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.

Read more short news at the SuppVersity to learn more about training & nutrition.

LLLT Can Almost Double Your Gains in 8 Weeks

LLLT Doubles Fat Loss, Improves Insulin Sens.

Weight Loss Supplements Exposed

Exercise Supplementation Quickie

Exercise Research Uptake Jan 12, 2015

Read the Latest Ex. Science Update

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.

You can learn more about the zero-calorie sweet stuff at the SuppVersity

Aspartame & Your Microbiome - Not a Problem?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Chronic Sweeten-er Intake Won't Effect Microbiome

Stevia, the Healthy Sweetener?

Sweeteners In- crease Sweet- ness Threshold

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.

Creatine Uptake, Bioavailability, and Efficacy - We've Gotten it all Wrong and Low Serum Creatine Levels are Better!?

Creatine Uptake, Bioavailability, and Efficacy - We've Gotten it all Wrong and Low Serum Creatine Levels are Better!?

bioavailability build muscle build strength creatine performance strength supplementation supplements

If you put some faith into the marketing campaigns of supp producers, there's a creatine for everyone: one to get lean, one to get strong and one to get big and buffed... bullocks!

It has been a while since I've discussed the bioavailability of different forms of creatine. On various supplement sites, the notion that there was one form of creatine that was significantly more bioavailable and would thus allow you to 'load' muscle phosphocreatine (PCr) faster and more efficiently is obviously still a matter of constant debate... a debate of which the latest study by Ralf Jäger et al. (2016) indicates that it may argue based on a fundamentally flawed premise, i.e. that higher serum levels of creatine after the ingestion of a given product would signify an increased efficacy in terms of performance / strength / size gains.

How come? Well, the previously mentioned, as of yet unpublished data from a study by Ralf Jäger, Martin Purpura, and Roger C Harris did not just confirm the results of previous studies, which indicate that glucose (75g) and alpha lipoic acid (ALA | 200mg) will increase the bioavailability of creatine, i.e. "the proportion of a drug or other substance [in this case creatine] that enters the circulation when introduced into the body" (Merriam-Webster.com), it also indicates that the practically relevant predictor of creatine's efficacy is - assuming equal dosing and complete absorption - not a high, but rather a low level of creatine in the blood.

You can learn more about creatine at the SuppVersity

Creatine Doubles 'Ur GainZ!

Creatine Loading = Unnecessary

Creatine Pre or After Workouts?

1st Benefits of Creatine-HCL

Creatine Blunts Fat Loss?

Build 'Ur Own Buffered Creatine

What? Let me explain: Initially, it may be worth pointing out that we are talking about a small scale study the results of which have not yet been published in the peer-reviewed journal. In that study, Jäger et al. aimed to compare the effects of ingesting tricreatine citrate (5g, TCrC),

• in combination with 75g of glucose and 200mg of alpha-lipoic acid, or
• without the former bioavailability enhancers.

on only six subjects. These three men and three women (35.5+/-14.5 yrs, 172.5+/-12.2 cm, 75.3+/-9.0 kg), who were all healthy, normal-weight and non-vegetarian and thus not, with creatine being a deficiency nutrient in vegetarians, extraordinarily susceptible to creatine supplementation (Burke. 2003), participated in two testing sessions during which they received the previously explained two treatments (the powdered supplements were simply dissolved in 450 ml of water).

Adding carbohydrates or cinnamon to creatine may well increase its uptake to the muscle. What it does not do, however, is to enhance creatine's efficacy - at least not in a 2015 3-week creatine loading study Islam et al. conducted in 25 recreational gymrats.

What's the increased absorption worth? If we rely on a a recent study by Islam, et al. (2015) the answer is (unfortunately) nothing. In their 2015 study, the scientists from the Wilfrid Laurier University and the University of Lethbridge in Canada found no (=zero) significant differences in anaerobic power, strength, and endurance when creatine was administered solo, with the same 70 g carbohydrate (CHO) that were used in Jäger et al. (2016), or 500 mg cinnamon extract (CIN), of which the authors believed that its proven ability to improve insulin sensitivity and up-regulate glucose transport in skeletal muscle would likewise enhance the uptake of creatine in the muscle and thus make it more effective.

