points that were used for LEDT (Hemmings. 2016)

A total of 34 recreationally resistance trained athletes between the ages of 18 and 26 participated in four trials. Each trial included pre/post exercise blood lactate measurements, the previously hinted at MVIC and a single set of eccentric leg extensions (at 120% of the previously determined MVC) to exhaustion that was done three minutes after the initial exercises and used as a yard-stick for the recovery benefits of using 30s, 60s and 120s of LEDT compared to a 45s placebo treatment of which the subjects thought that it was yet another irradiation time that was to be tested.

LLLT therapy has also been shown to almost double the muscle gains in a study with an 8-week eccentric training program | more

LLLT and LEDT - What does the science say?: Here's how the authors explain the difference, between different forms of laser light therapy (LLT) and light emitting diode therapy (LEDT): "The difference between LLT and LEDT is the power output and depth of penetration due to various patterns in wavelengths" (Hemmings. 2016). The potential mechanism, on the other hand is always the same: "[r]esearch suggests that LLLT can prolong the binding of nitric oxide to the cytochrome C oxidase enzyme, which permits the muscle to produce more ATP in the preferred oxidative pathway" (Hemmings. 2016).

A recent meta-analysis (Nampo. 2016) evaluated both, the effects of LLLT and LEDT, on exercise capacity and muscle performance of people undergoing exercise when compared to placebo treatment. Sixteen studies involving 297 participants were included in the meta-analysis that shows a mean improvement of the number of repetitions of 3.51 reps (0.65–6.37; P = 0.02), a 4,01 second delay in time to exhaustion (2.10–5.91; P < 0.0001), and - unlike the study at hand - a sign. reduction in lactate levels (MD = 0.34 mmol/L [0.19–0.48]; P < 0.00001) and increased peak torque (MD = 21.51 Nm [10.01–33.01]; P < 0.00001).

Exercise capacity - Number of reps (left), time to exhaustion (right | Nampo. 2016)

Reason enough for the authors to conclude that their "results suggest that LASERtherapy is effective in improving skeletal muscle exercise capacity" - one thing Nampo et al. rightly add is that "the quality of the current evidence is limited" (Nampo. 2016).

As you would expect it for any effective ergogenic, the scientists observed a "significant increase in the number of repetitions performed between the placebo treatment" (Hemmings. 2016). In that, it is interesting to see that both treatments, i.e. 60 seconds (p= 0.023), as well as the 120 seconds (p=0.004) LEDT treatment triggered a significant increase in the number of reps the subjects completed - without, however, significantly affecting the accumulation of blood lactate levels in the subjects' blood. Another thing the data in Figure 1 tells us that must not be forgotten is the lack of effect of applying LEDT for only 30 seconds per irradiation point (see Figure 1, right).

Lactate is not the enemy - remember? Caffeine and Bicarbonate (NaHCO3), two proven ergogenics increase, not decrease blood lactate accumulation while still boosting subjects' performance during a standardized yo-yo performance test | learn more.

While the last-mentioned lack of effect of a shorter treatment is probably something you'd expect, the lack of effect on the accumulation of lactate may come as a surprise. Eventually, however, the exercise duration was probably simply too short to accumulate exuberant lactate levels. It is imho also questionable why the scientists used lactate, not CK or another potential measure of muscle damage (or a biopsy) to judge the effects of the LEDT treatment on a molecular level. After all, the often-heard hypothesis that the accumulation of lactate would be the reason you fail due to muscular exhaustion is - in view of the existing evidence - at least questionable.

What about gains and does timing matter? No, you don't have to be afraid that LLLT would have the same negative effects on your gains as ice-baths. It has, after all, already been shown to double the gains in a 2015 8-week study in healthy volunteers | read more! And the timing, yeah... Well, yes timing does matter! You have to apply it before the workout to see effects... at least for immediate 1RM strength gains this is the case according to a very recent study by Vanin (2016) - future studies will tell if using it post, as a recovery tool can be effective in the long-term.

As a SuppVersity reader you will, for example, remember that proven ergogenics such as bicarbonate and beta alanine increase the accumulation of lactate significantly... ok, you may argue that they simply protect the muscle from the tiring effects of lactate, but eventually there are other more likely candidates to explain the onset of fatigue such as the accumulation of other muscle metabolite, a decrease in free energy of adenosine triphosphate, limited O2 or other substrate availability, increased glycolysis, pH disturbance, increased muscle temperature, reactive oxygen species production, and altered motor unit recruitment patterns (Grassi. 2015; Poole. 2015), which could eventually explain why our muscles fatigue and why the lactate levels increase (reduced ATP, for example, will necessarily increase glycolysis and eventually the lactate accumulation).

This is only one of of several LLLT studies I've discussed in detail in older SV articles. Examples? What about this one from Aug 2015: Phototherapy Doubles Fat Loss (11 vs. 6%) & Improvements in Insulin Sensitivity (40 vs. 22%) and Helps Conserve Lean Mass in Recent 20 Weeks 'Exercise for Weight Loss Trial' | read more

Bottom line: Yeah, the scienists are right to conclude that "light emitting diode therapy had a positive effect on performance when irradiating six points on the superficial quadriceps for 60 seconds and 120 seconds prior to an eccentric leg extension" (Hemmings. 2016).

What can be refuted based on their results, however, is that this effect was a consequence of reduced lactate levels. That's in contrast to another recent study in a particularly vurnerable subgroup of hobby athletes, i.e. the hospitalized patients with heart failure in a pilot study by Bublitz et al. who found a significant decrease in lactate accumulation, albeit in response to a 6-minute walking exercise, during which LLDT was able to reduce the subjective fatigue and the previously discussed lactate concentrations, but not the subjects' performance.

Overall, it seems reasonable to conclude that further research is necessary to (a) elucidate the underlying mechanism behind the (pro-)recovery / performance enhancing effects, as well as LEDT's / LLLT's previously reported beneficial effects on insulin sensitivity and body composition and the most promising areas of application (according to the study at hand this could be resistance training / any sport that requires maximal anaerobic performance) | Comment!

