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marylin monroe
Showing posts with label SOD. Show all posts
Showing posts with label SOD. Show all posts

3.2g of Beta Alanine Reduce Rate of Perceived Exertion, Increase Time to Exhaustion and Ventilatory Threshold. Vegetarians, Older People and Diabetics May Benefit Most.

Image 1: If you are into running, ladies, beta alanine is for you ;-)
Those of you who make sure that they are getting their highly educative daily dose of the SuppVersity *rofl* will be aware that today's blogpost is, once again, dealing with beta alanine. Contrary to yesterday's post, which dealt with its pharmacokinetics, we are today going to have another look at what kind of real world performance outcomes the average (female!) physical culturist can expect from taking at least 3.2g of the beta amino acid per day - a dosage that has been shown in previous studies to increase intra-muscular carnosine levels by 27–39% in fast- and slow-twitch muscle fibers, respectively (Baguet. 2009). And though I do not want to spoil things, I can already tell you that the results make it quite clear why beta alanine is not the next creatine.

Somehow ergogenic, yet not really antioxidant

For the study that was conducted at the Applied Physiology Laboratory at the University of North Carolina, study that was conducted by A.E. Smith recruited 24 "recreationally active" women, of which the authors state that they "engag[ed] in 3–7 days per week of aerobic, resistance or recreational activities, but were not highly trained competitive athletes". With a mean age of 21.8 years, a height of 165cm and a body weight of 61.5kg the subjects are thusly representative of the average young woman who goes to the gym to either get or keep in shape. I am specifically emphasizing this, because - at least in the early days - beta alanine was heavily marketed as "the creatine for women" who fear the water retention people still claim was an inevitable side effect of creatine supplementation.
Image 2: If you retain water, this is not due to creatine monohydrate. Either you are taking to much (creatine loading is a thing of the past) or you have bought a product with shitloads of carbs in it - in that case, chances are its not only water you are gaining ;-)
Does creatine supplementation inevitably lead to water retention and weight gain? Just because this myth is still perpetuated, especially among female figure competitors, I thought it may be worth addressing this again: Pure creatine monohydrate without the sugar and the other bullshit you will find in many creatine supplements does not necessarily lead to increases in either total body or water weight. A study by Rawson et al. showed only recently that the consumption of 0.03g/kg creatine for six weeks did not result in statistically significant changes in body weight or water in men or women, despite significantly increased plasma creatine concentration and enhanced resistance to fatigue during repeated bouts of high-intensity contractions (Rawson. 2011).
The women were advised to simply stick to their usual routine and to refrain from taking any supplements and medications except from their 2x800mg beta alanine tablets. The latter were to be taken 3x a day... so according to Cocker, they should have consumed 2x0.8g x3/day = 4.8g/day and not, as the scientists state "3.2 g daily". Now, according to Smith et al. this was the "required dosage" all participants met. I can however not say, whether this means that the third dose was optional... and this is not the only oddity in this study, where it is well worth to look beyond the assessments and conclusions of the authors.

At the beginning and the end of the 28-day supplementation period, the women had to perform a graded oxygen consumption test (VO2max) to evaluate VO2max, time to exhaustion, ventilatory threshold and establish peak velocity (PV), as well as a "non-damaging treadmill run (oxidative stress run) for 40 min at 70% PV [peak velocity]". Before, immediately after and in the 2-6h post running window total antioxidant capacity (TAC), superoxide dismutase (SOD), 8-isoprostane (8ISO) and reduced glutathione (GSH) were measured. In addition to that, heart rate and ratings of perceived exertion were recorded during the 40 min run. The two main metrics of the study were thusly the potential anti-oxidant effects (TAC, SOD, 8ISO, GSH) and the anticipated immediate ergogenic effects (VO2Max, time to exhaustion, heart rate and perceived exertion) of beta alanine supplementation.
Figure 1: Effect of 28 days of beta alanine supplementation on maximal oxygen consumption (VO2max), time to exhaustion during a graded exercise test (VO2TTE) and ventilatory threshold (VT) and qualitative practical significance (data and caption adapted from Smith. 2011)
If you now have a look at the my graphical rehash of the scientists own evaluation of the effect beta alanine supplementation had on VO2Max, the time to exhaustion (VO2TTE) and the ventilatory threshold (VT), you will have to concede that mean improvements of 0.28%, 6.6% and 3.7%, respectively, as well as the large discrepancies among the subjects (from beneficial over negligible to harmful) do not actually speak for beta alanine.
Figure 2: Effect of beta alanine supplementation on oxidative stress markers measured as total
antioxidant capacity (TAC) and glutathione (GSH) and the qualitative practical significance
for women (data and caption adapted from Smith. 2011)
Things get even more confusing when we take a look at the antioxidant effects of beta alanine. Not only were the levels of superoxide dismutase (SOD) and 8-isoprostane (8ISO) not different between groups, and the effect of beta alanine on the total antioxidant capacity (TOC) of the subjects negligible, the scientists' summary of the effects does even suggest that, after an initial amelioration of the negative effect of treadmill running on GSH, there was some sort of a "likely harmful" rebound 6h after the 40 min exercise bout. Before you do now flush your beta alanine stores down the toilette, I suggest you first take a look at the actual (absolute) effects beta alanine supplementation had on the exercise induced changes in GSH levels:
Figure 3: Absolute GSH levels (in µM) immediately before (pre), post, 2h and 4h after treadmill running in the placebo and beta alanine supplemented women before (pre) and after (post) the 28-day supplementation period (compiled based on data from Smith. 2011)
As you can see in figure 3, there was an (unexplained) increase in GSH in the course of the 28-day supplementation period in both groups. With 2%, the latter was statistically non-significantly greater in the beta alanine group, and the "likely harmful" effect of beta alanine supplementation 6h after the end of the treadmill-run is simply the result of a smaller increase in GSH, when you compare the pre- to post-supplementation levels at the 6h mark - and I guess, you would agree that a +27% increase in GSH is not exactly something that deserves to be called "likely harmful", wouldn't you?

