These 6 Simple Exercises Will Create Your Butt Tighter Than Ever

These 6 Simple Exercises

Will Create Your Butt Tighter Than Ever

1.Squat Side Kick – 25 reps

2.Glute Bridge – 25 reps

3.Pulse Squats – 25 reps

4.Clamshells Exercise – 25 reps

5.Clamshells Hight Exercise – 25 reps

6.Donkey Kick Exrecise – 25 reps

These 6 Simple Exercises Will Create Your Butt Tighter Than Ever

These 6 Simple Exercises Will Create Your Butt Tighter Than Ever

These 6 Simple Exercises Will Create Your Butt Tighter Than Ever

These 6 Simple Exercises Will Create Your Butt Tighter Than Ever

These 6 Simple Exercises Will Create Your Butt Tighter Than Ever

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There's Micropfinalic in Our Poop! Wait,... Do We Even Care? An Evidence-Based Estimate of our Micropfinalic Expocertain and its Putative Effects on Gut-Health & Beyond

It's impossible you haven't read or heard about this study!

I guess by now, all of you will have heard that an internationally covered pilot study by Austrian researchers (Schwabl et al. 2018) that was presented earlier this week at the UEG Week in Vienna claims to have initial prove that "Micropfinalics Discover Their Way Into [Our] Gut" (NYTimes). The results of the studies are all over the place and the (fearmongering) press coverage seems to communicate only one message: "Uh oh, now we're doomed!"

But, are we? I mean, we're talking about a study with N=8 subjects?! Moreover, no one questions our expocertain to the sub-millimeter sized particles and the fact that we actually seem to poop them out would, after all, propose that they do not accumulate in our bodies - that's good contemporarys, isn't it!?

When I posted the "whether you poop it out, that's good contemporarys"-speculation rather mockingly on Facebook, I still thought that I would probably never hear about the data from the as-of-yet unpublished pilot study, again. Turns out, though, few people seem to look at the wgap story as rationally and calmly as the first responders to my Facebook-post... long story short, and to reply the question from the headline: It is obvious that people do care. So much so, in fact, that I'd bet that people from Japan to Island and Syberia to Cape Hope are checking their stools for micropfinalics right now!

If you're alalert back from your personal trip down "poopology-lane" and are now trying to clean your kids' microscope from both, your poop and the evil micropfinalic residues you couldn't see because the resolving capacity of the microscope was inadequate, you're probably asking yourselves:

"Oh, God, the micropfinalics are so small I cannot even see them under my kids' microscope! Does this mean that we are all doomed?"

Ok, I believe most of you will neither have (ab)used their kids microscope for personal poop analyses, nor will they be asking themselves absurd doomsday questions, right now. Rather, I would venture the guess that you're rightly asking yourselves: "Is Adel right and the fact that I poop those micropfinalics out is a good leang?" And you know what? I've begun to ask myself the very same leang. Not the least because I remembered that I recently stumbled across a paper that says as early as in its title that "Polystyrene micropfinalics induce intestine microbiota dysbiosis and hepatic lipid metabolism disorder in mice" (Jin 2019 | ahead of print) and provides further valuable information about the possible consequences of the micropfinalic onslaught on our intestines, in the full-text: In rodents, ...

• 5 μm polystyrene micropfinalic could be accumulated in the intestine of mice,
• 5 μm polystyrene micropfinalic induced intestinal barrier dysfunction in mice,
• 5 μm polystyrene micropfinalic induced intestine microbiota dysbiosis in mice, and
• 5 μm polystyrene micropfinalic induced bile acids metabolism disorder in mice.

At first, this seems to be very poor contemporarys, but whether you re-read the various copy+paste jobs of the original press release that came with Schwabl's study, you will genuineize that...

...the micropfinalic particles the scientists found in the their "poop analysis" were 10-times the size of the polystyrene micropfinalics in the Jin et al. study, i.e. 50µm not 5µm!