References:

• Bublitz, Caroline, et al. "Acute effects of low-level laser therapy irradiation on blood lactate and muscle fatigue perception in hospitalized patients with heart failure—a pilot study." Lasers in medical science (2016): 1-7.
• Byrne, Christopher, Craig Twist, and Roger Eston. "Neuromuscular function after exercise-induced muscle damage." Sports medicine 34.1 (2004): 49-69.
• Grassi, Bruno, Harry B. Rossiter, and Jerzy A. Zoladz. "Skeletal muscle fatigue and decreased efficiency: two sides of the same coin?." Exercise and sport sciences reviews 43.2 (2015): 75-83.
• Hemmings, Thomas J. "Identifying Dosage Effect of LEDT on Muscular Fatigue in Quadriceps." Journal of Strength and Conditioning Research (2016): Publish Ahead of PrintDOI: 10.1519/JSC.0000000000001523..
• Poole, David C., and Thomas J. Barstow. "The critical power framework provides novel insights into fatigue mechanisms." Exercise and sport sciences reviews 43.2 (2015): 65-66.
• Vanin, Adriane Aver, et al. "What is the best moment to apply phototherapy when associated to a strength training program? A randomized, double-blinded, placebo-controlled trial." Lasers in Medical Science (2016): 1-10.

Resistant Starch (RS4) for Fat Loss & Exercise Performance

Resistant Starch (RS4) for Fat Loss & Exercise Performance

cycling lose fat performance resistant starch RS RS4

RS4 is still relatively difficult to come by. Options I know of are ActiStar® from Cargill and Fibersym® fom MGP. RS2 and RS3 alternatives are raw potato starch and, as previously discussed, banana starch or reheated starches. They'll have (presumably) very similar effects, but come directly from food.

You will probably remember the good old "Waxy Maize Reloaded" article from 4 years ago that caused quite a stir!? Well, I guess four years is a long time - more than enough to revisit the idea of designer resistant starches and their effect on your physique and performance. To do so, I've picked two recent studies from the South Dakota State University (Upadhyaya. 2016) and the Florida State University (Baur. 2016) that have one thing in common: they add to the hitherto still inadequate number of studies on resistant starch type 4 (RS4), one out of five forms of "resistant", i.e. (partly) undigestible, starches with significantly different chemical properties and corresponding functional differences such as their fermentability or their influence on the microbiota in the gut and their applicability as ergogenics in sports drinks and/or functional foods.

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To elucidate the effects on the gut microbiome and the production of health-relevant short-chain fatty acid (SCFA) production, of which the previously cited article about WM-HDP from 2012 explains how they affect GLP-1, glycemia and metabolism (read it), Upadhyaya et al. conducted an experiment with twenty individuals with signs of, but not fullly established metabolic syndrome (MetS).

Table 1: Overview of the study design (Upadhyaya. 2016).

With a total duration of 26 weeks that included two 12-week interventions periods, with one each for RS4 (30%, v/v in flour that is currently not available in supermarkets) and control flour (CF), and a two-week washout in between the interventions, the randomized cross-over study is one of the longest dietary interventions with any form of resistance starch I have read and thus also the one with the highest potential of yielding relevant insights into the long-term effects of RS-4 consumption. As previously pointed out, ...

"[...] all twenty participants who had signs of metabolic syndrome at baseline and submitted adequate stool samples at four data collection time points were included in the current investigation, which allowed for comparison of the gut microbial and SCFA profiles before and after the interventions and also between the endpoints of the RS4 and CF (control) interventions" (Upadhyaya. 2016). 

In view of the fact that adverse gastrointestinal side effects from the interventions were not evaluated in this cohort, we have to simply follow the scientists' reasoning that no bloating, belching or other unwanted sides would occur - an assumption that appears to be at least reasonable in view of the observations the scientists made in a previous study w/ similar design (Nichenametla. 2014).

The visible performance decrements in the low HMS group was sign. correlated with gastrointestinal distress (Baur. 2016).

What about performance? Those were evaluated by Daniel A. Baur in a study which investigated the metabolic and gastrointestinal effects of a hydrothermally-modified starch supplement (HMS) before and during cycling for ~3 h (1 h at 50% Wmax, 8 x 2-min intervals at 80% W max, and 10 maximal sprints) in 10 in male cyclists who underwent three nutritional interventions (crossover design): (1) a commercially available sucrose/glucose supplement (G) 30 min before (60 g carbohydrate) and every 15 min during exercise (60 g/h); (2) HMS consumed at the same time points before and during exercise in isocaloric amounts to G (Iso-HMS); and (3) HMS 30 min before (60 g carbohydrate) and every 60 min during exercise (30 g/h; Low HMS).

Interestingly enough, the supplement had no effects on sprint performance with Iso HMS vs. G, being identical and G and Iso HMS resultin in nothing but a "likely", yet small performance enhancement of 5.0% compared to the "low carb" = Low HMS trial.

What may  be considered a success, though, is the sign. increase in fat oxidation (31.6%+/-20.1%; very likely (Iso); 20.9%+/.16.1%; likely (Low)) and corresponding reduction in carbohydrate oxidation (19.2%+/-7.6%; most likely; 22.1%+/-12.9%; very likely) during exercise relative to the plain glucose trial (G). That the latter was dearly bought by increased during repeated sprints with ingestion of Iso HMS (17 scale units +/-18; likely) and Low HMS (18 +/-14; likely) that also explained the decreased performance with Low HMS vs. G (likely), future studies will have to either find ways to make HMS more gut friendly or test whether the repeated administration of HMS solves the issue by the means of intestinal adaptation - a corresponding study could also yield insights into whether the increased fatty oxidation would also trigger long-term mitochondrial growth that goes beyond what you'd see with regular Gatorade aka a sugar-containing workout beverage.