All-clear: Beta alanine is not ergolytic ;-)

Now that we have gotten that straight, let's get to the last (and most) significant benefit the women in the beta alanine group had from taking the supplement: a statistically significant reduction in the rate of perceived exertion during treadmill running (cf. figure 4).
Figure 4: Rates of perceived exertion during 40 min treadmill running before (pre) and after (post) 28 days of supplementation with beta alanine or placebo; small graph: relative difference post supplementation in women receiving BA vs. placebo (data calculated based on Smith. 2011)
It goes without saying that being 18% less fatigued is something that could well be worth spending the roughly 7$ for a 28-day supply on (calculation based on a dose of 3.2g per day taken over 28 days and assuming you buy your beta alanine in bulk at one of the major suppliers). This, by the way, could be particularly true if you belong to one of the following groups, who have been found to have low intra-muscular carnosine levels, to begin with:
    Image 3: Older people are only one of the three groups who are "at risk" of low carnosine levels and are thusly most likely to benefit from beta alanine supplementation.
  1. vegetarians - a 2011 study by Evaraert et al. found that "Vegetarians have a lower carnosine content of 26% in gastrocnemius compared to omnivores" (Everaert. 2011); and according to another recent study, the soleus carnosine content of vegetarians was "non-significantly" reduced by -9% after 5 weeks of sprint training, while the same protocol elicited increases of +11% in omnivores (Baguet. 2011)
  2. older people - Evaraert et al. found a linear decline (ca. -10% in 20 years) in carnosine levels with age (correlation r=-0.26; Everaert. 2011); and Stout et al. report a highly significant +29% increase in physical working capacity at the fatigue threshold in twenty-six men (n = 9) and women (n = 17) (age ± SD = 72.8 ± 11.1 yrs) who  had been supplementing with 800 mg three times per day for 90 days (Stout. 2008)
  3. type-2 diabetics - according to Gualano et al. type-2 diabetics have "significantly lower carnosine content (−45%) in gastrocnemius muscle", a relative deficiency of which the scientists argue that it "may be partially associated with defective mechanisms against oxidative, glycative and carbonyl stress in muscle." (Gualano. 2011)
After all, it does yet not really matter whether you are a type-2 diabetic, a vegetarian or simply getting older, compared to many (if not most) of the other overpriced ergogenics that are advertised all over the web, beta alanine is certainly not only one of the cheapest, but also one of the most promising candidates for the 3rd place on your list of staples, where (whey) protein and creatine should nevertheless still occupy position 1 and 2, respectively. And the fact that it did not prove to be a potent antioxidant in this study need not really be a disadvantage, after all, we still do not know whether the exercise-induced oxidative "damage" is not what actually triggers the highly desirable adaptive responses (cf. previous posts on "hormesis"), we are all looking for, when we are hitting the gym.

    Update on Antioxidants & Exercise - Neither Vitamin C Nor E Have ANY Effect on the Response to Intense Exercise.

    Image 1: If you add some reactive oxygen species to this mitochondrium, this will trigger beneficial, (mito-)hormetic adaptations, that could be blunted by too many antioxidants.
    As a diligent reader of the SuppVersity, you have probably been following my posts on antioxidants and their potentially negative effect on the adaptive (hormetic) response to the exercise induced formation of reactive oxygen specimen. Although, I still believe that the theory may have its merit - especially in metabolically deranged people, where the exercise induced ROS formation would initially have to overcome the low-grade chronic "background" stress - it appears that for healthy people, and "moderately trained young men" on an intense exercise protocol, in particular, the ingestion of reasonable amounts (<1g of vitamin C and <400IU of vitamin E) does not pose a problem. At least this is what the results of two relatively recent studies by scientists from Washington School of Medicine (Higashida. 2011) and researchers from universities in Denmark and France (Yfanti. 2011) would suggest.