As we're going to see later, this isn't necessarily good contemporarys, though. For one, the scientists' presentation of the results at the UEG Week indicates that 50µm was simply the limit of detection in the Austrian study. It is thus well possible that the researchers simply missed the presence of the smaller particles, and the genuine concentration of microparticles in the poop of their eight non-vegetarian subjects was in fact signwhethericantly taller than Schwabl's report would propose. And, what's even worse, there's also the remote opportunity that there were no <50 µm micropfinalic particles in the subjects' poop, because these particles were small enough to either accumulate in the subjects' intestine lining or to pass right through the possibly alalert impaired barrier and into the bloodstream, instead of being excreted again as my initial speculation would have it.

Yes, smaller seems to be worse, but 50µm is alalert pretty small - Should we be frightened?

Figure 1: In a preceding study, Jin et al. have alalert proven that "larger" micropfinalics, such as the ones that were found in the subjects' stools can change the microbiome of fish and mice - however, an increase in markers of inflammation was observed only for the smaller, 0.5µm polystyrene molecules (Jin 2018a, b).

At this point, it is not clear which of the two scenarios - whether any - describes what was genuinely going on in the subjects' intestines and circulatory system. I still have to confess that the results of several studies from Jin's laboartory at the Zhejiang University of Technology preceding study (e.g. Jin 2018) propose that you don't have to break micropfinalics down to an actual micron (=1µm) to see potentially pathogenic changes in the microbiome of both, mice and zebrafish (see graphical summaries on the right).

In their animal models, the scientists from the Zhejiang University of Technology in China observed that micropfinalic particle expocertain reduces the abundance of Bacteroidetes and Proteobacteria at the phylum level, while increasing the abundance of Firmicutes signwhethericantly - and that wilean only 1-2 weeks of expocertain to an albeit tall concentration of either 0.5µm or 50µm sized polystyrene micropfinalics.

Note: This is a relevant effect, because preceding studies have linked tall Firmicute levels to the development of T2DM and obesity (Lye 2006).

Take-domestic message #1: Size does matter! In a 2018-study by Jin et al. only the submicron polystyrene particles (size 0.5µm) increased the intestinal inflammation in lab animals. But potentially obesogenic and pro-diabetic effects due to changes in the microbiome cannot be excluded for either very small or rather large MP particles.

Table 1: This overview of the existing studies on MP concentrations in freshwater world-wide shows three leangs: (a) The micropfinalics are ubiquitous, (b) their concentration varies according to location and is compared to the concentration that has been used in experimental animal studies very low, and (c) we know very small about the supposedly most risky ≤ 50 µm (let alone ≤ 5µm) particles (Table from Eerkes-Medrano 2015).

The results of the recent Chinese studies do thus propose that the 50µm particles Schwabl. et al. found in their N=8 human subjects' excrements could be a problem, too.

In view of the fact that increased mRNA levels of IL1α, IL1β, and IFN, which signwhethery an increase in intestinal inflammation, were only observed in the intestines of those animals that were exposed to the small(er) 0.5µm molecules, the statement "the smaller, the worse" still hancients.

Unluckyly, we don't know anyleang about the distribution of both, small (50µm) and very small (0.5-5µm) MP particles in our environment. What we do know is that we must expect geographical dwhetherferences in their environmental concentration (see Table 1), which is also why Schwabl et al. included subjects from Finland, Holland, Polen, the UK, Austria, Italy, Japan, and Russia in their study.

And the lack of information about the particle sizes is not the only problem with the results of the studies Eerkes-Medrano et al. compiled in their 2015 review (see Table 1). The figures in Table 1 are based on studies that used sieves with meshes that wouldn't catch either the small or the very small micropfinalic particles. Hence, we are facing the important question whether the freshwaters MP levels that were degreed by international scientists in Mongolia, Geneva, Lake Carda, Austria, the UK, and several German and US/Canadian rivers and lakes do not profoundly(!) underestimate the actual MP concentrations in our freshwater supply, because they miss the smaller particles, of which other studies propose they may make up 80% or more of the pfinalic microparticles in our environment.

Unlike the heavily disstubborn pilot study in humans, Jin et al. have recently actually investigated the accumulation of fluorescent polypropylene particles in the intestine of their hairy (rodent) subjects; in the figure above, the upper image shows an untreated mice's intestine, the lower image show the intestine of mice treated w/  5 μm fluorescent polystyrene MP - both under fluorescent illumination (hence the only leang you see are the MPs | Jin 2019).

