Tribulus is Good for Something: 1.25 g/day Modulate IGF-1 Availability and Alleviate Muscle Damage While Promoting Anaerobic Performance of Intensely Trained Male Boxers

Tribulus is Good for Something: 1.25 g/day Modulate IGF-1 Availability and Alleviate Muscle Damage While Promoting Anaerobic Performance of Intensely Trained Male Boxers

athletes boxers IGF-1 IGF1 IGFBP-3 performance saponins testosterone booster tribulus tribulus terrestris

Tribulus terrestris extracts - While the boxing gloved protect a boxers fists from damage, the TT extracts may protect his muscle. Recent study yields surprising results and insights into the performance enhancing effects of TT and why it may have failed to work in previous studies.

Yes, it's (a) not a rodent study, (b) published in a peer-reviewed journal, (c) not sponsored by a supplement company (but the Chinese government), and was (d) conducted not just with untrained and mostly sedentary or "recreational trained" human beings, but even with fifteen highly trained male boxers (national second-level athletes, 2–3 years of training) who were recruited from the boxing team of Shanghai University of Sport Affiliated School of Sports in China. This alone makes the latest study from the Shanghai University of Sport newsworthy. The fact that the scientists actually observed significant and practically effects when they 'fed' their subjects 1.25g of a standardized tribulus terrestis (TT) extract (bought on the free market from Pronova Biocare, Sweden) with a saponin content of >40% per day, however, makes the study even more interesting.

If you want to build muscle forget T-booster and optimize your protein intake 

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5x More Than the FDA Allows!

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In contrast to previous studies that focused exclusively on testosterone and (sometimes) DHT, when it comes to identifying mechanisms for potential performance increases, the study at hand was designed to investigate the effects of Tribulus terrestris (TT) extracts on muscle mass, muscle damage, and anaerobic performances of trained male boxers and whether those may be brought about by androgen, IGF-1, and/or changes in IGF-1 or the concentration of its binding protein (IGFBP-3). To this ends, the previously mentioned fifteen male boxers were divided into an exercise group (E, n = 7) and an exercise plus TT group (E + TT, n = 8). The two groups both undertook 3-weeks of high intensity and 3-weeks of high volume training. The latter were separated by a 4-week rest period.

Table 1: Training protocol of the boxers with high intensity and high volume training (Ma. 2015) | Abbreviations: HR, heart rate; RM, repetition maximum.

"All athletes received similar 3-week high intensity training and 3-week high volume training separated by a 4-week rest. Besides special technical training, the main part of the high intensity training was strength training including maximum strength training (twice a week, on Tuesday and Friday) and speed strength training (twice a week, on Monday and Thurs day). For high volume training [see Table 1], the boxers undertook endurance training (10,000 m race every day and low to moderate intensity rope skipping twice a week, on Tuesday and Friday), and special technical training and speed strength training similar to high intensity training" (Ma. 2015).

The supplement, the aforementioned TT extracts (1,250 mg/day), was orally administered only in the E + TT group, obviously. Before the pills were handed out to the subjects, their exact compositions had been analyzed and their saponin content had been confirmed by UHPLC–Q-TOF/MS.

Not all TT extracts are created equal! If you've previously taken tribulus supplements and have seen no results, the reason could well be that they did not contain the right amount or type of saponins. As Ma et al highlight, the content of 25(R)-Spirostan-3,6,12-trione/25(R)-Spirostan-4-ene-3,12-dione and TT saponin A varies "depending on geographical region, climate23 and part of herb, which may partly explain the divergent results of TT extracts from different studies" (Ma. 2015).

The results of the pre- and post assessments of muscle mass, anaerobic performance, and blood indicators revealed no inter-group differences for testosterone, DHT, muscle mass or total IGF-1. Creatine kinase (CK), the IGF binding protein IGFBP-3 and the subjects' absolute and relative muscle power, on the other hand, increased significantly more in the supplement (E + TT) vs. control (E) group (Figure 1 shows the relative difference of the change from baseline, i.e. ΔE+TT - ΔE).

Figure 1: Differences in relative changes of IGF-BP3, the ratio of IGF/IGF-BP3, mean power, relative mean power and creatine kinase (CK) - higher values denote significant increases compared to control (E), lower values decreases in (E+TT) vs. (E) (all p < 0.05) | data calculated based on Ma. 2015

Against that background it is only logical that the scientists speculate that the performance increase and reduction in muscle damage they observed could be a result of the increased availability of IGF-1 (the total IGF-1 to IGF1BP-3 ratio is an indicator of the amount of insulin growth factor 1 that's actually floating around unbound in the blood).

Figure 2: Overview of the general role of IGF-1; focus on what is missing when it declines as we age (Berryman. 2013).

If you look at the far-reaching effects of IGF-1 on muscle (Frystyk. 2010) and its general effects on human metabolism as depicted in Figure 2 from Berryman, et al (2013), it certainly appears reasonable to assume that the significant increase in IGF-1 availability could explain the decreased muscle damage in the study at hand as well as similar results from a human study by Milasius, et al (2009) and studies in overtrained and intensely trained rodents by Zhang, et al (2010), Wang et al (2010) and Yin et al (2013), respectively.