    The hormetic benefits of inflammation

    According to the mitohormesis hypothesis, the beneficial effects of exercise on health, in general, and glucose metabolism, in particular, are at least partly mediated by an increase in reactive oxygen species, which triggers downstream "hormetic" adaptation processes which result in increased oxidative capacity and insulin sensitivity, as well as a reduction in total inflammation (cf. previous posts on the work of S. Schmeisser and M. Ristow from the Department of Human Nutrition at the University of Leipzig. If this theory held true, or let's be more specific, if this theory which is largely based on observations in metabollically derranged, i.e. obese and/or type II diabetic subjects, was applicable to healthy people and athletes, as well, this could mean that the multi-vitamin, the vitamin C pills, the alpha-tocopherol (vitamin E) and all the other little helpers you have been taking religiously to increase your exercise performance would actually have hampered, not promoted your muscle gains, fat loss and whatever else you may have had in mind, when you hit the gym, the road, the field, the court or the green ;-)
    Figure 1: Neither the high-dose supplementation protocol in rodents (HED: Human Equivalent Dose for 80kg), nor the moderate dose protocol in humans did block any of the measured beneficial adaptations to exercise in the studies by Higashida (2011) and Yfanti. (2011), respectively.
    Let me say this right away: As long as you have not been following the recommendations of dubious nutritional gurus and self-proclaimed fitness "experts" to take 10g+ of vitamin C and vitamin E supplements in the 3000IU+ range, the little vitamin pills and powders are probably not the reason that your biceps is not growing and your belly is just as fat as it was, when you began training.
    Figure 2: Serum vitamin C and vitamin E levels (µmol/L) in 21 subjects before, at the beginning and after 12 weeks of 5x a week strenuous cycling exercise with and without supplemental vitamin C & E (adapted from Yfanti. 2011)
    As you can see in figure 2, supplementation with 500mg of vitamin C and 400 IU of vitamin E (more on the protocols used in the studies in figure 1) before and during 12 weeks of strenuous bicycle exercise training with a frequency of 5 sessions per week (HIIT, HIT and stead state, cf. figure 6) did increase the concentration of antioxidants in the blood of the 21 healthy, physically active subjects (age 18-40years) of the Yfanti study, who had not participated in physical exercise more than twice a week before the experiment. Despite higher vitamin C and E plasma levels, and contrary to the research hypothesis of the scientists, who had expected that the anti-oxidant supplementation would blunt the adaptive response to the exercise protocol,
    [...] the present study showed that combined supplementation with vitamins C and E before and during 12 weeks of supervised, strenuous bicycle exercise training of a frequency of 5 days/week had no effect on maximal oxygen consumption, maximal power output, workload at lactate threshold, glycogen content, and CS and β-HAD activity in muscle.
    In other words, supplementing with "reasonable" amounts of vitamin C and vitamin E had absolutely NO EFFECT (!) on the exercise induced metabolic adaptations or performance increases - that does yet also imply that taking anti-oxidants is of little benefit as long as the minimal dietary requirements are met... and if you still insist to poor money down the literally rat hole, you may be interested to hear that (assuming that the results from Higashida's rat study translate to humans), even 10g of vitamin C and 3000IU of vitamin E a day probably would not really make a difference - as long as you train heavy enough.
    Figure 4: Exercise induced changes in GLUT-4 expression (arbitrary units) and 2DG transport (µmol/ml/20min) in rats subjected to 8 weeks of high dose antioxidant supplementation and 6days/week swimming exercise in the last 3 weeks (data adapted fro Higashida. 2011)
    Of particular interest in this context is the effect of "mega-dosing" anti-oxidants on the exercise induced increase in insulin sensitivity, which has been reported to be impaired in previous studies (Ristow. 2009). As the data in figure 3 shows, the increase in glucose transporter (GLUT4) expression is slightly greater in the non-supplemented rats, BUT neither this difference nor the difference in measured 2-Deoxy-D-glucose (2DG) transport reach statistical significance.
    Figure 5: Exercise induced changes in MDA, SOD and PGC-1α in rats subjected to 8 weeks of high dose antioxidant supplementation and 6days/week swimming exercise in the last 3 weeks (data adapted fro Higashida. 2011)
    Moreover, Higashida et al. found no statistically significant differences in the increases of malondialdehyde (MDA), superoxide dismutase (SOD1 & SOD2) or PGC-1α, a marker for the mitochondrial fatty acid oxidation, between the rats in the two groups (cf. figure 5).

    Now, I a confused and don't know what to believe

    So what does all that tell us? Well, we can now be relatively certain that supplementing with vitamin C and vitamin E is a waste of time and money for most of us. What we still cannot say for sure, though is why the Ristow study from 2009, which even made it to mainstream media news, found detrimental effects of supplementing with 1g of vitamin C and 400IU of vitamin E on the adaptive response to 4 weeks of 5days/week 20min steady state aerobic training + 45 minute circuit training + 20 min warm up + cool down (Ristow. 2009), while the Yfanti study, with 500mg of vitamin C and 400IU of vitamin E did not find any effects of supplementation...
    Figure 6: Exercise protocol that was used in the Yfanti study.
    ...the only reasonable explanation I have is that the protocol in the Ristow study may not have been intense enough. Unfortunately there is no detailed information on what the subjects did in the course of the "circuit training", but if that was your usual sissy type walk from one machine to the next, chances are that the level of ROS that was induced by this "exercise" protocol was so low that it was completely blocked by the supplemental anti-oxidants. The "cycling protocol" in the Yfanti study, on the other hand, is pretty intense. If you look at the schedule in figure 6 you will concede that this is almost the way athletes (and maybe you) train.

    All that being said, it appears that all is coming back to what I have been writing (and also saying on SHR) several times before: Controlled oxidation is likely to be beneficial. It's like the fire in the oven that keeps you warm - the one you carefully take care of, in order to prevent your whole house to catch fire... if you are a marathon runner, the latter can happen pretty quickly and you will need (tons of ;-) antioxidants and even that will probably not suffice. If you are the housewife on the treadmill, who walks at 5km/h for 20min two times a week, on the other hand, even a few milligrams of vitamin C and a few units of vitamin E will blunt the little oxidative "damage" that you do and your "efforts" to increase your insulin sensitivity or whatever your intentions may be will be sabotaged by your vitamin supplements.

    Transfats the Last Bastion of the "Bad Fats"!? Two New Studies Shed Some Light onto Their Impact on Your Health.