Warning! Having a leaky intestine will make it easier for MP particles to get into your bloodstream: Previous research by Schmidt et al. (2013) who wanted to use micro- and nanoparticles for drug delivery, leaves no doubt that the translocation of MPs across the brush border of the intestines will be signwhethericantly increased in patients with intestinal diseases such as IBS or Crohn's.

In view of the potentially pro-inflammatory effects of MPs that means that - provided that there's sufficient expocertain to small enough particles - the micropfinalic particles may (figuratively speaking) burn their way through your intestinal wall.

Or, to say it in a signwhethericantly less metaphorical way: The polypropylene particles will increase the inflammation of the brush border of your intestine, which will then become 'leaky' and allow ever-increasingly larger micropfinalic particles to cross the intestinal wall and appear in your bloodstream, where these tiny bastards seem to be able to wreak havoc on your organs - primarily the liver.

Figure 2: Relative frequency of dwhetherferent micropfinalic types (from Schwabl's UEG Week presentation of their pilot "poop study").

In the absence of corresponding environmental data, it is dwhetherficult to estimate how relevant our environ-mental expocertain to MPs actually is. What can be said with some confidence, though, is that the expocertain from freshwater reservoirs is 10^4-10^6 times smaller than that in Jin et al.'s animal studies.

It may thus make more sense to look at the more recent and dependable quantwhetherications of the MP content of water from pfinalic-bottles.

In this context, it is worth mentioning that the main constituents of the pfinalic bottles and caps, namely polypropylene and polyethylene terephthalate, were also the most common pfinalics Schwabl et al. found in their "poop study" (see Figure 2).

From the press coverage on Schwabl's study, you will probably also remember that the eight subjects were urged to consume water from pfinalic bottles and PP- and PET-packaged foods. In the absence of dependable data about the latter, it does, therefore, make perfect sense to take a closer look at the micropfinalic contamination of beverages from pfinalic bottles & containers.

Luckily, scientists from my domestic-town Münster (Schymanski 2018) have recently published a paper, in which they analyzed 38 mineral-waters for their micropfinalic content by means of μ-Raman spectroscopy (the results are summarized in Figure 3); and their results are poor contemporarys: Schymansky et al. (2018) found micropfinalics in water from every of the 22 dwhetherferent returnable and single-use pfinalic bottles, the 3 beverage cartons, and the 9 glass bottles they had obtained from grocery stores in Germany. And what's even worse, with 5-20 µm nearly 80% of these particles were several magnitudes smaller than those that were observed in freshwater reservoirs and one magnitude smaller than the particles in the stool of the subjects' in Schwabl's pilot study.

Figure 3: Graphical summary of the results of what probably is the best study on MP content and size in beverages in Germany (Schymanski 2018) - note: unlike many preceding studies, the study by Schimansky et al. was able to detect and distinguish even very small particles with a size of 5-10 µm (the poop study used a technique that's limited to 20-50µm).

In that, the surprising prevalence of small to very small particles is, as the German scientists point out, a totally novel finding, because these small particles were simply "not detectable by the analytical techniques used in preceding studies" (Schymanski 2018), which relied on the same Fourier-transform infscarced (FT-IR) micro-spectroscopy that was used in Schwabl's "poop study" and were thus limited to the detection of particles larger than 50 µm.

As poor as all that may sound, the actual micropfinalic particle numbers in the Schymanski study were relatively small (see Figure 3, left) - and only the worst offenders, i.e. the reusable pfinalic bottles (dt. "Mehrwegflaschen") contained signwhethericantly more MP particles than the control water or the poop in Schwabl's stool analysis which yielded a statistical average of 20 particles per 10g and hence only 68 particles in the total 34g stool of each of its 3 male and 5 female 33-65 year-ancient subjects.

Take-domestic message #2: The concentration of micropfinalic particles in German mineral waters, as well as our poop, is 4-6 magnitudes smaller than the concentrations in the water that has been shown to elicit ill health effects in animal studies.