Read this highly suggested SuppVersity Classic: Beware of falling victim to the "Brocebo Effect", Bros! Brocebo? Add 10kg to Your Bench in Days with Sugar-Based "Anabolic Steroids". Old Study Shows, Many "Natural Anabolics" Could Work Solely via Placebo Effects | learn more

What's the verdict, then? In view of the large influence the exact ratio and concentration of saponins will probably have on the effect of a given TT extract and its variability according to region, harvest and the part(s) of the plant that was/were used to prepare the extract (see red box) it is not impossible that previous studies by Antonio et al (2000) and Rogerson et al (2007) simply didn't find performance benefits in resistance-trained men and rugby players, because they used the 'wrong' extracts (or the training was not intense enough, some of the benefits in the study at hand were after all blunted performance decreases during intense training).

While it is hard to determine whether or not this hypothesis is true, there's no reason to debate the conclusion Ma et al draw based on their more recent results in trained boxers - a conclusion that reads: "Taking 1,250 mg capsules containing TT [...] alleviated muscle damage and promoted anaerobic performance of trained male boxers, which may be related to the decrease of plasma IGFBP-3 rather than androgen in plasma" (Ma. 2015) | Comment on Facebook!

References:

• Antonio, et al. "The effects of Tribulus terrestris on body composition and exercise performance in resistance-trained males." International Journal of Sport Nutrition and Exercise Metabolism, 10 (2000): 208–215.
• Berryman, Darlene E., et al. "The GH/IGF-1 axis in obesity: pathophysiology and therapeutic considerations." Nature Reviews Endocrinology 9.6 (2013): 346-356.
• Frystyk, Jan. "Exercise and the growth hormone-insulin-like growth factor axis." Medicine and science in sports and exercise 42.1 (2010): 58-66.
• Ma, Yiming, Zhicheng Guo, and Xiaohui Wang. "Tribulus Terrestris extracts alleviate muscle damage and promote anaerobic performance of trained male boxers and its mechanisms: Roles of androgen, IGF-1 and IGF binding protein-3." Journal of Sport and Health Science (2015).
• Milasius, K., R. Dadeliene, and Ju Skernevicius. "The influence of the Tribulus terrestris extract on the parameters of the functional preparedness and athletes’ organism homeostasis." Fiziol Zh 55.5 (2009): 89-96.
• Rogerson, Shane, et al. "The effect of five weeks of Tribulus terrestris supplementation on muscle strength and body composition during preseason training in elite rugby league players." The Journal of Strength & Conditioning Research 21.2 (2007): 348-353.
• Wang et al. "Effects of Tribulus terrestris on exercise ability, endocrine and immune functions of over-trained rats." Journal of Shanghai University of Sport 46 (2010).
• Yin, Liang, et al. "The Effects of Tribulus Terrestris on the Time of Exhaustion in Rats with High Intensity Training and Its Mechanism." Journal of Shanghai University of Sport 5 (2013).
• Zhang, Shuang, et al. "[Effect of gross saponins of Tribulus terrestris on cardiocytes impaired by adriamycin]." Yao xue xue bao= Acta pharmaceutica Sinica 45.1 (2010): 31-36.

Two-A-Day Training - That's Bogus, Right? No - Increased Fat Oxidation in Endurance, 2.4x Higher Max. Volume, 2.6x Higher Time to Exhaustion in Resistance Training Study

Two-A-Day Training - That's Bogus, Right? No - Increased Fat Oxidation in Endurance, 2.4x Higher Max. Volume, 2.6x Higher Time to Exhaustion in Resistance Training Study

AM/PM build muscle citric acid synthase endurance fat oxidation intensity techniques performance RER training training frequency two-a-days workout routines

If you feel totally wasted after every workout, I have bad news for you. In the two-a-day studies at hand the rest between the first and second workout was only 2h! Not exactly much time to recover, but the idea is to "train low" (on glycogen) on the second workout.

It sounds like madness or something for the "enhanced" athletes, but an older scientific study I recently dug out, accidentally, says that "training twice every second day may be superior to daily training" (Hansen. 2005). When I tried to learn more about this topic, though, I had to realize that the evidence is scarce. Similar results have been presented by Yeo et al (2008), though, albeit for trained triathletes and cycling.

In their study, Yeo and colleagues determined the effects of a cycle training program in which selected sessions were performed with low muscle glycogen content on training capacity and subsequent endurance performance, whole body substrate oxidation during submaximal exercise, and several mitochondrial enzymes and signaling proteins with putative roles in promoting training adaptation.