I know that you will probably me most interested in the effects on the subject's body composition. Therefore I plotted those in Figure 1 and postponed the presentation and discussion of the authors' actual research interest, the microbial composition of their subjects guts on a later paragraph.

Figure 1: Effects of control and RS4 diet on body composition and lipid variables (Updahyaya. 2016).

As you can see, the consumption of the RS4 diet had significant (beneficial) effects on the subjects' waist lines (~2% or 2 cm vs. baseline and control). In conjunctions with the beneficial effects on HDL (p = 0.001) and total cholesterol (p = 0.01), which were 10% higher and lower, respectively, after the RS4 vs. control diets, and a significant increase in adiponectin (p < 0.01), and none-significant improvements in fasting blood glucose (+5% and -4% vs. baseline in control and RS4, respectively) and HbA1c (-1% and -2% vs. baseline in control and RS4, respectively), there appears to be little doubt that the significant improvement in the firmicute to bacteriode ratio, which is frequently perceived as an indicator of a leaner phenotype (although the previously reported results are not always consistent | Fernandes. 2014) in the RS4 weeks, as well as specific results, such as ...

• the previously observed increase of species from Clostridial cluster XIVa, but not cluster IV, that was triggered by RS4 supplementation of the diet; at the species level, RS4 consumption increased the abundance of Bifidobacterium adolescentis (90.5 fold, q= 0.087) and Parabacteroides distasonis (1180.2 fold, q< 0.001) but not Ruminococcus bromii (−3.2 fold, q > 0.05), Faecalibacterium prausnutzii (−1.2 fold, q > 0.05), or Dorea formicigenerans (1.1 fold, q> 0.05)

• 

  Timing Matters if You Want to Turn Regular into Resistant Starch | more

  a not previously observed RS4-induced increase in Christensenella minuta abundance (119.7 fold, q= 0.038, 97% query coverage, 88% identity and E< 0.001 in NCBI-BLAST) as well as in several OTUs in the family Ruminococcaceae and genus Bacteroides; at the species level, Bacteroides ovatus (37.6 fold, q= 0.087), Ruminococcus lactaris (2866.7 fold, q< 0.001), Eubacterium oxidoreducens (3.3× 105 fold, q< 0.001), Bacteroides xylanisolvens (47.8 fold, q= 0.037), and Bacteroides acidifaciens (92.4 fold, q= 0.038) were enriched after RS4 intervention
• changes in the individual proportions of the SCFAs, butyric (69.5%, p= 0.03), propionic (50.2%), valeric (44.1%), isovaleric (20.3%), and hexanoic (19.2%) acids increased post intervention from baseline in the RS4 group (p< 0.05) but not in the CF group (data not shown)
• correlations between significant changes in the gut microbiota composition induced by RS4 and altered SCFA level that were not observed after the control treatment

provide reasonable evidence for the use of RS4 as a food additive (in place of regular starches, obviously). In that, it is also important point out is that the changes in body composition, lipoproteins, glucose control and the bacterial composition of the subjects' microbiome occured in the absence of significant differences in macronutrient intake,... well, aside from the dietary fibre intake, which was obviously significantly higher in the RS4 group (p< 0.001). After all, RS4 is officially being classified as a prebiotic dietary fibre.

Figure 2: Differential gut microbial composition after RS4 intervention at the species level (left) and correlations with important metabolic outcomes from total cholesterol (TC) to adiponectin (right | Upadhyaya. 2016).

Overall, the average calories (~1,774 Kilocalories) consumed at baseline were estimated to come from carbohydrate (~49%), protein (~17%), and fat (~34%) - values you may criticize, but of which the authors rightly point out that they "fall within the Dietary Reference Intakes (DRI) for macronutrients, which are 45–65%, 10–35%, and 20–35% for carbohydrate, protein, and fat", respectively.

Is RS4 different from other prebiotics?It obviously is structurally different, so it is not 100% surprising that a previous parallel design study u-sing other prebiotics, na-mely inulin and oligofruc-tose, suggests that the ensuing improvement in metabolic functions and body composition are more pronounced with RS4 compared to other prebiotics.

Bottom line: In sum the two studies provide reasonable evidence for the addition of RS4 to your diet and/or functional foods. There is one thing you should keep in mind: the potential ergolytic effect that comes with the intestinal side effects in those who cannot handle the RS4-laden Gatorade alternative. Before you buy a few pounds of RS4 at the bulk-supplier of your trust, you should thus better test-drive your individual RS4 tolerance.

Since similar effects were not observed by Nichenametla and Updahyaya in their 2014 and 2016 studies, it is yet safe to assume that this effect may be exposure dependent with the use of  30% v/v RS4 in flour - a strategy that could also be employed in processed foods having no significant effect on the digestive health of the average customer, but a sign. effect on his waist circumference | Comment!

References:

• Baur, Daniel A., et al. "Slow-Absorbing Modified Starch before and during Prolonged Cycling Increases Fat Oxidation and Gastrointestinal Distress without Changing Performance." Nutrients 8.7 (2016): 392.
• Dewulf, Evelyne M., et al. "Insight into the prebiotic concept: lessons from an exploratory, double blind intervention study with inulin-type fructans in obese women." Gut (2012): gutjnl-2012.
• Fernandes, J., et al. "Adiposity, gut microbiota and faecal short chain fatty acids are linked in adult humans." Nutrition & diabetes 4.6 (2014): e121.
• Nichenametla, Sailendra N., et al. "Resistant starch type 4‐enriched diet lowered blood cholesterols and improved body composition in a double blind controlled cross‐over intervention." Molecular nutrition & food research 58.6 (2014): 1365-1369.
• Upadhyaya B, et al. "Impact of dietary resistant starch type 4 on human gut microbiota and immunometabolic functions." Sci Rep. 2016 Jun 30;6:28797. doi: 10.1038/srep28797.