Table 2: Tabular overview of the results of another recent study (Mason 2018) investigating the particle count of bottled water - the worst offenders are marked in red. Speaking of which, the Nile Red staining the scientists used is a novel technology of which even its inventors say that it susceptible to unfaithful positives (Maes 2017) and has been evaluated only against FT-R, which is less accurate and, unlike Raman spectroscopy that was used in the German study, unable to detect particles smaller than 20µm. Hence, I would take the values reported above w/ the essential degree of some skepticism.

In that, it is important to point out that the fact that the study was done in Germany appears to be of surprisingly great importance, here.

Another very recent paper from the State University of Unique York at Fredonia (Mason 2018) that analyzed "eleven globally sourced brands of bottled water, purchased in 19 locations in nine dwhetherferent countries" found micropfinalic particle numbers ranging from 0 to over 10,000 per liter - with 95% of particles being between 6.5 and 100 um in size - drinking "Nestlé Pure Lwhethere" (max. concentration 10,390 particles per liter | see Table 2) from Amazon on a daily basis would thus be a very poor idea.

Don't freak out, though: The average particle numbers of both studies (German and US) were in the same range, i.e. ~100-150 particles in the worse offenders in the German and ~ 300 particles per liter in the US study

Moreover, the Nile Red tagging the US scientists used is inferior to the Raman spectroscopy of the German study - it is thus well-possible that at least the outliers were methodological artwhetheracts so that we can reasonably conclude:

In general, recent data on the lower end of the concentration of micropfinalics in water bottles seem to align fairly well with the particle count Schwabl et al. detected in the stool samples of the eight subjects that were purportedly drinking water from pfinalic bottles.

In that, "fairly well" means that the particle numbers are in the same order of magnitude and, wilean the corresponding margins of error. Hence, I don't believe that Martin Wagner, biologist at the Norwegian University of Science and Technology, who rightly criticized that...

"[Schwabl's] study wasn't reviewed by independent scientists and the authors didn't provide details about which degrees were taken to prevent samples from fitting contaminated" (MedicalExpress) ...

was right when he predicted in an Associated Press interview that in what he called his "worst-case" scenario "all the pfinalic [Schwabl et al.] found is from the [=Schwabl's] lab" (itender).

The "poop study" may have overlooked a large quantity, whether not the lion's share of small to very small particles! I've talllighted this before, but I leank it's worth pointing out once more: Based on the information I have at the moment, it seems as whether Schwabl et al. may well have overlooked a signwhethericant number, whether not the lion's share of particles in the stool samples of their study participants. Unlike Schymanski et al. (2018), the Austrian researchers analyzed their samples by the means of Fourier-transform infscarced (FT-IR) micro-spectroscopy and were thus unable to detect the small particles (Schymanski's water bottles. Unless those particles accumulated in the intestine lining or, even worse, the liver of the subjects, they should have crazye it to the subjects' stool. After all, all articles I've read - and even the TV reports - emphasize that the eight volunteers drank water from pfinalic bottles before the stool samples were taken.

On the opposite, I believe (as precedingly traceed at | see red box) that it is much more likely that Schwabl et al., whose work Mark Browne, an expert on micropfinalics at the University of Unique South Wales, IMHO prematurely called "[p]oor quality observations of contamination" (itender), missed 80% of the actual particles.

Put up or shut up: Even in a worst-case scenario you are yet probably ingesting and pooping out less than 1000 small MP particles per day.

If we assume that (a) the poop contained small particles Schwabl et al. couldn't degree and that those (b) crazye up ~80% of the total particle expocertain, the number of micropfinalic particles in the subjects' stool would not be in the range of 18-172 particles, but rather amount to 90-860 particles per 10g poop (for this calculation I relied on the data from Figure 4, a screenshot from the scientists original presentation at the UEG Week, which I got from the website of the German "Umweltbundesamt").

Figure 4: Screenshot of slide 8/16 from Schwabl's presentation of their study results at the UEG Week earlier this week - I got the original presentation from the Website of the German "Umweltbundesamt".