    Image 1: The Meet the Fats campaign is part of the stultification... ah I mean educational program of the American Heart Association
    Meanwhile, even mainstream dietitians are beginning to understand that fats, which have been a, if not THE staple energy source in human history are not the bad boys the anti-fat hysteria of the 1980s would make us believe. Even the American Heart Association begins to advocate the use of "healthy fats" as part of a "heart healthy diet" - unfortunately, the AHA guys still lump Sat (that is the obese guy in the left) Trans (that is the sleazy guy in green) together, although the evidence against poor Sat (who obviously represents all saturated fats) is less conclusive than that against Poly, his money-grubbing sister who would do everything for her sponsors from the corn-industry... well, be that as it may, today's charge is against Trans who is accused of arson, or whole body inflammation, to be precise ;-)

    New evidence against Trans is provided by two teams of experts, one from Europe (Bendson. 2011) and the Middle East (Dhibi. 2011). In what I personally would consider battery, Nathalie T. Bendson and her colleagues from Denmark and France assigned 52 (formerly ;-) healthy women randomly to receive
    either 15.7g partially hydrogenated soybean oil or control oil without any industrially produced  trans fatty acids (IP-TFA) on a daily basis. The results were not life-threatening, but certainly not desirable:
    After 16 weeks, IP-TFA intake increased baseline-adjusted serum tumor necrosis factor (TNF) by 12% more in the IP-TFA group compared with controls. Plasma soluble TNF receptors 1 and 2 were also increased by IP-TFA.
    With TNF-alpha's role in the modulation of endothelial and vascular smooth muscle cell function as well as endothelial cell-blood cell interaction and "the importance of such alterations for vascular dysfunction, the initiation and progression of atherosclerosis" (Kleinbongard. 2010), Bendson et al.'s asssumption that
    the IP-TFA-associated increase in cardiovascular risk beyond the adverse effect explained by changes in blood lipids may be partly due to induction of systemic low-grade inflammation
    is possibly correct. Nevertheless, the jury is still out on how bad TNF-alpha actually is, as its role in cardiovascular disease is actually quite ambiguous with the aforementioned low-grade inflammation on the one hand and its ability to protect your heart by ischemic conditioning on the other hand.
    Figure 1: Trans fat content of fresh soy oil, oxidized soy oi and margarine (data based on Dhibi. 2011).
    More comprehensive evidence comes from a rodent study by Dhibi et al. who fed 48 male Wistar rats one out of four experimental diets which were either high in fat and included 20% fresh soybean oil diet (FSO), 20% oxidized soybean oil diet (OSO) and 20% margarine (MG) or based on the standard chow (control) with a protein/carbohydrate/fat ratio of 17/62/4 for 4 weeks (Dhibi. 2011). The liver function of the rats, as evidenced by the elevated transaminase levels (ALT, AST) and the increases in alkaline phosphatase (ALP) and lactate dehydrogensase (LDH) in figure 2, took a major beating.
    Figure 2: Relative changes in transaminases (ALT, AST), alkaline phosphatase (ALP) and lactate dehydrogensase (LDH) in rats after 4 weeks on diets containing 20% fresh soybean oil, oxidized soybean oil or margarine (data calculated based on Dhibi. 2011)
    I suppose the sponsors of the American Heart Association won't like this observation, but it is as plain as the nose in your face that even the "transfat free, heart-healthy polyunsaturated soybean oil" led to statistically significant increases in alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels... what, ah... of course that is because the diet was high in fat - how could I forget that 20% fat is still way too much and humans, just like rats should eat a 62% carb 4% fat diet ... I guess that was enough sarcasm for one blogpost, so let's back to the facts, now.
    Figure 3: Correlation  between  fatty  acid  isomers  in  the  diet  and  oxidative  stress
      parameters in rat’s liver and plasma hepato-specific enzymes (data based on Dhibi. 2011).
    The changes in liver function were accompanied by profound reduction in antioxidant enzyme activity (SOD: superoxide dismutase; GPx: glutathione peroxidase; CAT: catalase) and increased accumulation of conjugated dienes (CD) and malondialdehyde (MDA), the respective correlations of which with the fatty acids isomers (trans fats from mono-unsaturated and poly-unsaturated fatty acids, as well as total transfat content) are plotted in figure 3.

    Image 2: Rat liver histology.
    Due to its scale (only two different transfat profiles, i.e. oxidized soybean oil and margarine) the study's statistical power is yet so small that we can only make a definite case against the total transfat content for decreases in catalase activity and oxidized polyunsaturated fatty acids for the accumulation of conjugated dienes. With correlations in the the >0.5 and <-0.5 range for many other suspects and crimes, I will yet leave it up to you, the jury, to decide, which members of the transfat family (I suppose the American Heart Associations Trans character must have a whole bunch of children, then - just like in every honorable mafia family ;-) are to be held responsible for which of these crimes against health, the ultimate result of which you see in the histological changes in the livers of the rats fed with oxidized soy oil (OS) and margarine (MG)... So, members of the Jury, on the Case of Trans Fatty Acid (and his mafia clan) vs. the Suppversity, what you say?

    Eccentric Exercise IGF1 & Athlete's Heart; Long or Short Intervals, Both Improve Arterial Stiffness. Plus: Exercise Heals Wounds & Makes You Rust Proof Within One Year!

    Controlled exhaustion = positive adaptation; continuous exhaustion = wear and tear = one out of 57,002 who suffer from cardiac arrest during a marathon (data based on Webner. 2012)
    As announced on Saturday, already this is a "special edition" of the On Short Notice series, focusing exclusively on exercise related studies. With
    • two studies on heart health
    • one on wound healing and the last one on the 
    • bullet proof endogenous anti-oxidant system of trained athletes, 
    this installment of the "Exercise News Roundup" and two studies on different HIIT, it does however have both a health, as well as a HIIT focus.

    I know that does not sound as sexy as being big and buffed, but what's the use of that if you don't fit the coffin, you're about to need, when your looks are more important to you than your health?