With their cross-over after the initial test and a 7 day break between the tests, the scientists would have been able to compare the effect of adding glucose and alpha lipoic acid to the tricreatine citrate (Creapure™ Citrate, AlzChem, Trostberg, Germany | 65% w/w creatine) on an individual level. Corresponding data, however, is not (yet?) available. Instead, we get the likewise interesting statistical averages (see Figure 1):

Figure 1: Mean plasma creatine concentration over 8 hours following ingestion of 5g tricreatine citrate (TCrC) and 5g tricreatine citrate + 75g glucose + 200mg alpha-lipoic acid (TCrC+Glu+ALA | Jäger. 2016).

And these data present a quite intriguing result. More specifically, they indicate that the increase in peak concentration and the area under the curve (indicative of the total amount of creatine that appeared in the blood of the subjects) were significantly lower in the TCrC+Glu+ALA group in comparison to TCrC (75.3%, p<0.05, and 82.2% respectively).

Less creatine in the blood with sugar + ALA? That's bad, right? No that's good!

Just as the likewise lower 0.5 and 1h plasma concentrations of creatine, in the TCrC+Glu+ALA group (in comparison to TCrC), these reductions do not indicate a reduced efficacy of the supplement. On the contrary! The significantly elevated mean 8h urinary creatine elimination in the control group (TCrC | 26.5 ± 13.9% of the dose administered  vs. 17.2 ± 13.0% for TCrC+Glu+Ala) rather indicates that the addition of glucose and ALA "enhanced rate of creatine uptake into the muscle" - as previous studies indicate probably due to the presence of raised insulin (by glucose) and / or an increased insulin sensitivity (by ALA / Koszalka. 1972; Steenge. 1998; Pittas. 2010).

Figure 2: The study on creatine + glucose and creatine + cinammon by Islam et al. (red box) is not the only one that shows that the increased deposition of creatine in the muscle doesn't give you athletic advantages. The exact same results have been observed in an 8-week study comparing 70 g of a dextrose placebo (PL), 5 g creatine/70 g of dextrose (CRD) or 3.5 g creatine/900 mg fenugreek extract (CRF) by Taylor et al. (2011)

Why's this study relevant? Well, the answer should be obvious. The few allegedly 'advanced creatine products' on the market that actually have scientific back-up of their efficacy often refer to studies showing increases in plasma creatine of which the study at hand shows that they are no valid predictor of the actual efficacy of the supplement. The latter obviously depends on muscle creatine uptake, not serum peak levels or AUC. Don't be a fool, though: This does not mean that lower serum levels after ingestion were automatically better. After all, those lower levels of creatine in the blood may well be a mere result of an impaired / incomplete absorption in the gut.

Confusing? Well, let's summarize: By measuring the creatine level in the blood and the excretion of creatine in urine, Jäger et al. were able to refute the (ostensibly) logical assumption that higher serum creatine levels would indicate an improved efficacy. What they did not prove conclusively, however, is that the creatine levels in the muscle were in fact significantly higher (no biopsies) and, most importantly, that this makes a performance difference. The latter has after all been refuted in previous studies, such as Islam et al. (2015 | see red box and Figure 2). The hunt for the "best form" of creatine will thus probably go on, albeit with different experimental means, i.e. either the measurement of serum and urinary creatine as it was done in the study at hand or (even better) the direct assessment of muscle creatine stores and the actual performance benefits | Comment!