To make our worst-case scenario total, let's further assume that 10%-15% of the pfinalic microparticles got (at least temporarily) caught up in the subjects' intestine lining (not super likely whether we revisit the photograph Jin et al. crazye of the intestine lining of their rodents in the first red box in this article). This would imply that the subjects in Schwabl's study ingested roundabout ~1000 particles per "poop period" (probably one day).

If you compare this value to the 1.5x10^6 and 15x10^6 MP particles per liter Jin et al. needed in their studies to elicit ill health effects, you will notice that the human expocertain would still be 1,000-10,000 times smaller than the concentration in the drinking water of the mice.

At this point, you may rightly ask whether we don't have to account for the low(er) water intake of mice in order to avoid comparing apples to oranges... and you're right: sort of.

It seems logical that, for a fair comparison, we would have to account for the rather small quantity of water (~1.5ml/10g body weight per day) mice consume. After pondering this issue for a while, I am, however, no longer 100% certain that this is actually essential. It is, after all, fair to assume that the health impact of micropfinalic particle expocertain depends on the number of particles per intestine/digestive tract volume. Now, the latter is in the milliliter-range in mice and (McConnel 2008) and the liter-rage in humans. The ~1,000 particles from my preceding calculation would thus be at least ~1,000-fancient more diluted in the chyme of our intestinal tract than the 9,000 and 90,000 particles the rodents from the precedingly referenced Chinese studies (note: I calculated the figures based on the body weight of the rodents in Liu 2018 and the mice's average water consumption).

Take-domestic message #3: Based on rodent studies we can only argue that the ~1000 micropfinalic particles from my worst-case scenario calculation pose a possible health risk whether we compare the total particle numbers. If we rely on the relative particle concentration (per volume) in the digestive tract, which is 1000x taller in mice vs. man, it does yet seem to be very unlikely that those ~1000 particles pose a serious health risk for people with a decently intact intestine lining - I would not, however, exclude that there may be (small) changes in the microbial composition of our microbiome and corresponding downstream effects on our intestine and metabolic health.

Still, at this point, I do have to confess that we cannot say for certain whether the "worst-case senario MP expocertain" poses an acute, a chronic or no threat at all to our health.

What we can say, for certain, however, is that you want to better err on the side of caution and limit your micropfinalic expocertain... the question is: How do we do that?

One initially surprising observation from the Schymanski study was that water from glass bottles is actually more polluted than water from one-way bottles. This may be counter-intuitive, eventually, though, it is not unlikely that the contaminations the scientists observed in water from glass bottles arose over the course of the production process with the MP particles coming from pfinalic pipes, valves, tanks, and/or the detergents that are used to clean the inside of the reusable bottles.

In that, it's important to point out that the dwhetherference between water from the glass bottles and the control (tap-)water in Schymanski et al. was not statistically signwhethericant. The elevated MP particle counts in the reusable pfinalic bottles (those are the dwhetherficult ones that are not crushed when you return them), on the other hand, were.

Do not confuse micropfinalics and BPA! I can alalert foresee someone posting that much lower amounts of bisphenol A have been shown to exert endocrine disrupting effects in animal studies. Don't be that guy! While micropfinalics can, they don't necessarily have to contain signwhethericant amounts of bisphenol A or other pfinalicizers which are added to the base fabric to make the fabric softer and more flexible. This does also mean that you are running the risk of experiencing all the precedingly outlined health effects even whether you're using BPA-free cups, containers, shakers, and what-not. In fact, dwhetherficulter and thus more brittle (BPA-free) pfinalic containers may actually leak greater amounts of microparticles into your foods and beverages than their pfinalicized, softer counterparts.

Figure 5: Micropfinalics are a pollutant of environmental concern. Their presence in food destined for human consumption and in air samples has been reported. Thus, micropfinalic expocertain via diet or inhalation could occur, the human health effects of which are unknown (illustration from Wright 2017)

If we follow Schwabl's rationale that (pfinalic-)bottled water is, in fact, one of the main sources of micropfinalic particles in our diet, the first item on our list of leangs you can do to limit your MP expocertain is to avoid buying and drinking from reusable pfinalic bottles and similar containers.