Overtraining can obviously still be an issue | Learn how to check your training status:

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Now, the interesting thing about Yeo's study and the reason I want to discuss their results first is that the scientists from the School of Medical Sciences at the RMIT University in Victoria, Australia used trained subjects - seven endurance-trained cyclists/triathletes who were used to training daily anyway. During the three week study period, however, the subjects had to stick to one of the following training schedules:

• Daily training (Daily - aka "High") - In this group the subjects alternated between 100-min steady-state aerobic rides (AT) one day, followed by a high-intensity interval training session (HIT; 8x5 min at maximum self-selected effort) the next day.
• Twice every second day training (Two-A-Day - aka "Low") - Subject who had been randomly assigned to this group performed the AT, first, then 1–2 h later, the HIT. 

Forty-eight hours before and after the first and last training sessions, all subjects completed a 60-min steady-state ride (60SS) followed by a 60-min performance trial. Muscle biopsies were taken before and after 60SS, and rates of substrate oxidation were determined throughout this ride and the results were... well, let's say interesting:

Figure 1: Markers of fact glycogen use and fat oxidation during steady state exercise after 3 weeks of training (Yeo. 2008)

As you can see markers of mytochondrial beta oxidation (citrate synthase), as well as the glycogen concentrations and whole body fat oxidation during the 60 minute steady state ride pre-/post-test increased exclusively in the "two-a-day" group. That's a relevant results, even though the increase in cycling performance improved by 10% in both Low and High and the performance during the HIIT trials, which were performed after the aerobic rides, suffered in the LOW, i.e. the "Two-a-Day" arm o the study (see Figure 2, right).

Figure 2: During the training sessions the HIIT performance is initally lower, but even then the increased capacity to oxidize fat and thus ability to spare gluocose pays off in slowly increasing performance markers (no sign. difference anymore) after only 7 HIIT sprints - during a race the fat oxidation boost (right) may be even more important (Yeo. 2008)

Why's that beneficial? Well, while it is not relevant for short bouts of HIIT, the significant increase in fat oxidation during the exercise test (see Figure 2, right) indicates that, the subjects' ability to use fuel as substrate during steady state, as well as longer interval rides increased significantly. The spared glycogen may then, during a longer race, for example, decide victory and defeat when the glycogen depleted every-day trainer cannot keep up with the glycogen sparing two-a-day every other day trainer during a sprint at the end of a race.

Want to learn more? At this point you may be reminded of a previous article of mine with the telling title "8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Intensity Exercise in Glycogen Depleted Elite(!) Cyclists: Training Revolution or Recipe for Disaster?". If not, I suggest you head back and read it now!

The obvious question that's probably preying on your minds already is: How on earth does that relate to strength training, bro? Well, let's see... so, in the strength training study by Hansen, et al., the authors actually speculated to observe an effect as it was observed in the study I discuss in the article I referenced in the red box, i.e.  that "training at a low muscle glycogen content [during a second workout on the same day] would enhance training adaptation" (Hansen. 2005). Therefore, the Hansen et al performed a study in which seven healthy untrained men performed knee extensor exercises with one leg trained in a two-a-day fashion (2h rest between the 1h sessions), the other one in everyday. Luckily, the study duration in this study was 10 and not just 3 weeks.

Against that background it is not surprising that the training load increased significantly. Since the latter has little to do with the mitochondria, it is also not that surprising that the increase in maximal workload was identical for the two legs. What may be surprising for those who think that training twice a day would be bogus, however, is that the time until exhaustion and total volume during the post-test was "markedly more increased" in the leg that was trained twice a day, albeit only every other day vs. the one that was trained daily, but only once (see Figure 3).

Figure 3: Relative performance increases from pre- to post-test (left) and glycogen levels before and after exhausting bouts of knee extensor exercises (right) | high = daily training, low = twice a day, but only every other day (Hansen. 2005).

Just like in the previously cited cylcling study by Yea et al, the effect may be attributed to (a) increased resting muscle glycogen and (b) higher activities of the mitochondrial enzyme 3-hydroxyacyl-CoA dehydrogenase and citrate synthase which are both involved in the oxidation of fat in the mitochondria of your muscle.

"Just One More Set" (1/2): Metabolic Response to 10,000kg vs. 20,000kg Regimen. EPOC: Do Reps and Loads Both Figure? And What About Elite Athletes Do They Need More? Find answers to these questions, here!

Bottom line: While it should be obvious that (a) further research is necessary and (b) the benefits of two-a-day training will depend on your training goals, the (older) studies presented in this article clearly support what Hansen et al phrase like this: "training twice every second day may be superior to daily training" (Hansen. 2005).

Ok, while the benefits for cyclists are obvious, it will have to be proven that the additional one or two reps or the extra high intensity set you may be able to do due to the improvements in glycogen sparing fatty oxidation will actually increase your muscle gains, but the mere possibility that training twice a day every other day could be better than training everyday, which is something I see people do at the gym regularly, is intriguing, isn't it? Comment!

References:

• Hansen, Anne K., et al. "Skeletal muscle adaptation: training twice every second day vs. training once daily." Journal of Applied Physiology 98.1 (2005): 93-99.
• Yeo, Wee Kian, et al. "Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens." Journal of Applied Physiology 105.5 (2008): 1462-1470.