    IGF-Response to exercise implicated in "athletes heart" A group of polish researchers describes in their latest paper that's been published ahead of print in the International Journal of Sports Medicine, how the differential IGF-1 response to eccentric (ECC) and concentric (CON) arm exercise in 10 trained strength athletes (1.5-2.0 h on 3-5 days weekly) and 10 age-matched healthy non-trained subjects could explain the differences in the degree of left ventricular hypertrophy, the scientists had measure via M-mode and 2D Doppler echocardiography beforehand (Zebrowska. 2012).

    IGF1 and left ventricular hypertrophy (LVH): The correlation stands out of question, but what about the implications? Is this a causative relationship? And what's more: How dangerous are LVH  and having an athlete's heart, at all?
    The athletes with LVH did not only have higher IGF-1 levels at baseline (52±5 nM vs. 46±7 nM for controls, p<0.05), they also showed a significantly more pronounced IGF-1 response during the eccentric (ECC) exercise test, with athletes with LVH exhibiting 30% higher and athletes without LVH 15% higher IGF-1 levels than untrained controls (54±6 nM). Moreover, both CON and ECC exercise resulted in higher serum IGFBP-3 levels in LVH athletes compared to controls (242±57 and 274±58, athletes, vs. 215±63 and 244±67, controls, nM, p<0.05), while no differences in other hormones were found between groups. Yet though the scientists' conclusion that these findings would "suggest a role of IGF-1, possibly released from contracting muscle, in stimulating LV hypertrophy in resistance training" is certainly right, we would be ill-advised to jump to any conclusions, hastily by simply (and faultily) equating correlation and causation, here.

    Moreover, we should acknowledge that the previously accepted paradigm that LVH, per se, is a bad thing that has to be avoided at all costs is actually not supported by empirical evidence, or as Florescu et al. have it "'Supranormal' cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with 'supranormal' cardiac function, and there are no markers of myocardial fibrosis." (Florescu. 2010)... in short: in the absence of myocardial fibrosis, a big heart is nothing you will die from - how IGF-1 could actually prevent the latter, i.e. the occurrence of fibrotic structures due to uncompensated growth of the heart muscle, would yet be the topic for another quite lengthy blogpost ;-)



    This image shows a study participant of another study during a VO2 max test on the exact same bike Rakobowchuk et al. used (WSCU.edu). Wrt to the protocols the researchers remark "the protocols involved an identical total training volume and time commitment but differed regarding metabolic stress" With the HIIT trial inducing greater metabolic stress due to the longer periods at supra-amaximal workloads (cf. Turner. 2006).
    Heavy or moderate interval training equally heart healthy - at least if you take their effect on arterial stiffness and heart rate dynamics as a measure. That's the message of an article that was published ahead of print in the European Journal of Applied Physiology at then end of last week. During a six-week experiment, Mark Rakobowchuk and his colleagues from the University of Essex and the University of Leeds investigated which of the following protocols (all performed three times per week, for a total of 18 session; 2min warm-up for each; cf. Rakobowchuk. 2012),
    • MIIT - moderate intensity interval training consisting of 10s : 20s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression), or
    • HIIT - high intensity interval training consisting of 30s : 60s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression),
    would elicit more favorable changes in carotid artery stiffness, blood pressure, and heart rate variability in a group of 20 healthy, previously untrained young men and women (n = 7 men and 13 women; age 23.5y; BMI 23).

    Trainees who want to increase their VO2max should still do HIIT, because only the subjects in the HIIT training group achieved statistically significant increases with respect to this outcome measure (+14% in HIIT vs. +3% VO2 max in MIIT).
    Just as the scientists had speculated, their hypothesis that irrespective of the metabolic stress, which would be higher in the HIIT vs. the MIIT trial, the total volume, which was identical would determine the overall adaptive response. For them it was therefore not surprising that all measured parameters of  heart health, i.e.blood pressure, heart rate dynamics and carotid arterial stiffness, improved without significant inter-group differences. Most notably, though, those with the highest arterial stiffness before the trial saw the greatest reductions!



    Figure 2: Additional exercise sped up the wound healing process only in the obese rodents, not the lean ones (Pence. 2012)
    Exercise speeds healing of subcutaneous wounds in obesity. This was allegedly observed only in obese rodents, but since the underlying mechanism was neither mediated by gene or protein expression of proinflammatory cytokines interleukin-1A and tumor necrosis factor-alpha or the anti-inflammatory cytokine interleukin-10 in the wounds, I felt it was still worth mentioning, also because it is, as the scientists point out,
    "the first report of an exercise effect on wound healing that is unrelated to alterations in wound site inflammation." (Pence. 2012) 
    Future trials will have to elucidate whether clotting and homeostasis, which occur in the earliest stage of wound healing, approximately 30 min after the trauma may be involved in this phenomenon.

    In this context, some of you will probably remember my recent post on the "Antithrombotic effects of caffeine blunt platelet activity in response to interval training" that exercise increases the tendency of your blood to clot - a tendency that does obviously come handy, when you are bleeding. That the increase in coagulation factors came into effect only in the obese, yet not in the normal weight control, in turn, could be related to the presence of existing hemostastic imbalances due to obesity which would have been corrected by the 30min of treadmill running the rodents in the exercise groups performed at a pace of 12 m/min on a 5% incline for the final 30 min of the light period (0930–1000 h), three days before until five days after the wounding.