When "No Load Training" Builds Muscle and Classic Biceps Curls Diminish Your Triceps Size, Science Must be Involved

When "No Load Training" Builds Muscle and Classic Biceps Curls Diminish Your Triceps Size, Science Must be Involved

build muscle gains gainz high load hypertrophy low load muscle gains no load training

Do not misunderstand the results of the study at hand. It does not "proof that you don't have to use weights to make size gains" and it does not even suggest that "training without load works as effectively as training with loads for every muscle".

I suspect you will remember that I have previously written about the potential muscle building effects of posing. Now, the isometric contractions you perform when you "pose", are not exactly the same, but at least related to the "maximal contractions through a full range of motion" Counts et al. investigated in their latest study. Accordingly, it doesn't seem to be totally far-fetched to assume that (1) increases in muscle size would be similar with this type of NO LOAD compared to HIGH LOAD training and that (2) HIGH LOAD training would still result in a greater strength increases compared to NO LOAD due to the principle of specificity.

To elucidate whether these hypotheses are accurate, Counts et al. recruited fifteen (6 men, 9 women) participants for a 6-week study (see Figure 1) ... untrained subjects.

It could be a good idea to use NO LOAD training as part of your periodization schemes.

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Untrained? I know what you're thinking, but you got to start somewhere and to measure significant muscle gains in only 6 weeks, your subjects almost have to be untrained; even if this means that it is neither necessarily nor likely possible to transfer your results to trained individuals. It is thus well possible, that the NO LOAD conditions, the authors describe as follows, ...

"[t]he NO LOAD training condition is defined as voluntarily maximally contracting the muscle through the full range of motion without the use of an external load. During each NO LOAD training session, surface electromyography (EMG) electrodes were applied to the biceps to provide feedback to the participant and to help encourage greater activation during each repetition. The participants completed 4 sets of 20 repetitions with 30 seconds of rest between sets. This protocol was based off of pilot work performed in our laboratory which suggested that 4 sets of 20 repetitions should result in increases in both fatigue and muscle activation" (Counts. 2016).

... will have smaller or even no effect at all on the muscle size of already trained individuals - and that would obviously be much in contrast to the tried-and-proven HIGH LOAD training in which the authors completed 4 sets of 8–12 repetitions with 90 s of rest between sets at 70% of their 1RM (weight was increased if more than 12 reps could be done).

Figure 1: Study design outline. 1RM – one repetition maximum (Counts. 2016).

But enough of the "could"s and "might"s. Let's take a look at what we can says for sure: In the study at hand, where both conditions exercised to a metronome at a cadence of 1.5 s for the concentric and eccentric portion of the lift, totaling a 3 s contraction, the subjects were assigned to the NO or HIGH load condition according to a counterbalanced design and the results were quite intriguing:

• Contracting muscle through a full range of motion with no external load increases muscle size similar to high load training.
• High load training produced larger increases in 1RM strength & muscle endurance compared to contracting with no external load.
• Muscle growth can occur independent of the external load provided sufficient tension is produced by the muscle.
• Muscle strength is proportional to the load being used and the modality of exercise being performed (specificity)

More specifically, the study results show that anterior muscle thickness increased similarly from Pre to Post, with no differences between conditions for the 50% [Pre: 2.7 (0.8) vs. Post: 2.9 (0.7)], 60% [Pre: 2.9 (0.7) vs. Post: 3.1 (0.7)] or 70% [Pre: 3.2 (0.7) vs. Post: 3.5 (0.7)] sites, that there is a significant condition × time interaction for one repetition maximum (p = 0.017), with HIGH LOAD (+2.3 kg) increasing it more than the NO LOAD condition (+1 kg) and thus that it is, as Counts et al. write "generally possible to make gains [at least in untrained individuals] across a vast range of external loads and muscle actions" - even independent of external load "provided there are enough muscle fibers undergoing mechanotransduction" (Counts. 2016).

Figure 2: Mean muscle thickness from pre to post training at 50%,60% and 70% sites of the anterior (biceps) & posterior (triceps) upper arm (left) and individual differences in anterior muscle thickness (right | Counts. 2016).

Before you drop the weights altogether, though, you should know that there are a few other limitations of the study (next to the previously hinted at lack of training experience in the subjects) the scientists discuss: They range from the lack of quantitative data on the volume of work completed in the NO LOAD condition (workload is distance times weight - with no weight, you cannot calculate it), of which the scientists say that it "may explain some of the variability in the growth response following NO LOAD training" to the choice of tests which are "more specific to the HIGH LOAD condition and less specific to the NO LOAD condition[. Consequently] it stands to reason that NO LOAD training's effect on strength may be underestimated" (Counts. 2016).

Eventually, the results of the study at hand, as intriguing as they may be, must thus be considered preliminary evidence in support of the mechanotransduction theory of muscle building and its implications, namely that no external load is necessary to stimulate the transcription factors that will eventually initiate the adaptive response to "no-weight lifting" (see Figure below)

Overview of the main events during signal transduction and gene regulation leading to muscle hypertrophy (my orange emphasis in a figure from Rennie, et al. 2004)

So, yes further research is war-ranted to evaluate whether training w/out load could make sense for trained individuals as well.  I have to admit, though, that the existing evidence on the underlying mechanisms of muscle growth supports the notion that training for size does not necessarily involve high weights or muscle damage. After all, the hypertrophy driving trans-criptional factors (see Figure on the right) can be induced by Ca2+ increa-ses, stretch and hypoxia, which can all be achieved in the absence of high loads or sign. muscle damage (Rennie. 2004)... and still, I have my doubts about the effects on trained individuals.

What? Oh, yes... the hint at the reduced posterior muscle (=tripecs) size from the headline. I almost forgot that. Well, the scientists were probably not less surprised than you were when you looked at Figure 2 and realized that the tried and proven "HIGH LOAD condition decreased posterior upper arm muscle thickness following 6 weeks of bicep curl training" (Counts. 2016). Just like me Counts et al. are "not aware of any studies that investigated HIGH LOAD resistance training that targeted only the biceps and measured muscle size of both the biceps and triceps"; and in contrast to what I previously suggested, this cannot be a methodological artifice, because the ultrasound measures the scientists used could distinguish between muscle and fat. What exactly the reason for the ostensible 'atrophy' of the triceps muscle is, may thus still be called a 'mystery' - one that needs to be addressed in future studies, though... (thx Jeremy for spotting this mistake) | What do you think, any ideas on the mechanism? Comment on Facebook!