References:

• Burke, Darren G., et al. "Effect of creatine and weight training on muscle creatine and performance in vegetarians." Medicine and science in sports and exercise 35.11 (2003): 1946-1955.
• Jäger, Ralf, Martin Purpura and Roger C Harris. "Reduction of Plasma Creatine Concentrations as an Indicator of Improved Bioavailability." Upublished data from privatt conversation (2016).
• Koszalka, Thomas R., and Carole L. Andrew. "Effect of insulin on the uptake of creatine-1-14C by skeletal muscle in normal and X-irradiated rats." Experimental Biology and Medicine 139.4 (1972): 1265-1271.
• Pittas, G., et al. "Optimization of insulin-mediated creatine retention during creatine feeding in humans." Journal of sports sciences 28.1 (2010): 67-74.
• Steenge, G. R., et al. "Stimulatory effect of insulin on creatine accumulation in human skeletal muscle." American Journal of Physiology-Endocrinology And Metabolism 275.6 (1998): E974-E979.
• Taylor, Lem, et al. "Effects of combined creatine plus fenugreek extract vs. creatine plus carbohydrate supplementation on resistance training adaptations." Journal of sports science & medicine 10.2 (2011): 254.

Training in Line W/ Your Genetic Potential Can Boost Your Performance Gains More Than 600%, DNAFit™ Studies Say

Training in Line W/ Your Genetic Potential Can Boost Your Performance Gains More Than 600%, DNAFit™ Studies Say

athletes build muscle elite athletes gains gainz genes genetics performance training programming training programs training protocol

While the study at hand appears to confirm that the DNAFit test can tell you if you're an endurance or strength athlete, it won't help you achieve goals you were not "made for" - it eventually you may thus have to give up your dream of being the fastest, strongest or most chiseled guy / gal on the track, field or in gym.

You probably know that: There's that guy at the gym who has been training only half as long as you and still made twice the gains, ... must be juicing that idiot, right? Well, even if we assume that you're not one of the >50% of trainees who overtrain (and undereat) that's by no means the most likely explanation for the astonishing discrepancies.

A recent study that was conducted by a consortium of European researchers is now the first to impressively demonstrate that "matching the individual’s genotype with the appropriate training modality leads to more effective resistance training" (Jones. 2016) What the scientists some of whom work for a company that offers corresponding DNA tests won't tell you, though is that their test will eventually just help you to select the right sport, not to excel in the one sport you have already chosen.

Learn more about workouts, supplements, diet and more at the SuppVersity

Vitargo, Red Bull, Creatine...

Pump Supps & Synephrine...

High Protein, Body Comp...

Keto Diet Re- search Update

The Misquantified Self & More...

BCAA, Cholos-trum, Probiotics...

Eventually, none of this should surprise you, though. Scientists and practitioners alike have suspected for centuries and known for decades that elite athletes are born, not formed in the gym. Association studies have identified dozens of genetic variants linked to training responses and sport-related traits (Table 1 provides a glimpse at the peak of a hitherto largely unknown iceberg of genetic variants that will influence your adaptation to specific training types).

Table 1: List of known genetic variants that influence your adaptation to specific (resistance) training stimuli that were analyzed with the patented DNAFit Peak Performance Algorithm™ in the study at hand (Jones. 2016).

Yes, the way and consistence with which you train will obviously have an effect on the way your physique, strength, speed, conditioning, etc. develops, but when all is said and done, you are simply lucky if you're not lapped by somebody who has trained just as intense- and persistenly who was gifted with a more appropriate gene set for the sports you love. It is thus no wonder that scientists have been pondering about ways to (a) select the right candidates for the right sports and (b) personalizing athletes' training based on their genetic profiles.

In the previously cited study, Jones et al. proposed to do just that by the means of an algorithm that would allow athletes to achieve "greater results in response to high- or low-intensity resistance training programs by predicting athlete's potential for the development of power and endurance qualities" (Jones. 2016).The DNAFit algorithm which is designed to predict the response to high- or low-intensity resistance training programs invokes the 15 performance-associated gene polymorphisms from Table 1.

Figure 1: Both studies used the same randomized, double-blinded crossover design (based on Jones. 2016).

To validate it, its designers from DNA Sports Performance Ltd. and scientists from the University of Central Lancashire, the Universitat Pompeu Fabra and the Parc Científic i Tecnològic Agroalimentari de LleidaPCiTAL performed two studies in independent cohorts of male athletes using in ...