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

appetite breakfast exercise fructose health hiking hunger lose fat pre-workout walking

About to go for a walk? Have fructose for breakfast to keep the hunger at bay.

I know very well that fructose is the nutritional boogyman of the 21st century, but avoiding it altogether is about as unwarranted as consuming it by the pound is unhealthy. A recent study from the Department of Health and Physical Education at the Hong Kong Institute of Education and the Department of Sports Science and Physical Education at the Chinese University of Hong Kong does now show a new, hitherto unknown, or at least under-appreciated effect of fructose: The ingestion of a fructose containing, albeit not fructose only (not tested, though) breakfast will significantly reduce the desire to eat that will usually rise sharply after a 60 minute bout of "cardio" training in form of walking at 50% of one's individual VO2max.

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As a SuppVersity reader you will know that low-intensity cardio, much more than HIT or HIIT (learn more), will trigger significant increases in hunger and one's desire to eat. To ameliorate this effect, you could - that's at least what the aforementioned study shows - simply replace part of the starchy or high GI carbs of your breakfast with high fructose fruits and/or other fructose containing food items.... that's at least - as  previously mentioned - what the study at hand suggests; a study in which Hong Kong researchers compared the effects of three isocaloric breakfasts with identical amounts of carbs (1.0 g/kg body weight) from different food sources with different GIs (41, 39, and 72) and fructose contents on the appetite scores of ten healthy young male volunteers (21.7 ± 1.5 yr, 20.9 ± 1.1 kg/m²) who had to rate different aspects of appetite every 30 min during the 2-hr postprandial period after the meal, as well as during the 1-hr recovery period that followed the 1h of brisk walking (46% VO2max) all subjects had do perform 2h after consuming the standardized breakfasts.

"Three isocaloric meals were used in the present study. [...] Briefly, all meals had similar macronutrients and provided 1.0 g∙kg−1 body weight CHO for each participant. The LGI meal was composed of cooked spaghetti, egg, and full-fat milk. The LGIF meal comprised rice vermicelli, egg, ham, and fructose. The HGI meal involved rice vermicelli, egg, ham, and glucose. In the LGIF and HGI meals, approximately 25% of energy was derived from the fructose or glucose beverage (nearly 25 g for a 60 kg person). The calculated GI values for the LGI, LGIF, and HGI breakfasts were 41, 39, and 72, respectively. All meals were freshly prepared in the morning of each main trial, and the preparation procedure was standardized."

As you can see in Figure 1 the three test-meals initially had very similar effects on the subjects' appetite ratings, i.e. their desire to eat, hunger, fullness, and perceived ability to eat.

Figure 1: Appetite Sub-Score. b: P < 0.05 vs. LGIF. LGI: Low-GI meal without fructose; LGIF: Low-GI meal including fructose beverage; HGI: High-GI meal (Sun. 2015).

Only the 25% fructose meal, however, kept the rapid increase (or decrease in the case of fullness) in all four parameters after the 1h of brisk walking (Rec-X in Figure 1) at bay. That's quite an interesting observation, even though one could argue that the study cannot serve as a definite litmus test, because it lacks a post-exercise test-meal where the practical significance of the reduced appetite scores was measured against the reduction in food intake in the fructose group.

But isn't fructose the appetite increasing, liver clogging devil? While it may be the devil in the books of a couple of researchers who have nothing else to publish, the specific effect of fructose on appetite are far from being proven to be good or bad. (Rodin. 1990 & 1991). While it appears as if the isolated consumption of high amounts of free fructose has negative effects on appetite control (Lowette. 2015); and still, there's  no debating that fructose has the general ability to blunt food intake compared to an isocaloric amount of glucose in healthy individuals, as it has been shown by Rodin in 1991 (see Figure on the left).

Irrespective of the previously mentioned methodological short-coming, it is, as the authors highlight, quite striking that "the increased fructose content in LGIF breakfast suppressed the appetite score, compared with isocaloric HGI and LGI breakfast" (Sun. 2015). Previously, scientists often argued that the satiety promoting effect of fructose must be mediated by the lower GI and correspondingly lower insulin spikes as well as reduced glucose excursions after fructose vs. glucose containing meals. The data in Figure 2, however, tells us that neither the insulin spikes (Figure 2, right) nor the glucose excursions (Figure 2, left) differed significantly between the LGI (low GI) and the LGIF (low GI + fructose) meals over the relevant last part of the study period - an observation which does by the way also show us that "[w]hen exercise is included as a co-intervention strategy, the effect of GI on appetite may be highly complex" (Sun. 2015) and in most cases relatively irrelevant.