References:

• Counts, Brittany R., et al. "The acute and chronic effects of “NO LOAD” resistance training." Physiology & Behavior (2016).
• Rennie, Michael J., et al. "Control of the size of the human muscle mass." Annu. Rev. Physiol. 66 (2004): 799-828.

Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review

Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review

cheese dairy diet health healthy diet healthy eating lose fat

Cheeses come in all forms and colors.

Cheese is not exactly the first food that comes to mind when we think about "healthy eating". Rightly so? Today's overview of recent cheese studies tries to answer this question.

The article will, among other things, also address the claim that cheese was addictive (see red box) and / or that the consumption of a dairy product with a saturated fat content that is second only to that of butter would harm your cardiovascular and metabolic health.

So, where do we start? Netherlands? Well, even though the Dutch are famous for the many different types of cheese they produce and consume, they are probably not the ones who "invented" it. Rather than that it appears to be certain that the first cheeses were produced 5,000 BC - accidentally.

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Back in the day, humans had not invented pottery and thus stored their foods - including their milk - in animal stomachs, ... stomachs the cuagulating enzyme content of which turned milk into curd during storage (Fox. 1993). The first recorded "production" of cheese, in that case Gorgonzola dates back to the year 897, however (see Table 1).

Table 1: First Recorded Date for some Major Cheese Varieties (Fox. 1993).

Another cheesy fact about the Netherlands is that the Dutch would be the world's #1 cheese producer and consumer. Both is not the case! Rather than that, France holds both the title of the greatest producer (1.3 m tonnes) and consumer (22kg / per capita | Fox. 1993 // relative to their total dairy consumption, the Italians are the kings of cheese w/ up to 28% and 33%  of the dairy intake from cheese of women and men in the province Ragusa | Hjartåker. 2002). It is thus also France, where we will probably find the most significant evidence with regards to the health effects of cheese consumption. The most prominent study investigating this issue comes from the Aarhus University (Zheng. 2015)..

Is cheese the reason for the "French paradox"?

In said study, Zheng et al. used an NMR-based metabolomics approach "to investigate the differentiation between subjects consuming cheese or milk and to elucidate the potential link to an effect on blood cholesterol level" (Zheng. 2015). To this ends, the researchers recruited fifteen healthy young men for a full crossover study during which all subjects consumed three isocaloric diets with similar fat contents that were either (1) high in milk, (2) high in cheese or (3) contained only limited amounts of dairy for 14 days.

Only the fat "Norvegia" gouda has cholesterol-lowering effects in an 8 week RCT (Nilsen. 2015).

Question 1 - Does the type of cheese matter? High fat may matter. Well, "fake cheese" that's made from vegetable oils + tons of additives, as you will find it on most frozen Pizza from the supermarket is obviously not an option, but even among "real" cheeses there appear to be differences in terms of their individual health effects. The results of a 2015 study from Norway, for example, show that only fat gouda (80g/day), yet not fat- and salt-free Gamalost, a traditional form of Norwegian cheese will significantly reduce elevated cholesterol levels in non-medicated men and women over 18 years of age (Nilsen. 2015).

As the data from the scientists urine and feces analyses shows, the cheese diet significantly reduced the urinary citrate, creatine, and creatinine levels and significantly increased the microbiota-related metabolites butyrate, hippurate, and malonate compared to the milk diet. Overall, the study shows...

"[...] that cheese consumption is associated with an increased level of SCFAs in the gut, possibly induced by stimulation of beneficial gut microbiota, as well as an increased extent of lipid excretion with resultant beneficial effects on cholesterol metabolism"(Zheng. 2015 | my emphasis).

In conjunction with the significant reduction of the subjects' TMAO production [Trimethylamine N-oxide has been associated with increased CVD and even cancer risk] of which the authors rightly say that it could "also contribute to potential beneficial effects of cheese intake on the risk of CVD" (Zheng. 2015), the results of this controlled human trial are in stark contrast to the cheese = "high cholesterol" = "bad for your heart" myth that's still so prevalent:

"Overall, this metabolomics study suggests that cheese could be an important piece in the French paradox puzzle. However, further studies are needed to explore the exact metabolic mechanisms linking cheese consumption, stimulation of the gut microflora, and cholesterol metabolism" (Zheng. 2015 | my emphasis)

Just as many other researchers working in this area, Zheng et al. received support for their study from the dairy industry - a factor that is as prevalent in other areas of nutrition research, but interestingly most heavily criticized for dairy (Armstrong. 2005) and, obviously, artificial sweeteners.

Percentages of women reporting a craving for a given food at four different timepoints during their menstrual cycle (Rodin. 1991). 

Question 2 - Is cheese addictive? Prolly not! Even though the whole concept of food addiction is still contested (Rogers. 2000; Corwin. 2009; Albay-rak. 2012; Ziauddeen. 2012; Hebebrand. 2014), the Internet is full of "information" about the addictive nature of cheese. Claims that are not really backed up by science, as the data from Judith Rodin et al.'s study of the food cravings of women during different phases of the menstrual cycle in the Figure (left) shows (Rodin. 1991) - the real world does thus not confirm the relevance of the theor. addictive potential of casomorphines (Freye. 2004).

In general, rather than a role for individual molecules, the existing data appears to suggest "addictive", or rather hyperpalatable foods share common macronutrient compositions that distinguish a dairy queen chocolate ice cream cone with 34 g sugar 10 g fat and 160 mg sodium (+22 extra ingredients) per serving from roasted chicken breast or an apple (Gearhardt. 2011). This does not exclude that you can be "addicted" to cheese, but the same goes for carrots of which Kaplan reported 10 years ago that they got a 49-year-old woman addicted (Kaplan. 1996).