• study 1: athletes from different sports (n=28) / 55 Caucasian male University athletes, all aged 18-20 years, volunteered for the study, and 28 of them (height 180.7 ± 1.5 cm, weight 77.0 ± 2.1 kg) successfully completed it (27 athletes had not completed all aspects of the study due to either injury or illness); each participant was a member of first or second team, actively competing in British Universities and Colleges Sports (BUCS) leagues. The athletes competed in squash (n = 1), swimming (n = 7), running (n = 1), ski/snowboard (n = 4), soccer (n = 1), lacrosse (n = 2), badminton (n = 1), motorsport (n = 1), cycling (n = 4), cricket (n = 2), volleyball (n = 1), fencing (n = 1) and rugby union (n = 2). and 
• study 2: soccer players (n=39) / 68 male soccer players, all aged 16-19 years, volunteered to participate in the study, and 39 of them (height 176.1 ± 1.0 cm, weight 68.9 ± 1.5 kg) successfully completed it (29 participants were withdrawn from the study due to non-adherence of set training volumes over the 8 weeks, or injury); each subject was a member of college soccer academy who actively competed in British Universities & Colleges Sport (BUCS) league.

In both studies athletes completed an eight-week high- or low-intensity resistance training program, which either matched or mismatched their individual genotype. In that, participants of both studies were initially randomly allocated to an eight-week high- or low-intensity resistance-training program, after undergoing performance tests for both explosive power and endurance. After another set of performance tests, they then transitioned to the respective other 8-week intervention, the results of which were then compared with the previous ones and correlated with the subjects gene types.

No, the muscle or strength gains were not assessed: I am not sure why the scientists decided against measuring the lean / fat mass gains / losses. After all, their gene set included the thyrotropin-releasing hormone (TRH) receptor gene where polymorphisms at rs16892496 A/C that influences the secretion of thyroid-stimulating hormone (TSH) and prolactin (PRL) and has been found to modulate the amount of lean mass by Liu et al. in 2009. My best bets are that the reasons are financial ones (DXA is expensive, everything else inaccurate)strategic ones, with 8-weeks of training being unlikely to produce sufficiently inter-group differences in already trained athletes, given the small sample size(s) and range of sports that were included (esp. in study 1), or a mere consequence of the choice of protocols, which did not include a hypertrophy protocol (thus no measurement of muscle gains) and/or would obviously produce greater strength gains with the high intensity protocol (measuring those would thus be useless, too).

As the authors point out, "[t]he study was double blinded, in that all were unaware of their ‘genetic potential status’, as determined by the DNAFit Peak Performance Algorithm™" (Jones. 2016). Since this also included the lead investigator who coached the participants during the 8 weeks of resistance training, the notion that 'this is the optimal training type for me / my trainee' should not have influenced the study outcomes.

Figure 2: Intergroup comparisons of CMJ increases (%) in response to high- or low-intensity training; the %-ages over the bars indicate the difference to the mean effect (all) - It's easy to see that training 'according to your genotype' makes a 40-80% difference even if you compare the speficic to the average success; >100% for inter-group comparisons (Jones. 2016)

And still, as the data from the explosive power and aerobic fitness tests that involved countermovement jumps (CMJ) and an aerobic 3-min cycle test (Aero3) revelead, training 'according' to your genes (or rather the assessment of the DNAFit test), i.e.

• high-intensity trained with power genotype or 
• low-intensity trained with endurance genotype,

significantly increased results in CMJ (P=0.0005) and Aero3 (P=0.0004). Athletes from the mismatched group (i.e. high-intensity trained with endurance genotype or low intensity trained with power genotype), however, demonstrated non-significant improvements in CMJ (P=0.175) and less prominent results in Aero3 (P=0.0134).

Figure 3: Inter-group comparisons of Aero3 increases (%) in response to high- or low-intensity training; left axes = power and endurance genes groups, right axes = all subjects (data from both cohorts | Jones. 2016).