Figure 2: Glucose and insulin response to the test meals; significant differences were observed for high GI (HGI) compared to the other meals and initially for the fructose meal, where the glucose levels increased slightly more rapidly than in the low GI (LGI) reference meal -  in spite of identical calculated GI values, by the way (Sun. 2015)

Previous studies show that even though exercise exerts the most profound effect on human energy expenditure, it seems that post-exercise energy intake is not affected by exercise itself (Blundell. 1999; Melzer. 2005). In that, a study by Stevenson et al appears to confirm the finding of the study at hand which is that there is no difference relevant appetite scores between HGI and LGI trials during the postprandial period if the time between breakfast and moderate intensity exercise is sufficiently long.

Figure 3: The appetite suppressing effects of fructose preloads in the absence of exercise have been known ever since Rodin's 1990 study on the effects of fructose vs. glucose and water preloads on food intakes (Rodin. 1990).

What's new with the present study, though, is that "eating an LGIF [25% fructose] breakfast resulted in decreased appetite scores compared with HGI breakfast and LGI breakfast [25% non-fructose carbs]" (Sun. 2015). This and the fact that this difference cannot be explained by the usual suspects, i.e. insulin and blood glucose levels leads Sun et al to emphasize that ...

"[t]he effect of fructose on appetite has been substantially investigated. Earlier studies have indicated that fructose beverages suppressed energy intake more than glucose beverages did (Rodin, 1990 and Rodin, 1991). The underlying mechanism has been attributed to the metabolism of fructose in the liver and the effect of insulin" (Sun. 2015).

In fact, scientists have previously speculated that fructose may affect appetite through slow and incomplete absorption. This effect, however, is eliminated when fructose is consumed with other CHOs (Anderson. 2003). As far as potential mechanisms are concerned, we are thus left with changes in satiety hormones and peptides like ghrelin, cholecystokinin, glucagon-like-peptide-1 and peptide-YY and/or direct or indirect effects on the gut-brain axis as potential mechanisms that would explain the results of Sun's study. Unfortunately, neither of these mechanism was assessed in their study.

Make you choice - cholesterol and regular sugar (left), or fat free and fructose-laden? In the end it all may not even matter. In spite of that, you shouldn't forget that fruit is not the enemy, isolated fructose in drinks is.

So, what's the verdict? I'd like to cite the original conclusion first, before adding my two cents: "It appears that fructose content in, rather than the GI of, a pre-exercise breakfast meals affect subjective appetite score during the recovery period after 1-hr of brisk walking" (Sun. 2015).

There's no doubt that this is right, but there are important qualifications with respect to the real-world significance of the results: Firstly, the absence of a post-recovery test meal, where the actual food intake would have been measured, is a major methodological problem of the study at hand. Even though changes in appetite of a similar magnitude will usually translate in changes in food intake, this is not a necessity. Therefore the actual food intake and the mechanism for the appetite suppression have to be elucidated in future trials.

In the mean time, I'd suggest you do your own test-run. If it works, fine. If not, you don't have to care about the results of follow-up studies, anyway. Why? Well, what works for the virtual average study participant does not necessarily have to work for you | Comment on Facebook!

References:

• Anderson, G. Harvey, and Dianne Woodend. "Effect of glycemic carbohydrates on short-term satiety and food intake." Nutrition Reviews 61.5 (2003): S17.
• Blundell, John E., and Neil A. King. "Physical activity and regulation of food intake: current evidence." Medicine and science in sports and exercise 31 (1999): S573-S583.
• Lowette, Katrien, et al. "Effects of high-fructose diets on central appetite signaling and cognitive function." Frontiers in nutrition 2 (2015).
• Melzer, Katarina, et al. "Effects of physical activity on food intake." Clinical nutrition 24.6 (2005): 885-895.
• Rodin, Judith. "Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake." The American journal of clinical nutrition 51.3 (1990): 428-435.
• Rodin, Judith. "Effects of pure sugar vs. mixed starch fructose loads on food intake." Appetite 17.3 (1991): 213-219.
• Sun, Feng-Hua, Stephen Heung-Sang Wong, and Zhi-Gang Liu. "Post-exercise appetite was affected by fructose content but not glycemic index of pre-exercise meals." Appetite 96 (2016): 481-486.

True or False: Adolescent Athletes at Risk of High Tendon Stress due to Non-Uniform Tendon/Muscle Adaptation

True or False: Adolescent Athletes at Risk of High Tendon Stress due to Non-Uniform Tendon/Muscle Adaptation

adolescence adolescents build muscle health hypertrophy ligaments muscle growth resistance training tendons TOF

Not allowing young athletes to lift weights may in fact increase, not decrease, their injury risk and hamper their recovery.

I am not sure why, but people won't stop inventing new reasons why professional athleticism would be bad for adolescents. One of the more recently heard claims is that early resistance training will lead to a "non-uniform adaptation of muscle and tendon in young athletes" that may "result[] in increased tendon stress during mid-adolescence" (Mersmann. 2015).

In a recent longitudinal study Mersmann et al. investigated the development of the morphological and mechanical properties of muscle and tendon of volleyball athletes in a time period of 2 years from mid-adolescence to late adolescence and the results are quite unambiguous.