The reasons why I would argue that you can still put faith into the accuracy of the results Zheng et al. present in their paper are: (1) they openly declared the funding, i.e. support by The Danish Council for Strategic Research, Arla Foods, and the Danish Dairy Research Foundation in the project “FIAF - Milk in regulating lipid metabolism and overweight. Uncovering milk’s ability to increase expression and activity of fasting-induced adipose factor” (10-093539) and (2) the supporting evidence from various previous studies:

• Beneficial effect on CVD health - "The majority of prospective studies and meta-analyses examining the relationship between milk and dairy product consumption and risk of CVD show that milk and dairy products, excluding butter, are not associated with detrimental effects on CVD mortality or risk biomarkers that include serum LDL-cholesterol" (Lovegrove. 2016).
  

  

  Figure 1: Unlike 40 g dairy fat from butter, 40g of fat from matured cheddar cheese do not sign. affect the levels of total cholesterol and LDL in a 4 weeks cross-over study in healthy subjects (Nestel. 2005).

  With the latest evidence for this claim coming from an impartial source, namely Iran, where Sadeghi et al. found that higher cheese intakes are are associated with 19% reduced risk of metabolic syndrome and 13% reduced risk of suffering from (too) low HDL-C level, one may still doubt the objectivity of this claim being made at a conference about animal products, but can hardly argue that there was only potentially biased research to support Lovegrove's claim and the conclusions of the latest meta-analysis of its effects on blood lipids (de Goede. 2015):

  "Compared with butter intake, cheese intake (weighted mean difference: 145.0 g/d) reduced low-density lipoprotein cholesterol (LDL-C) by 6.5% (−0.22 mmol/l; 95%CI: −0.29 to −0.14) and high-density lipoprotein cholesterol (HDL-C) by 3.9% (−0.05 mmol/l; 95%CI: −0.09 to −0.02) but had no effect on triglycerides" (de Goede. 2015).

  In addition every regular gouda (and many other classic cheeses) contains peptides that have proven to have anti-hypertensive effects (Saito. 2000) and will thus lower the #1 risk factor for stroke and related cardiovascular problems - including death (Fagard. 2008).
• Reduced breast cancer risk -  A case-control study from the Netherlands suggests that each 60g increase in gouda intake will reduce the breast cancer risk of 25-64 year-old women (analysed according to age groups) with a 34% reduced risk of breast cancer.
  

  

  Figure 2 A high intake of gouda is associated with highly significant reductions in breast cancer risk even after adjusting for familial history, smoking,education, contraceptive use, age at menarche and first full-term pregnancy, parity, body mass index, and geographic area in Dutch women (van't Veer. 1989)

  What is also interesting about the effects plotted in Figure 2 is that a similar beneficial effect was not observed for milk (had no negative effect, either) or similarly low intakes of other fermented dairy (van't Veer).
• Anti-NAFLD and prometabolic effects - At least in comparison to a butter-fat based diet a similarly low fat (20%) likewise AIN76 (that's std. rodent chow) based diet with freeze-dried cheese powder significantly reduced the accumulation of triglyceride and cholesterol in the liver (P = 0.016 and P < 0.001, respectively) of rats who received the cheese or control diet in a 9-week study.
  

  

  Figure 2: Liver triglyceride (a) and total cholesterol (b) concentrations in rats fed control or cheese diet. Mean ± standard error. Asterisks indicate significant differences between groups (Higurashi. 2016)

  Just like the previously reported human studies, the rodent study als found significant increases in HDL and decreases in non-high-density lipoprotein (non-HDL) cholesterol, as well as elevated levels of metabolically healthy serum adiponectin concentration at week 9 in rats fed the cheese diet. To which degree this effect was due to or related to the increase in fat excretion in the feces will have to be determined in future studies. What appears to be clear, though, is that these "results suggest that cheese mediates various beneficial effects for preventing the development of metabolic syndrome by suppressing the accumulation of fat in the liver" (Higurashi. 2016).
• High nutritional value - Cheese is a low carbohydrate food that's packed with high concentration of essential amino acids saturated fats that could be good, not bad for your health (e.g. conjugated linoleic acid and sphingolipids present in cheese may have anti-carcinogenic properties, too), a lot of highly bioavailable calcium with beneficial effects on bone, teeth, blood pressure and weight loss (when combined with low-energy diets). Reason enough for researchers to state that "[c]heese is an important dairy product and an integral part of a healthful diet due to its substantial contribution to human health" (Walther. 2008).

Whether the average young, whites, female knows all the above or whether there's another reason that this part of US society consumes the highest amounts of cheese (Glanz. 1998) is something I cannot tell you. What I can tell you, though, is that the previously presented evidence suggests that weight concerns should not, as they still were in 1998 in the US (Glanz. 1998), be a reason for you not to consume cheese (in controlled amounts). Rather than that you should follow the example of the rich and intelligent of which a more recent study shows that they tend to consume the most cheese in Europe (Sanchez-Villegas. 2003).

A high cheese will also increase the level of the "good lipoproteins" HDL and apo A-I (Thorning. 2015a).

Bottom line: Don't get me wrong. The purpose of today's article is not to promote a "cheese only diet" or to tell you to consume at least X amounts of cheese per day. It is rather meant to critically evaluate the irrational fear that still characterizes the relationship of many health-conscious dieters to (esp. fatty) cheeses.

When consumed in moderation, cheese is not just a highly nutritious food, but can, as a lot of the more recent studies indicate, even have beneficial effects on your cardiovascular and metabolic health that are probably mediated by key nutrients and the beneficial effect cheese will have on your microbiome | Comment!