Similar results were observed in the 2nd study, where  soccer players from the matched groups saw significantly greater (P<0.0001) performance changes in both tests compared to the mismatched group. In that, the following facts are particularly noteworthy:

• the advantage of training 'according to your genotype' ranges from ~40% to ~80% even if you compare it to the average training response (Figure 1, "all");
• comparing training according to training in discordance with your genotype(s) yields differences that range from 55% up to 610% (the latter in the soccer players on the low intensity regimen for CMJ; Figure 1, study 2 / low intensity)

What is maybe even more important than the statistically significant differences in the mean gains is the consistency of failure, i.e. the fact that Among non- or low responders of both studies, 82% of athletes (both for CMJ and Aero3) were from the mismatched group (P<0.0001).

Remember? Your Post-Workout Testosterone Levels Can Predict Your Gains - Study Takes Novel Approach to the T ↔ Muscle Link | Learn more

Bottom line: As the (maybe biased) authors of the study point out, their well-designed and appropriately blinded trial clearly "indicate[s] that matching the individual’s genotype with the appropriate training modality [as determined with 'their' proprietary DNAFit test] leads to more effective resistance training" (Jones. 2016). It does therefore stand to reason that "[t]he developed algorithm may be used to guide individualised resistance-training interventions" (Jones. 2016). Whether that's actually useful for the average gymrat, whose goal may diverge sign. from what he was 'born to achieve', though, is another story... at least until you'll be able to home-brew / -tweak your genes with CRISPER ;-)

Another thing we shouldn't forget is that getting big and buffed, the goal of a majority of male gymgoers, wasn't even investigated in the study at hand... I bet, though, that future studies with different training regimen and study populations (e.g. untrained individuals) will assess and probably find similar results for muscle and strength gains - And you know where you will be able to read about their results, right? | Comment on Facebook!

References:

• Jones, N., et al. "A genetic-based algorithm for personalized resistance training." Biol Sport 33.2 (2016): 117-126.
• Liu, Xiao-Gang, et al. "Genome-wide association and replication studies identified TRHR as an important gene for lean body mass." The American Journal of Human Genetics 84.3 (2009): 418-423.

The Bitter Taste that Gets You Going: Quinine Mouthrinse Provides Instant 4% Power Boost During 30s All-Out Sprint

The Bitter Taste that Gets You Going: Quinine Mouthrinse Provides Instant 4% Power Boost During 30s All-Out Sprint

ergogenic mean power mouthrinse peak power performance power powerlifting quinine sprinting sprints

Getting ready for an all-out sprint? A bitter mouth rinse W/ quinine will provide instant power boost of 4% in ‘ur 30s cycle sprint more than a sweet mouth rinse could do .

If you're a powerlifter, the idea that rinsing your mouth with a bitter substance can improve your performance is probably no news for you... even though, powerlifters smell, not taste ammonia, smelling and tasting are, after all, more or less two sides of the same coin (Rozin. 1982).

Against that background and in view of the similar brain activation patterns scientists have observed in response to bitter and sweet taste perception, it appears only logical for Sharon Gam et al. to speculate in a 2014 paper, which is still worth its own SuppVersity article (!), that rinsing w/ quinine, a distinctly bitter substance, could produce the same or at least similar power increments as sweet substances.

For longer sprints bicarbonate may be the more effective choice

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

Creatine + BA = Perfect Match

Bicarb Buffers Creatine

Instant 14% HIIT Boost

Of the latter, previous research has shown that they will elevate both peak power (+22.1 ± 19.5 W; ES, 0.81; p = 0.0667) and mean power (+39.1 ± 26.9 W; ES, 1.08; p = 0.0205 | Beaven, et al. 2013), during all out sprints. The goal of the researchers from the University of Western Australia was thus to elucidate, "whether combining mouth rinsing with the ingestion of a bitter-tasting solution composed of quinine acutely improves mean and peak power during a 30-s maximal cycling sprint effort" (Gam. 2016) would yield similar benefits.