    A bunch of maggots on a diabetic wound.
    Be that as it may, there are more than enough sedentary, "SAD dieting" (and the standard high fat diet rodents are fed in studies like this is nothing but a clone of the S-tandard A-merican D-diet) full-blown or pre-diabetic obese human beings who could likewise benefit from as little as 30min of daily aerobic activity. I mean think about it, if you could thus avoid having 50-100 maggots being placed on those nasty diabetic wounds (see picture on the right) that would never heal without those tiny critters secreting their salivary juices onto the wound to liquefy and subsequently ingest and further degrade the dead tissue in their gut, you can hardly argue that this is too much to ask for, can you?



    "Rust proof" athletes don't need vitamin pills with copious amounts of anti-oxidants and don't have to be afraid of fruit with their synergistic blend of small, but highly effective and synergistic amounts of vitamins and polyphenols, either.
    Oxidation proof after 1 year+ of regular aerobic + anaerobic training. According to a paper that's soon going to be published in Medicine & Science in Sports & Exercise trained athletes between the ages of 21 and 35yrs who had been participating in a structured exercise training program (including both aerobic and anaerobic) for the past 12 months, with each session lasting no less than 45 min per session, as well as no less than three sessions per week, are virtually "rust proof".

    That's at least my allegedly nonchalant interpretation of the non-existent increases in serum markers of oxidation the scientists from the University of Memphis observed in their 12 male subjects (BMI 25kg/m², body fat 12.8%; VO2Max 20 ml/kg/min) in response to four training sessions separated by 1 wk.

    The Sessions were counterbalanced and included either a no-exercise condition (subjects simply rested for the entire period) or one of the these three:
    • MISS - moderate intensity + duration steady state: 70% HR reserve for 60min; total time: 60min with 60min of actual work
    • HIIT - high intensity + moderate duration interval sprints: 5x60s at 100% + 225s recovery yielding a 1:3.75 work-to-rest ratio ("Within each interval, subjects were instructed to pedal between 80 and 100 rpm for the first 45 s, and then for the final 15 s, subjects were instructed to pedal as fast as possible"); total time: 20 min with 300s of actual work
    • MaxIIT - maximal intensity + short duration interval: 10x15s at a wattage of 200% of VO2max, followed by 116s of recovery (1:7.7 work-to-rest ratio); total time: 20 min with 150s of actual work
    All exercise bouts were performed on the same cycle ergometer used for the GXT, and subjects reported to the laboratory in the morning (0600–0900 h) after a minimum 10-h overnight fast. The HR was continuously monitored via Polar (TM) HR monitors and blood was drawn at the end of the 20-min rest period  (corresponding to the immediate postexercise blood samples) and 30 and 60 min after the 20-min rest period (corresponding to the postexercise blood samples).
    Figure 3: Total antioxidant capacity (TEAC), SOD, CAT and GPx values immediately (0min), 30min and 60min after the respective exercise bouts (data based on Farney. 2012)

    The respective total work performed during the trials was 461.1kJ, 96.9kJ, 96.9kJ for the MISS, HIIT and MaxIIT trials, respectively, the perceived exertion was highest in the MaxIIT trial (16.7 vs. 15.6 for HIIT and 13.5 for MISS), while the maximal heart rate 171.7bpm was achieved in the HIIT trial. Still,
    "No differences were noted in malondialdehyde, H2O2, advanced oxidation protein product, or NOx between conditions or across time (P > 0.05) [while the a]ntioxidant capacity was generally highest at 30 and 60 min after exercise and lowest at 0 min after exercise." (Farney. 2012; my emphases)
    If you will, you could even go one step further and argue that the total antioxidant capacity increases in well-rested, well conditioned athletes in response to exhaustive exercise bouts. Though, this increase reaches statistical significance in the MaxIIT trial only (see figure 3).
    Hungry for more news? Visit the SuppVersity on Facebook!
    That's it for today, ... but only as far as SuppVersity posts go. In about 2h at 1PM (EST), to be precise you can - if you want - listen to me on Super Human Radio. I am going to pick up on the topic of the first hour which is "Moderate Alcohol Consumption how (Un-)Healthy is it really" and do my best to provide some insights into the discrepancy that exists between reliable scientific evidence, the media coverage on the topic and Mr Average Joe's interpretation of the latter. And if you ain't into booze, just work out ;-) [update: download the podcast]

    References:
    • Farney TM, McCarthy CG, Canale RE, Schilling BK, Whitehead PN, Bloomer RJ. Absence of blood oxidative stress in trained men after strenuous exercise. Med Sci Sports Exerc. 2012 Oct;44(10):1855-63.
    • Pence BD, Dipietro LA, Woods JA. Exercise Speeds Cutaneous Wound Healing in High-Fat Diet-Induced Obese Mice. Med Sci Sports Exerc. 2012 Oct;44(10):1846-1854.
    • Rakobowchuk M, Harris E, Taylor A, Cubbon RM, Birch KM. Moderate and heavy metabolic stress interval training improve arterial stiffness and heart rate dynamics in humans. Eur J Appl Physiol. 2012 Sep 16.
    • Turner AP, Cathcart AJ, Parker ME, Butterworth C, Wilson J, Ward SA (2006) Oxygen uptake and muscle desaturation kinetics during intermittent cycling. Med Sci Sports Exerc 38:492–503.
    • Webner D, Duprey KM, Drezner JA, Cronholm P, Roberts WO. Sudden cardiac arrest and death in United States marathons. Med Sci Sports Exerc. 2012 Oct;44(10):1843-5.
    • Zebrowska A, Waśkiewicz Z, Zając A, Gąsior Z, Galbo H, Langfort J. IGF-1 Response to Arm Exercise with Eccentric and Concentric Muscle Contractions in Resistance-Trained Athletes with Left Ventricular Hypertrophy. Int J Sports Med. 2012 Sep 7.