References:

• Albayrak, Ö., Sebastian Mathias Wölfle, and Johannes Hebebrand. "Does food addiction exist? A phenomenological discussion based on the psychiatric classification of substance-related disorders and addiction." Obesity facts 5.2 (2012): 165-179.
• Corwin, Rebecca L., and Patricia S. Grigson. "Symposium overview—food addiction: fact or fiction?." The Journal of nutrition 139.3 (2009): 617-619.
• de Goede, Janette, et al. "Effect of cheese consumption on blood lipids: a systematic review and meta-analysis of randomized controlled trials." Nutrition reviews 73.5 (2015): 259-275.
• Fagard, Robert H., et al. "Daytime and nighttime blood pressure as predictors of death and cause-specific cardiovascular events in hypertension." Hypertension 51.1 (2008): 55-61.
• Fox, P. F. "Cheese: an overview." Cheese: chemistry, physics and microbiology. Springer US, 1993. 1-36.
• Freye, Enno. "Exorphine (exogene Opioidpeptide) und β-Casomorphine." Opioide in der Medizin. Springer Berlin Heidelberg, 2004. 323-324.
• Gearhardt, Ashley N., et al. "Can food be addictive? Public health and policy implications." Addiction 106.7 (2011): 1208-1212.
• Glanz, Karen, et al. "Why Americans eat what they do: taste, nutrition, cost, convenience, and weight control concerns as influences on food consumption." Journal of the American Dietetic Association 98.10 (1998): 1118-1126.
• Hebebrand, Johannes, et al. "“Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior." Neuroscience & Biobehavioral Reviews 47 (2014): 295-306.
• Higurashi, Satoshi, et al. "Cheese consumption prevents fat accumulation in the liver and improves serum lipid parameters in rats fed a high-fat diet." Dairy Science & Technology (2016): 1-11.
• Hjartåker, A., et al. "Consumption of dairy products in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: data from 35955 24-hour dietary recalls in 10 European countries." Public health nutrition 5.6b (2002): 1259-1271.
• Lovegrove, Julie A., and Ditte A. Hobbs. "Plenary Lecture 2: Milk and dairy produce and CVD: new perspectives on dairy and cardiovascular health." Proceedings of the Nutrition Society (2016): 1-12.
• Nestel, P. J., A. Chronopulos, and M. Cehun. "Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects." European journal of clinical nutrition 59.9 (2005): 1059-1063.
• Nilsen, Rita, et al. "Effect of a high intake of cheese on cholesterol and metabolic syndrome: results of a randomized trial." Food & nutrition research 59 (2015).
• Rodin, Judith, et al. "Food cravings in relation to body mass index, restraint and estradiol levels: a repeated measures study in healthy women." Appetite 17.3 (1991): 177-185.
• Rogers, Peter J., and Hendrik J. Smit. "Food craving and food “addiction”: a critical review of the evidence from a biopsychosocial perspective." Pharmacology Biochemistry and Behavior 66.1 (2000): 3-14.
• Saito, T., et al. "Isolation and structural analysis of antihypertensive peptides that exist naturally in Gouda cheese." Journal of Dairy Science 83.7 (2000): 1434-1440.
• Sanchez-Villegas, A., et al. "A systematic review of socioeconomic differences in food habits in Europe: consumption of cheese and milk." European journal of clinical nutrition 57.8 (2003): 917-929.
• Thorning, Tanja K., et al. "Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial." The American journal of clinical nutrition 102.3 (2015): 573-581.
• Thorning, Tanja K., et al. "Cheddar Cheese Ripening Affects Plasma Nonesterified Fatty Acid and Serum Insulin Concentrations in Growing Pigs." The Journal of nutrition 145.7 (2015b): 1453-1458.
• van't Veer, Pieter, et al. "Consumption of fermented milk products and breast cancer: a case-control study in The Netherlands." Cancer research 49.14 (1989): 4020-4023.
• Zheng, Hong, et al. "Metabolomics investigation to shed light on cheese as a possible piece in the French paradox puzzle." Journal of agricultural and food chemistry 63.10 (2015): 2830-2839.
• Ziauddeen, Hisham, I. Sadaf Farooqi, and Paul C. Fletcher. "Food addiction: is there a baby in the bathwater?." Nature Reviews Neuroscience 13.7 (2012): 514.

Taurine Boosts Good Gut Bacteria & Short-Chain Fatty Acid Prod. | 1st Study to Show Natural Beats Synthetic Taurine

Taurine Boosts Good Gut Bacteria & Short-Chain Fatty Acid Prod. | 1st Study to Show Natural Beats Synthetic Taurine

bacteria bacteriodetes bad bacteria firmicutes good bacteria health helicobacter microbiome natural taurine SCFA short-chain fatty acids synthetic taurine synthetic vitamins taurine

The bacteria in our guts are the latest rage in medical sciences... and taurine, especially natural taurine, may be a way to modulate them in beneficial ways.

It has been some time since the last taurine article on the SuppVersity (read all articles). There was simply a lack of interesting studies... until now, or rather until the latest study of scientists from the Zhejiang University of Technology which suggests that taurine "might be of benefit to health by inhibiting the growth of harmful bacteria, accelerating the production of SCFA and reducing LPS concentration" (Yu. 2016).

As the authors of the paper point out, taurine is a necessary amino acid that taurine plays an important role in the regulation of neuroendocrine functions and nutrition.

In previous studies, taurine was shown to improve immunity, resist oxidation, delay senility, reduce blood pressure, promote recovery from acute hepatitis, etc. (Averin. 2015; Wang. 2013; De Luca. 2015; Ito. 2012). In addition, taurine can also improve the metabolism of the nutrients and play an important role in the regulation of neuroendocrine (Cuttitta et al. 2013; Camargo et al. 2015).

You can learn more about taurine & other amino acids at the SuppVersity

Taurine Pumps Up Strength & Recovery?

Taurine Improves Insulin + Glucose Metabolism

Taurine ➲ 180% Testosterone Increase

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43% Reduced Performance W/ BCAAs

3g Taurine Boost Glycogen Re-synthesis Sign.

With their latest study, the Chinese scientists Haining Yu, Zhengzhao Guo, Shengrong Shen , an Weiguang Shan were now able to add yet another beneficial health effect of taurine to the previous, impressive list: taurine's effect on gut microbes and metabolism.