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A total of eighteen elite volleyball athletes participated in magnetic resonance imaging and ultrasound-dynamometry sessions to determine quadriceps femoris muscle strength, vastus lateralis, medialis and intermedius morphology, and patellar tendon mechanical and morphological properties in mid-adolescence (16 ± 1 years) and late adolescence (18 ± 1 years).

Figure 1: Mean values ± standard deviation of the muscle volume of volleyball athletes in mid-adolescence and late adolescence; %-ages indicate relative mid-to-late differences (Mersmann. 2015).

As the data in Figures 1 and 2 indicates, the muscle strength, anatomical cross-sectional area (CSA), and volume showed significant (P < 0.05) but only moderate increases of 13%, 6%, and 6%, respectively. In contrast to the muscular development, the patellar tendon CSA (P < 0.05) which is under constant stress in (semi-)professional volleyball players showed a substantially higher degree of hypertrophy (27%) that wen in line with increased stiffness (P < 0.05; 25%) and reduced stress (P < 0.05; 9%). Accordingly, the scientists conclude that - in contrast to the commonly heard prejudice - exercise during early adolescence will lead to

"pronounced hypertrophy of the patellar tendon led to a mechanical strengthening of the tendon in relation to the functional and morphological development of the muscle - [...] adaptive processes [that] may compensate the unfavorable relation of muscle strength and tendon loading capacity in mid-adolescence and might have implications on athletic performance and tendon injury risk" (Mersmann. 2015).

You know what, I can read your minds: "What about resistance training, then?" That's the question that's preying on your mind, right now - right? Well, as one of the more recent reviews says, "there is evidence that resistance training may reduce injury in a young athlete’s chosen sport" (Myer. 2006). The authors of the review point out that ...

Heyna et al. have demonstrated as early as 1982 that young athletes who regularly perform resistance training exercises are not just less likely to be injured, they also recover faster (Hejna. 1982).

"[t]his evidence is based on the beneficial adaptations that occur in bones, ligaments, and tendons following training and is further supported by epidemiologic-based reports. Lehnhard and colleagues were able to significantly reduce injury rates with the addition of a strength training regimen to a male soccer team. [...] Hejna and coworkers reported that young athletes (13-19 years) who included resistance training as part of their exercise regimen demonstrated decreased injuries and recovered from injuries with less time spent in rehabilitation when compared with their teammates" (Myer. 2006).

Similar results have been found specifically for female athletes for whom strength training - especially when performed in theh preseason and as regular part of in-season conditioning - reduced injury risk factors and anterior cruciate ligament injuries significantly.

Figure 2: Mean values ± standard error (bars) of (a) patellar tendon cross-sectional area (CSA) as a function of tendon length (in 10% intervals from proximal to distal; n = 18), (b) tendon force-elongation relationship (obtained from ramp contractions, see 'Methods' section; n = 12), and (c) maximum tendon force and stress (calculated for iMVCs; n = 12) of volleyball athletes in mid-adolescence (white) and late adolescence (black | Mersmann. 2015)

So, what's the verdict, then? The study at hand refutes the general claim that a non-uniform adaptation of muscle and tendon in young athletes may result in increased tendon stress during mid-adolescence. Furthermore the comprehensive overview of the effects of resistance training Myer et al. present in their 2006 review shows that additional "resistance training is not only a relatively safe activity for young athletes but that it may also be useful to reduce injuries during competitive play" (Meyer. 2006). To tell your young athletes to stay away from the gym is thus tantamount to telling them not to care about injury prevention.

As the 2014 International Consensus Statement on Youth Resistance Training in the British Journal of Sports Medicine (Lloyd. 2013) points out, it is yet important that your kids and youthsare following "[a]ppropriately designed resistance training programmes" if you actually want to make sure that they reduce, not increase, sports-related injuries. As such, LLoyd et al. even say that resistance training programs "should be viewed as an essential component of preparatory training programmes for aspiring young athletes" (Llyod. 2013 | my emphasis) | Comment on Facebook!

References:

• Lloyd, Rhodri S., et al. "Position statement on youth resistance training: the 2014 International Consensus." British journal of sports medicine (2013): bjsports-2013.
• Mersmann, F., et al. "Muscle and tendon adaptation in adolescent athletes: A longitudinal study." Scandinavian Journal of Medicine & Science in Sports (2015).
• Myer, Gregory D., and Eric J. Wall. "Resistance training in the young athlete." Operative techniques in sports Medicine 14.3 (2006): 218-230.

Cinnamon as Nutrient Partitioner and 1st-Line Treatment for Pre-Diabetes? 5% Decrease in Fasting Glucose per Month in Human Studies, Up to 24% in 40 Days W/ High(er) Doses

Cinnamon as Nutrient Partitioner and 1st-Line Treatment for Pre-Diabetes? 5% Decrease in Fasting Glucose per Month in Human Studies, Up to 24% in 40 Days W/ High(er) Doses

anti-diabetes cassia cinnamon cinnamon Coumarin diabesity diabetes fasting blood sugar glucose management HbA1c health insulin sensitivity lose fat

Yes, that's how real cinnamon look like. It does not grow as powder in plastic boxes on trees as I suspect the members of the generation McBurgerSubway believe ;-)

No, this is not absolutely new. In fact this is just "another" SuppVersity articles on the anti-diabetic effects of cinnamon, but I promise it's going to be the most comprehensive one. One that discusses the currently available evidence from human trials, as well as the things we know and believe to know about how cinnamon acts its anti-diabetic magic qualitatively and quantitatively.