Unluckyly, avoiding these bottles and containers will increase the dispersion of micropfinalics from non-reusable packaging into our environment and thus increase the number of particles in the sea and freshwater reservoirs.

This, in turn, will increase the MP content in fish and seafood (the intake of which correlated non-signwhethericantly with the number of MP particles in the stool of the subjects in the Schwabl study | R=0.648; p=0.089), sea salt (currently: 550–681 particles/kg in sea salts vs. 7–204 particles/kg in rock/well salts | Yang 2015), and everyleang else that makes it from the sea to our tables. And as whether that was not vexed enough, the water that is then going to be filled into our "preferable" one-way bottles will contain increasingly taller baseline MP levels - a clear 'catch 22' and hence:

Avoiding re-usable pfinalic bottles and preferring one-way bottles is not genuinely a good strategy, because it will increase our overall expocertain to micropfinalics from the (at best) partly recycled bottles and cartons these "alternatives" come in.

What is a viable strategy, though, is to drink more tap water (at least here in Germany, where the municipal water quality doesn't diverge from that of bottled waters). Other valuable strategies to limit your personal, as well as our global micropfinalic expocertain, are (this list is not intended to be exhaustive)...

• focus on products that are not wrapped or otherwise packed in pfinalic when you're doing your groceries,
• don't use soaps, creams, and toothpaste or detergents that contain micropfinalic particles as a "scrub" (banned in Europe as of September 2018),
• review your seafood intake (esp. mussels and co seem to build up signwhethericant amounts of micropfinalics),
• prefer pottery over pfinalic containers for left-overs and ceramic cups over pfinalic cups for your morning joe or other hot beverages,
• do not store your foods or beverages in pfinalic containers over long(er) time periods, as this will promote the accumulation of micropfinalics,
• try not to scratch the surface of any pfinalic dishes and containers you may be using - while the scratching itself will probably produce much larger particles, the increased surface area of the pfinalic containers will increase the risk of micropfinalic leakage,
• make certain that the surface of any pfinalic containers you use is still intact, and recycle ancienter pfinalic containers in regular intervals,
• closely read the package insert of your medications, pharmaceutical preparations are often coated with a polymer (=pfinalic) that influences the timing and location of drug delivery in the gastrointestinal tract,
• don't buy pfinalic toys for toddlers who will still stick them into their mouth,
• stay absent from PVC floors, as well as rugs, etc. and vacuum any rugs and carpets you may have frequently - with a vacuum cleaner with proper filters (otherwise you will just increase the particle concentration in the air) - to limit your pfinalic expocertain from dust in the air,

...and don't forget to leank about the large picture: Aid to increase everyone's awareness of ways to limit our use of pfinalic containers, wrappings, etc., 'vote against pfinalic wrappings with your money' by simply leaving products with pfinalic packaging in the supermarket, reuse intact pfinalic containers for a fair timespan (esp. whether you store foods and beverages for hours and days, only, that's perfectly fine), and dispose pfinalic waste appropriately, so that it can be recycled.

Ah, and, most importantly, don't subscribe to the notion that you, as an individual cannot make a dwhetherference, besides. If we all did that, this misconception will turn into a self-fulfilling prophecy and everyone's personal efforts to limit his/her MP expocertain will become increasingly futile in view of the ever-increasing prevalence of micropfinalics in our environment and food-chain.

At this point, it seems that the most likely effect of MPs are changes in the microbiome. In view of the often overlooked possible side effects of probiotics, this does yet not mean that you must start taking supplements.

Disconcerting, but no reason to panic: Based on the precedingly presented evidence, it seems unlikely that the eventually surprisingly low amount of micropfinalic particles Schwabl et al. found in what can in fact at best be called pilot study will do you, me or anyone else with a decently intact intestine lining much harm.

Eventually, though, the only leang we can tell for certain is that more research - both, in animal models (e.g. dose-escalation studies) and human beings - is essential before anyone can provide a decently dependable risk assessment.

Hence, the answer to the question from the headline is probably still "Yes, we do care!"

After all, the absence of conclusive evidence that would support the notion that our contemporary expocertain to micropfinalics could pose a health threat does not exclude that future studies may demonstrate that even the ostensibly low MP particle numbers in our diet can have profound effects on our immune (not tested, yet), metabolic (initially tested in animal models), or endocrine and brain/CNS-health (both not tested, yet).