Food	Amount	Taurine (mg)
Cheese	3 ounces	1000
Cheese,cottage	1 cup	1700
Milk,whole	1 cup	400
Yogurt	1 cup	400
Wild game	3 ounces	600
Pork	3 ounces	540
Granola	1 cup	650
Oatmeal flakes	1 cup	500
Chocolate	1 cup	400
Meat (luncheon)	1 cup	390
Wheat germ,toasted	1/4 cup	350
Egg	1 (medium size)	350
Turkey	3 ounces	240
Duck	3 ounces	240
Chicken	3 ounces	185
Sausage	3 ounces	185
Avocado	1/2 (medium)	75
Table 1: It doesn't always have to be supplements - Taurine content of selected foods (USDA Handbook #8)

As you'd expect it for a "first of its kind" study, the researchers used a rodent model to evaluate the effects of a human equivalent dose of ~1g of taurine in BALB/C who were randomly divided into three experimental groups:

• the first group was administered saline (CK),
• the second group was administered 165 mg/kg natural taurine (NE) and
• the third group one administered 165 mg/kg synthetic taurine (CS).

With the NE and CS group, this is also one of the few studies to distinguish between "natural" and "synthetic" taurine, which is obtained from isethionic acid (2-hydroxyethanesulfonic acid) and not extracted from animal bile, usually that of the ox, and subjected to a series of purification procedures by several different methods (Gioacchini. 1995).

Figure 1: Effects of taurine on gut bacteria abundance (Yu. 2016).

To assess the effects, the gut microbiota composition in mice feces was analyzed by metagenomics technology, and the content of short-chain fatty acids (SCFA) in mice feces was detected by gas chromatography (GC), while the concentrations of lipopolysaccharide (LPS) and superoxide dismutase (SOD) were detected by a LPS ELISA kit and a SOD assay kit, respectively.

Studies Confirm: Natural and Synthetic Vitamins Can Differ in Quantity & Quality of Effects! Vitamins A-E, B's & More | read more

Is "natural taurine" the "better taurine"? In the study at hand, it seems as if this was the case. The only evidence from other studies that suggests that the source of taurine matters, however, is 1995 paper by Gioacchini et al. who developed a method to distinguish the two and may thus have a vested interest in stating that "[n]atural taurine is an essential constituent of formula milk for infants and, because of the inferior nutritional value (δ), of synthetic forms, it is important to discriminate between these and taurines derived from a natural source" (Gioacchini. 1995). Another study shows that the allergy risk for synthetic taurine appears to be elevated (Lee. 2013).

Why this is the case or what triggers any differences in the effect on the microbiome is something I cannot tell you: if the molecules were structurally different, Gioacchini et al. would after all not have had to use the 13C/12C ratio that is also used to date bones and other relicts. It could eventually be solely a question of dosage - with "inferior nutritional value" the synthetic taurine may have to be dosed much higher... as high as in most previously published human studies which generated the most impressive results with 3-6g and thus 3-6x more taurine per day than the human equivalent dose (learn more about the HED concept) of the study at hand.

As the data in Figure 1 indicates, taurine had profound effects on gut microbiota could reduce the abundance of Proteobacteria, especially Helicobacter (see Figure 1, bottom right). In that, it is interesting to see that the natural taurine ...

• had more pronounced beneficial effects on the count of good bacteroidetes and was more potent than the synthetic version when it comes to reducing proteobacteria and helicobacter, and even more intriguingly
• had opposite effects on firmicutes which make up the largest portion of the mouse and human gut microbiome, can't be described as "beneficial" or "bad" as a whole, but have been shown to be involved in energy resorption and obesity

In line with the last-mentioned increase in firmicutes is the scientists' observation that the SCFA content was increased in feces of the NE group, but not the CS group that received the synthetic taurine supplement.

Figure 2: Short-chain fatty acid (SCFA) and Activity of superoxide dismutase (SOD) levels in response to natural (NE), synthetic taurine (CS) and saline control (CK) supplementation in mice (Yu. 2016).

That's interesting, also because this change went hand in hand with a 'natural exclusive' LPS content was decreased, but similar increases in the activity of the antioxidant SOD enzyme in serum and livers of the both taurine groups.

None of the previous taurine studies declared whether the chemical they used was "natural" or "synthetic", I thus suspect that a synthetic version was used in most if not all of them - that this could make a difference is still both surprising and intriguing.

Bottom line: While it is correct that both "natural taurine and the synthetic taurine could regulate the gut micro-ecology, which might be of benefit to health by inhibiting the growth of harmful bacteria" (Yu. 2016), it is quite intriguing that only the natural taurine accelerated the production of SCFA and reducing LPS concentration, while the synthetic taurine did not.

Unfortunately, I have no studies to tell you if there's (a) a general advantage of natural over synthetic taurine (see red box, too), or (b) whether your taurine is natural or synthetic. If the previous quote (see red box) from Gioacchini et al. is accurate, though, it would appear that (a) 'natural' was superior and that (b) your taurine supplement was almost certainly nor extracted from ox-bile or another expensive natural source | Comment on Facebook!

References:

• De Luca, Annamaria, Sabata Pierno, and Diana Conte Camerino. "Taurine: the appeal of a safe amino acid for skeletal muscle disorders." Journal of translational medicine 13.1 (2015): 1.
• Gioacchini, Anna Maria, et al. "Differentiation between natural and synthetic taurine using the 13C/12C isotope ratio." Rapid communications in mass spectrometry 9.12 (1995): 1106-1108.
• Ito, Takashi, Stephen W. Schaffer, and Junichi Azuma. "The potential usefulness of taurine on diabetes mellitus and its complications." Amino acids 42.5 (2012): 1529-1539.
• Lee, Seung-Eun, et al. "A case of taurine-containing drink induced anaphylaxis." Asia Pacific Allergy 3.1 (2013): 70.
• Yu, Haining, et al. "Effects of taurine on gut microbiota and metabolism in mice." Amino acids (2016): 1-17.