Before I even go into further details, though, I would like to address one of the "cinnamon myths" that says that only the highly expensive Ceylon or Sri Lankan Cinnamon would do the trick, while the commonly sold Cinamon cassia would be useless or even dangerous due to its high (and in fact toxic) coumarin content.

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Interestingly, all human studies have been done with the "cheap toxic stuff from the supermarket". In view of what you are about to learn about its effects on blood glucose later in this article, the first take-home-message from today's article is thus: "Cheap cinnamon cassia will work just fine as a blood glucose management supplement!" Unfortunately, long-term studies the safety of "common cinnamon" with its highly variable coumarin content (0.31 g = harmless to 6.97 g = potentially dangerous per kg raw powder | Wang. 2013 | see Table 1) are non-existent.

Table 1: Content of Coumarin 1, Cinnamyl Alcohol 2, Cinnamaldehyde 3, Cinnamic Acid 4, Eugenol 5, Cinnamyl Acetate 6 in Cinnamomum Species and Commercial Samples (g/kg) | DUL = Detected under limits of quantitation; ND = not detected (Wang. 2013).

The only advise I can give you is thus to rely on supplements with standardized (low to non-detectable) amounts of this potentially carcinogenic substance (Wang. 2014) if you plan to take it regularly for years. Using the next best cinnamon powder from the supermarket next door on the other hand is probably not advisable even though some of the scientists who conducted the studies Arjuna B. Medagama reviewed for his (or her?) latest paper in Nutrition Journal (Medagama. 2015) probably did just that: Buy cinnamon powder from the supermarket next door to test its effects on blood glucose management in 40-days- to 4-months-studies in cinnamon-naive patients with (pre-)diabetes.

If you take a closer look at the data, though, it becomes obvious that some studies used plain cinnamon powder, while others used regular or commercial water-extracts (CinSulin. Anderson).

Effect of 6g of cinnamon on post-prandial blood glucose in healthy subjects (Hlebowicz. 2007). This hefty dose also slowed down gastric emptying and triggered non-significant increases in satiety in 14 healthy subjects after high CHO meals.

What's the optimal dosage? Even though the overview in Figure 1 suggests that "more helps more", Anand, et al. (2010) observed negative effects on the liver of rodents at dosages that would tantamount to ~40g of cinnamon per day. Ok, I assume you already apprehended that this is madness, but in the world of fitness maniacs and mad bodybuilders I thought it would be worth mentioning that even the coumarin free Ceylon cinnamon appears to have ill side effects when it is consumed in extremely high dosages. It would thus appear to be more reasonable to target an intake of 3-6 g of cinnamon with every major meal (it slows down gastric emptying and reduces postprandial blood glucose, therefore it makes sense to take it with a meal | Hlebowicz. 2007, see Figure to the left).

If you scrutinize the results I've plotted for you in Figure 1, you will notice that (a) the improvements in fasting blood glucose were significantly more pronounced than those of the long-term blood sugar maker HbA1c, that (b) the former appear to increase with the dosage that was used (Klan and Mang observed the highest reductions and used the highest amounts of cinnamon powder), and that (c) the reductions in HbA1c take time, i.e. several months and are not guaranteed, even if there are significant reductions in fasting blood glucose (cf. Belvins).

Figure 1: Relative changes in fasting blood glucose and HbA1c levels of pre-diabetic subjects (Medagama. 2015)

On average, the fasting blood glucose levels of the study participants in all studies decreased by 4.7% in four weeks; the HbA1c, on the other hand, by only 1%. Since part of the effects on blood glucose are merely a results of the reduced gastric emptying and will thus affect the peak values, yet not the overall glycemia, it appears logical that the HbA1c reacts slowly to the intervention. As Medagama points out, the effects of cinnamon are yet more far-reaching, so that more pronounced effects on the slow-reacting HbA1c levels can be expected to be seen in the hitherto non-existent long-term (= 1-2 year) studies, because cinnamon will also have ...