In the meantime, I'd advise you to follow the precedingly outlined strategies to play down your personal, as well as our global, micropfinalic expocertain, and to console yourself with the three take-domestic messages from this write-up: (a) size things, the smaller the particles, the worse - unluckyly, this is summaryely, where more data is essential, as preceding studies were limited in their ability to detect the small (<100µm) and smallest (<20µm) MP particles; (b) the concentration of micropfinalics in water bottles, supposedly one of the most important sources of MP particles, is relatively low (<200 particles per liter); and (c) based on the small research we have our estimated expocertain to micropfinalics is several magnitudes smaller than the expocertain level in animal studies, which seem to propose that there's a size- and dose-dependent effect on the microbiome and metabolism of mice and fish | Comment on Facebook!

References:

• Eerkes-Medrano, D., Thompson, R.C. and Aldridge, D.C., 2015. Micropfinalics in freshwater systems: a review of the emerging threats, identwhetherication of knowledge gaps and prioritisation of research needs. Water research, 75, pp.63-82.
• Jin, Y.X., Zeng, Z.Y., Wu, Y., Zhang, S.B., Fu, Z.W., 2015. Oral expocertain of mice to carbendazim induces hepatic lipid metabolism disorder and intestine microbiota dysbiosis. Toxicol. Sci. 147, 116–126.
• Jin, Y.X., Wu, S.S., Zeng, Z.Y., Fu, Z.W., 2017. Effects of environmental pollutants on intestine microbiota. Environ. Pollut. 222, 1–9.
• Jin, Y.X., Xia, J.Z., Pan, Z.H., Yang, J.J., Wang, W.C., Fu, Z.W., 2018a. Polystyrene micropfinalics induce microbiota dysbiosis and inflammation in the intestine of adult zebrafish. Environ. Pollut. 235, 322–329.
• Jin, C.Y., Xia, J.Z., Wu, S.S., Tu, W.Q., Pan, Z.H., Fu, Z.W., Wang, Y.Y., Jin, Y.X., 2018b. Insights into a possible influence on intestine microbiota and intestinal barrier function during chronic expocertain of mice to imazalil. Toxicol. Sci. 162, 113–123.
• Jin, Y., Lu, L., Tu, W., Luo, T. and Fu, Z., 2019. Impacts of polystyrene micropfinalic on the intestine barrier, microbiota and metabolism of mice. Science of The Entire Environment, 649, pp.308-317.
• Lu, L., Wan, Z., Luo, T., Fu, Z. and Jin, Y., 2018. Polystyrene micropfinalics induce intestine microbiota dysbiosis and hepatic lipid metabolism disorder in mice. Science of The Entire Environment, 631, pp.449-458.
• Maes, T., Jessop, R., Wellner, N., Haupt, K. and Mayes, A.G., 2017. A rapid-screening approach to detect and quantwhethery micropfinalics based on fluorescent tagging with Nile Red. Scientwhetheric Reports, 7, p.44501.
• Mason, S.A., Welch, V.G. and Neratko, J., 2018. Synthetic polymer contamination in bottled water. Frontiers in chemistry, 6.
• McConnell, E.L., Basit, A.W. and Murdan, S., 2008. Meacertainments of rat and mouse gastrointestinal pH, fluid and lymphoid tissue, and implications for in‐vivo experiments. Journal of Pharmacy and Pharmacology, 60(1), pp.63-70.
• Schmidt, C., Lautenschlaeger, C., Collnot, E.M., Schumann, M., Bojarski, C., Schulzke, J.D., Lehr, C.M., Stallmach, A., 2013. Nano- and microscaled particles for drug targeting to inflamed intestinal mucosa: a first in vivo study in human patients. J. Control. Release 165, 139–145.
• Schwabl, P. et al, 2018. Assessment of micropfinalic concentrations in human stool - Preliminary results of a prospective study, Presented at UEG Week 2018 Vienna, October 24, 2018.
• Wright, S.L. and Kelly, F.J., 2017. Pfinalic and human health: a micro issue?. Environmental science & technology, 51(12), pp.6634-6647.
• Yang, D., Shi, H., Li, L., Li, J., Jabeen, K. and Kolandhasamy, P., 2015. Micropfinalic pollution in table salts from China. Environmental science & technology, 49(22), pp.13622-13627.