    Green Tea Extracts, Athletes and a Preliminary Answer to the Question: "Are Anti-Oxidants For Athletes Not?" No True Benefits or Negative Effects of 1g GTE in Sprinters

    The supplement that was used in the study at hand was a commercially available product from Olimp Labs, a Polish producer of bodybuilding and fitness supplements.
    Before I even go into more detail, I would like to point out that the study today's SuppVersity article will talk about is not able to answer the question whether anti-oxidants are for athletes once and for all. Why? Well, the subjects in the recently conducted experiment by Ewa Jówko, Barbara Długołecka, Beata Makaruk and Igor Cieslinski were sprinters from a University Sports Club, and they received a green tea supplement - so who can guarantee that a bodybuilder taking vitamin C would not have a totally different reaction to a totally different anti-oxidant?

    No one can and that's why I'd like to ask you to go back to some of the previous articles on that matter and remind yourself that there is evidence that the provision of significant amounts of supplemental antioxidant can blunt the beneficial adaptive response to exercise (learn more and even more).
    Learn more about hormesis and potential neg. effects of antioxidants at the SuppVersity

    Is Vitamin E Good for the Sedentary Slob, Only?

    NAC Impairs Anabolic Effects of Exercise

    Vitamin C + E Hamper Gains in the Elderly

    C+E Useless or Detrimental for Healthy People

    Vitamin C and Glucose Management?

    Antiox. & Health Benefits Don't Correlate
    Apropos "significant amounts"! If we take a look at the amount of green tea extract, the 16 male sprinters (21.6 y; 76.9kg; 11.8% body fat) received, a question arises: Are 2x250 mg of standardized GTE (245 mg polyphenols, including 200 mg catechins, among them 137 mg epigallocatechin-3-galate) a "significant amount" of green tea extract (GTE) if they are consumed twice daily?

    I guess there may be supplement junkies out there who consume way more than this 1g of green tea extract everyday. Based on the dosages in studies that report beneficial effects of GTE, 1g is yet already on the high(er) side of the dosing continuum and thus unquestionably a "significant amount" of green tea extract, which was administered in a randomized controlled crossover study that was conducted during preparatory phase of yearly training cycle (after transition period) of the sprinters all of whom had more than 4 years of training experience.
    What do the latest reviews say about exercise + antioxidant supplementation? In spite of the fact that you will find reviews with different undertones, the vast majority of reviewers concludes that convincing evidence of the long-assumed benefits of anti-oxidant supplementation does not exist.Whether this warrants conclusions as the one Mari Carmen Gomez-Cabrera, Michael Ristow and Jose Viña formulate in their 2012 paper(s) and "the vast majority of experimental evidence clearly advises against this supplementation" (Gomez-Cabrera. 2014), however is still a matter of open debate (Holloszy. 2012).
    The two 4-week treatment periods (during which half of the subjects received GTE and the other half PL, and vice versa) were separated by a 4-week washout period. The duration of the washout period was selected based on the results of one previous study (Brown. 2011), in which 6-week supplementation with higher amounts of catechins (800 mg/day) was used on obese subjects. In view of the fact that the plasma catechin concentration in this study returned to its baseline level after at least 2 weeks of washout period, we can safely assume that a 6-week washout in highly active non-obese individuals should be enough to get rid of all the effects of only 250mg of catechins.
    Both GTE and PL were administered in the form of dark gelatin capsules (Olimp Labs, De˛bica, Poland), identical in appearance (i.e., size, shape, and color); the same dosage regimen was used (two capsules twice a day). One GTP capsule contained 250 mg of standardized GTE (245 mg polyphenols, including 200 mg catechins, among them 137 mg epigallocatechin-3-galate) and additional substances (maltodextrin, microcrystalline cellulose, and magnesium stearate). Therefore, each participant was administered 980 mg polyphenols daily. PL capsules contained microcrystalline cellulose, magnesium stearate, and maltodextrin instead of GTP."
    Compliance was measured by counting the capsules the subjects returned. Participants who returned no more than 15 % of their capsule dose were classified as "compliant". At the end of each of the two 4-week treatment periods, the sprinters performed a repeated cycle sprint test (RST) on a cycle ergometer (Ergomedic 839E, Monark, Sweden).
    Based on the food logs, the scientists decided that there were no significant nutritional differences between the two phases of the study (Jówko. 2014)
    Dietary standardization: The participants were asked to not modify their diet for the duration of the study, except for refraining from consuming any products containing green tea and limiting the intake of caffeine-containing drinks to one cup per day. Moreover, they were asked to maintain a similar
    diet for both treatment periods. During both the first and the second treatment periods (during 7 days preceding each RST), the participants filled out a 3-day dietary record (covering 2 week days and 1 day of the week end).
    The test consisted of four consecutive 15-s bouts (4 x 15 s), each of them with base set according to the Wingate procedure and separated by 1-min rest intervals. The subjects were asked to cycle for 15 s, as fast as possible, against a constant load (75 g/kg body weight).