To be able to tell how similar sweet and bitter taste effects on sprinting performance actually are, they scientists compared the effects of 0.36 mL/kg body mass of a 2-mM quinine HCl solution (QUI; Sigma-Aldrich), not just to plain water and a no rinse control (CON), but also to a 0.05% w/v aspartame solution (ASP; Sigma-Aldrich), all of which were used immediately before the 30s all-out sprint on an Exertech EX-10 front access cycle ergometer.

Figure 1: My graphical "illustration" of the study design (based on facts from Gam. 2014).

As the authors explain, the "volume of 0.36 mL/kg was chosen to account for differences in body size, with each participant receiving approximately 25–35 mL of solution per session" (Gam. 2014) and the "[p]articipants were instructed to rinse their mouth for 10 s and then ingest the solution", a practice that was prescribed to ensure "that bitter receptors at the back of the tongue were activated because there is evidence that the strongest sensation of bitterness occurs in that area of the oral cavity" (Gam. 2014).

Bitter perception (Mennella. 2013).

Have you ever asked yourself how "bitter works"? Here is the answer from a 2013 paper by Mennella, et al. → "The generation of bitter taste starts when a bitter compound enters the oral cavity, where the ligand binds to a T2R G-protein coupled receptor expressed in the apical membrane of receptor cells found in taste buds, triggering a cascade of signaling events, leading to the release of neurotransmitter that activates an afferent nerve fiber that transmits the signal via the cranial nerve to the brain. Taste buds are distributed in distinct fields in the oral, pharyngeal, and laryngeal epithelia, with each field innervated by a different cranial nerve branch. Only the taste buds on the tongue are depicted in the figure."

As you can see in the selected performance markers I've plotted for you in Figure 2, the fourteen competitive male cyclists, who performed a 30-s maximal cycling sprint immediately after rinsing their mouth for 10 s and then ingesting the aforementioned solutions (QUI, water, ASP, CON), experienced significant increases in both mean power output by 2.4%–3.9% [P < 0.021, effect size (ES) = 0.81–0.85] and peak power output in the quinine condition.

Figure 2: Relative changes in mean & peak power (%) + effects sizes for quinine vs. CON, WAT or ASP (Gam. 2014).

For the latter, it is yet important to point out that a significant performance enhancement in terms of the peak power output was recorded only in comparison to the water (3.7%, P = 0.013, ES = 0.71) and the control (3.5% P = 0.021, ES = 0.84) conditions, yet not compared to the aspartame condition (1.9%, P = 0.114, ES = 0.47), in which the scientists observed a non-significant increase in performance compared to the water and control trial. Differences in heart rate, perceived exertion, or blood variables between any of the conditions were not observed.

Bitter taste increases ghrelin, ghrelin rapidly increases noradrenaline and adrenaline - if that's what explains the effects of quinine will yet have to be elucided in future studies.

So what's the mechanism, here? Unfortunately, the researchers don't speculate about the mechanism behind this, for sprinters and power athletes highly relevant effect of quinine (or other bitter tastants). My brief research of the existing research on bitter taste receptors, however, suggests various possible mechanisms with the release of ghrelin in response to bitter taste sensing (Janssen. 2011) and its effects on gluconeogenesis, noradrenaline and adrenaline (Enomoto. 2003 | see Figure on the right) being a candidate that would usually have us expect to see more pronounced increases in heart rate than they were observed in the study at hand, where quinine raised the heart rate only in the absence of exercise (by ~3-4 bpm).

It is thus questionable, whether the ghrelin => (nor-)adrenaline hypothesis provides the correct explanation - not just, but also because previous research suggests that the benefits of rinsing your mouth with bitter substances before sprinting may have the same origin as those that occur in response to carbohydrate mouth-rinsing, the triggers of which are likewise believed to "reside in the central nervous system" (Jeukendrup. 2010) and thus to be of non-metabolic origin.