• 

  Figure 2: Molecular mechanisms of Cinnamon by which it exerts hypoglycaemic activity. (Medagama. 2015).

  direct effects on the insulin receptor have been observed for Cinnamtannin B1, a proanthocyanidin isolated from the stem bark of Ceylon cinnamon that activates the phosphorylation of the insulin receptor β-subunit on adipocytes as well as other insulin receptors,
• indirect effects on glucose management that are mediated by increased GLP-1 levels, a satiety hormone that decreases the amount of insulin that is necessary to clear glucose from your blood - as Medagama points out, probably by improving glucose transport,
• direct effects on the GLUT-4 glucose uptake receptor, the expression of which is increased by 42.8 % to 73.1 % in brown adipose tissue and muscle by cinnamon in a dose dependent manner,
• indirect effects on insulin sensitivity that are mediated by the effects of cinnamon on the expression of PPAR (α) and PPAR (γ), the increase of which is linked to increased glucose uptake - unfortunately, also in fat cells,
• direct effects on carbohydrate availability that are mediated by the inhibition of the amylase enzyme that is responsible for breaking down complex carbs into simple sugars,
• indirect effects on the endogenous production of glucose in the liver that is inhibited by cinnamon (glucogenesis, i.e. the storage of sugar in the liver, on the other hand, is promoted), and
• indirect effects that are brought about by the reduced rate of gastric emptying that will naturally slow down the absorption of glucose after a meal.

If that was too much for you to remember, I guess the graphical overview Medagama created may serve as a memory aid, when you come back to this article to refresh your knowledge about cinnamon and pre-diabetes. Speaking of which...

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So, what's the verdict about cinnamon and pre-diabetes? As Medagama points out in the conclusion to the previously referenced recently published review, "[b]oth true cinnamon and cassia cinnamon has the potential to lower blood glucose in animal models and humans" (Medagama. 2015). The problem is yet that we do not have reliable long-term safety studies for both, the problematic, potentially coumarin-laden regular cinnamon, as well as the expensive 99% coumarin-free Ceylon cinnamon, which has actually never been tested in human studies (rodent studies suggest that it works at least as well, though).

Addendum: As previously hinted at, there is no evidence from human studies that the "healthier", "true cinnamon" aka Ceylon cinnamon even works. Well, I just noticed that there's a single, rarely cited study in healthy individuals from the Lund University in Sweden that says that Ceylon cinammon has no effect whatsoever on glycemia and thus concludes "The Federal Institute for Risk Assessment in Europe has suggested the replacement of C. cassia by C. zeylanicum or the use of aqueous extracts of C. cassia to lower coumarin exposure. However, the positive effects seen with C. cassia in subjects w/ poor glycaemic control would then be lost." (Wickenberg. 2012)

To recommend regular cinnamon as a standard-supplement, you'd take everyday for years, on the other hand cannot really be recommended - not for pre-diabetics and by no means for healthy, active individuals who have no reason to take supplements with non-muscle specific glucose partitioning effects, anyways. If you want to improve your glucose management folks, work out - a glycogen-depleting strength or HIIT workout, that's the only scientifically proven muscle specific glucose repartitioner | Comment on Facebook!

References:

• Akilen, R., et al. "Glycated haemoglobin and blood pressure‐lowering effect of cinnamon in multi‐ethnic Type 2 diabetic patients in the UK: a randomized, placebo‐controlled, double‐blind clinical trial." Diabetic Medicine 27.10 (2010): 1159-1167.
• Anand, Prachi, et al. "Insulinotropic effect of cinnamaldehyde on transcriptional regulation of pyruvate kinase, phosphoenolpyruvate carboxykinase, and GLUT4 translocation in experimental diabetic rats." Chemico-biological interactions 186.1 (2010): 72-81.
• Anderson, Richard A., et al. "Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose." Journal of Traditional and Complementary Medicine (2015).
• Blevins, Steve M., et al. "Effect of cinnamon on glucose and lipid levels in Non–insulin-dependent type 2 diabetes." Diabetes care 30.9 (2007): 2236-2237.
• Crawford, Paul. "Effectiveness of cinnamon for lowering hemoglobin A1C in patients with type 2 diabetes: a randomized, controlled trial." The Journal of the American Board of Family Medicine 22.5 (2009): 507-512.
• Hlebowicz, Joanna, et al. "Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects." The American journal of clinical nutrition 85.6 (2007): 1552-1556.
• Khan, Alam, et al. "Cinnamon improves glucose and lipids of people with type 2 diabetes." Diabetes care 26.12 (2003): 3215-3218.
• Mang, B., et al. "Effects of a cinnamon extract on plasma glucose, HbA1c, and serum lipids in diabetes mellitus type 2." European journal of clinical investigation 36.5 (2006): 340-344.
• Suppapitiporn, Suchat, and Nuttapol Kanpaksi. "The effect of cinnamon cassia powder in type 2 diabetes mellitus." Journal of the Medical Association of Thailand= Chotmaihet thangphaet 89 (2006): S200-5.
• Vanschoonbeek, Kristof, et al. "Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients." The Journal of nutrition 136.4 (2006): 977-980.
• Wang, Yan-Hong, et al. "Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States." Journal of agricultural and food chemistry 61.18 (2013): 4470-4476.
• Wickenberg, Jennie, et al. "Ceylon cinnamon does not affect postprandial plasma glucose or insulin in subjects with impaired glucose tolerance." British journal of nutrition 107.12 (2012): 1845-1849.