    The performance tests were performed in the morning following 12-hovernight fast, at air temperature between 19 and 21°C and with 40–60 % relative humidity. The subjects were instructed to not perform hard physical training for 48 h and avoid drinking tea and caffeinated beverages within
    24 h prior to each of the RSTs.
    Figure 1: Changes in blood indices of acid–base balance & lactate concentration induced by the repeated sprint test (49 x15 s) in sprinters (n=16) after 4-week supplementation with placebo (PL) or green tea extract (GTE; Jówko. 2014)
    As you can see in Figure 1, there were no treatment (only time) effects as far as the acute changes in blood indices of acid–base balance and plasma lactate concentration are concerned. Against that background it's not surprising that there were no changes in the performance results of the repeated sprint test, either. Peak power, mean power, total work output, and fatigue index during the Wingate protocol were identical.
    Table 1: Changes in blood parameters of oxidative stress and muscle damage induced by the repeated sprint test (49 x15 s) in sprinters (n=16) after 4-week supplementation with placebo (PL) or green tea extract (GTE; Jówko. 2014)
    An observation that certainly raises the question, whether the treatment effects that were observed for the total antioxidant capacity and Superoxide Dismutase (SOD) levels (see Table 2) are even physiologically significant. Personally, I'd say no, because higher TAC and SOD levels have no health or performance value on their own.
    Previous studies suggest that NAC impairs the adaptive response to exercise | learn more
    Bottom line: In spite of the fact that the study at hand does not provide evidence that the commonly assumed beneficial ergogenic effects of green tea supplements exists, the results are still good news for green tea supplement users. They do after all suggest that the provision of significant amounts of anti-oxidant catechins does not appear to hamper the adaptive response to exercise.

    In that, it's important to mention that the study at hand acquits only green tea, yet not vitamin C, NAC & co which act via different mechanisms of the charge of having potentially detrimental effects on the adaptive response of athletes, average joes and/or obese type II diabetics... and just to remind you: Theoretically the response of all three of them could be totally different | comment on Facebook!
    Reference:
    • Brown, A. L., et al. "Health effects of green tea catechins in overweight and obese men: a randomised controlled cross-over trial." British Journal of Nutrition 106.12 (2011): 1880-1889.
    • Gomez-Cabrera, Mari Carmen, Michael Ristow, and Jose Viña. "Antioxidant supplements in exercise: worse than useless?." American Journal of Physiology-Endocrinology and Metabolism 302.4 (2012): E476-E477. 
    • Holloszy, J. O., et al. "Response to letter to the editor by Gomez-Cabrera et al." American Journal of Physiology Endocrinology and Metabolism 302 (2012): E478-E479.
    • Jówko, Ewa, et al. "The effect of green tea extract supplementation on exercise-induced oxidative stress parameters in male sprinters." European Journal of Nutrition (2014): 1-9.

    2g Vitamin C Ameliorate Low Testosterone Levels and Sexual Dysfunction in Diabetic Rats. Usefulness in Normoglycemic Individuals Still Questionable.

    Illustration 1: In view of the increase in renal
    vitamin C clearance with higher plasma levels
    (Friedmann. 1940), it may be sensible to use a
    time-released vitamin C formula, or, even
    better, eat a serving of veggies or fruits that
    are high in vitamin C multiple times a day
    Yes, I know, supplemental vitamin C does not ward off the common cold... the same applies for taking super high doses of vitamin C as antioxidant buffers before or around workouts. In fact, studies have shown that the antioxidant overkill of a combination of vitamin C and other powerful antioxidants could negate the beneficial effects exercise has on human blood glucose management. Now, a group of Brazilian scientists has published a rodent study that seems to suggest that in the absence of exercise the addition of 2g (human equivalent for 80kg male) of vitamin C to your diet could partially restore sexually function and increase testosterone levels in diabetic patients (Fernandez. 2011).

    In their study, the Fernandez et al. had fed 10 out of 20 hyperglycemic rats vitamin C enriched chow (+150mg) and found that the addition of the water-soluble vitamin had beneficial effects on oxidative strees biomarkers in the erythrocytes, which have proven to be a valuable indicator of stress levels for the whole body (Naziroğlu. 2001; Garg. 2000)] (cf. figure 1),
    Figure 1: Stress markers TBARS, SOD, GSHt and GSH/Px in hyperglycemic rats after 30 days on normal (placebo) and vitamin C enriched chow; data expressed relative to normoglycemic controls (data adapted from Fernandez. 2011)
    as well as reproductive organ weights, sperm parameters, plasma hormone levels (FSH, LH and testosterone), testicular and epididymal histo-morphometry and histopathology.of the hyperglycemic rats (cf. figure 2).
    Figure 2: Organ weights (*visceral fat / 100g), reproductive hormones and sperm number and quality in hyperglycemic rats after 30 days on normal (placebo) or vitamin C enriched chow; values expressed relative to normoglycemic control (data adapted from Fernandez. 2011)
    Vitamin C supplemented or not, compared to the normoglycemic control,  the diabetic rats must still be regarded as partially impotent and overall sickly, which is an observation the scientists omit, when they conclude
    [...] the present study showed that vitamin C supplementation minimized some alterations in the male reproductive system caused by hyperglycemia such as reduction of testosterone and LH levels and impairment in sperm morphology. [italicization by Dr. Andro]
    After all, what's the worth of a "minimizing" the negative effect on testosterone levels to  -71%? This may be 10% less damage than without vitamin C, but wouldn't it be much better not to get yourself into such a misery in the first place?
    Note! Not everything that is good for sick people makes a viable addition to the supplementation regimen of a healthy or even athletic person. Even Fernandes and her co-workers emphasize that "is possible that the beneficial effects of vitamin C supplementation are only relevant to those individuals with low levels of vitamin C and high levels of oxidative stress that occur in hyperglycemic condition."
    Well, regular exercise and the avoidance of high fructose corn syrup and the other sweet suspects you poise yourself with on a daily basis would be the way to go - and you know that!