Since the quinine solution was also swallowed, effects that were triggered by bitter taste receptors (ghrelin remains the most likely candidate) in endocrine cells along the gut (figure from Depoortere. 2014) could also explain the performance increases.

Speaking of carbohydrate / sweet mouth rinses, it should be mentioned that the lack of significant performance differences (1.9%, P = 0.114, ES = 0.47) between the aspartame and the quinine trial in the study at hand appears to suggest that sweet and bitter mouth rinses work by the same, still to be elucidated mechanism (it should be said, though that structural analogues of aspartame have been found to active the bitter taste receptor, as well | Benedetti. 1995).

In view of the fact that this hypothesis is, as Gam et al. point out, in line with the results of "studies based on functional magnetic resonance imaging [, which] have shown that the brain areas activated in response to the bitter tastant, quinine, overlap to a great extent" with those brain areas that are stimulated when you rinse with CHOs / sweet solutions (Zald. 2002; Small. 2003), finding mechanistic explanations for one of these performance enhancer (e.g. the sweet mouthrinse) may also yield explanations for the performance enhancing effects of the other one. Whether that's the actual reason for the preformance increases does yet appear questionable. After all, a 2015 follow up study by the same researchers showed that that mouth rinsing with the same bitter quinine solution without ingesting it won't improve young athletes' sprint cycling performance (Gam. 2015) - in view of the presence of ghrelin producing cells in the digestive tract (see Figure in this bottom line), this does not falsify the "ghrelin" => (nor-)adrenaline hypothesis, which would also be in line with the increases in corticomotor excitability Gam et al. observed in yet another follow up study in male competitive cyclists (Gam. 2015b), in which the quinine was ingested, too | Comment!

References:

• Beaven, C. Martyn, et al. "Effects of caffeine and carbohydrate mouth rinses on repeated sprint performance." Applied Physiology, Nutrition, and Metabolism 38.6 (2013): 633-637.
• Benedetti, Ettore, et al. "Sweet and bitter taste: Structure and conformations of two aspartame dipeptide analogues." Journal of Peptide Science 1.6 (1995): 349-359.
• Depoortere, Inge. "Taste receptors of the gut: emerging roles in health and disease." Gut 63.1 (2014): 179-190.
• Enomoto, Mitsunobu, et al. "Cardiovascular and hormonal effects of subcutaneous administration of ghrelin, a novel growth hormone-releasing peptide, in healthy humans." Clinical Science 105.4 (2003): 431-435.
• Gam, Sharon, Kym J. Guelfi, and Paul A. Fournier. "Mouth rinsing and ingesting a bitter solution improves sprint cycling performance." Medicine and science in sports and exercise 46.8 (2014): 1648-1657.
• Gam, Sharon, et al. "Mouth rinsing with a bitter solution without ingestion does not improve sprint cycling performance." European journal of applied physiology 115.1 (2015a): 129-138.
• Gam, Sharon, et al. "Mouth rinsing and ingestion of a bitter-tasting solution increases corticomotor excitability in male competitive cyclists." European journal of applied physiology 115.10 (2015b): 2199-2204.
• Janssen, Sara, et al. "Bitter taste receptors and α-gustducin regulate the secretion of ghrelin with functional effects on food intake and gastric emptying." Proceedings of the National Academy of Sciences 108.5 (2011): 2094-2099.
• Jeukendrup, Asker E., and Edward S. Chambers. "Oral carbohydrate sensing and exercise performance." Current Opinion in Clinical Nutrition & Metabolic Care 13.4 (2010): 447-451.
• Rozin, Paul. "“Taste-smell confusions” and the duality of the olfactory sense." Attention, Perception, & Psychophysics 31.4 (1982): 397-401.
• Small, Dana M., et al. "Dissociation of neural representation of intensity and affective valuation in human gustation." Neuron 39.4 (2003): 701-711.
• Zald, David H., Mathew C. Hagen, and José V. Pardo. "Neural correlates of tasting concentrated quinine and sugar solutions." Journal of Neurophysiology 87.2 (2002): 1068-1075.