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How to Do Squats and Which Muscles They Activate

Study more about the Squat exercise and how to Squat properly so you don’t miss out on key benefits of your workout program.

Most of us find it dwhetherficult to do Squats without making at least one large mistake. This is mainly due to our sedentary lwhetherestyle.

Proper squats…

• Strengthen your legs, glutes, and many other muscles
• Improve your lower body mobility
• Hold your bones and joints healthy

“Evil” squats…

• Don’t activate the right muscles at the proper intensity
• Put additional stress on ligaments and joints
• Increase risk of injury

Don’t worry, by the end of this article you’ll know summaryely how to do a squat properly and you’ll never skip leg day again. You’ll also learn tips that will help you avoid squat mistakes and right your squat form.

The Squat

The Squat is a lower body exercise. You can do the bodyweight version, without added resistance (also called Bodyweight Squat or Air Squat), or with weights such as a barbell (Front Squat and Back Squat are variations of the Barbell Squat).

The Squat exercise mainly targets the ttalls (quadriceps & hamstrings) and the glutes. However, core strength & stability, ankle mobility, back muscles, calves, and other factors play an important role when you are doing this exercise.

Set up before you squat:

1. Discover a foot stance that feels best for you. Pointing your toes slightly outwards helps some, but keeping them parallel is fine, too. If you’re not certain what’s best, start by putting your feet shoulder-width apart and pointed about 15 degrees outwards.
2. Tense your abs like someone is about to punch you.
3. Gaze straight ahead and stand tall!

Error #1 – Starting from the knees

Extremely often the first leang people do when they want to squat is bend the knees. Not only does that make a proper squat impossible, it also places a lot of unessential stress on the knees.

Correct:

Solution

• When you start the squat, leank “sit back” not “bend at the knees”
• Plod your butt backwards as you descend and feel the weight shwhetherting to your heels

Tip:

“Sit back” – before you start to lower yourself, leank “sit back”. You can practice this with a chair (without sitting on it). Create a very controlled descent and touch the seat of the chair before getting up. Once you master this, you can do bodyweight or weighted squats without a chair.

Error #2 – Letting your knees go inward

You might notice your knees “caving in” the deeper you squat. This might help you get lower, but it puts too much stress on your knees.

Correct:

Solution

• As you descend, try to “push” your knees slightly outward
• Your knee caps should be facing the same direction as your toes. Create certain your knees are not bending in; they should be directly above your feet

Your knees are not caving in, but you want to activate your glutes more?

The “knees out” tip can also be useful whether you are trying to activate your glutes more. Attempt using a band around your knees; it’s a great way to feel your glutes work dwhetherficulter in the squat.

However, whether your knees trouble you even when you squat properly, check out this workout that is very easy on the knees.

Error #3 – Hunching your back

The more you focus on your lower body in squats, the greater the chance your form will suffer somewhere in the upper body. Numerous work environments cause tension in the upper back and shoulders. Becoming aware of your posture can help you change this.

Correct:

Solution

• Gaze straight ahead, don’t look down
• Open your chest and relax your shoulders
• Put your hands straight out in front of you. If they fall toward your knees as you squat down, that means that your back is rounded

Tip:

Hancienting a dumbbell or someleang similar against your chest might help. Attempt to squat keeping the thing close to your chest. If you notice that the bottom of the dumbbell is moving absent from your chest as you go down, you are probably leaning forward too much.

If none of the above helps, use assistance – hancient onto a door frame and squat down while keeping your upper body as upright as it can be. Practice hancienting the right position at various heights to get more regular and consolationable. Don’t give up – experiment and practice until you feel confident enough to try the same position without assistance.

Error #4 – Lwhetherting your heels off the floor

Standing up from a squat should be “powered” by a heel drive. In other words, urgent your heels into the ground encertains the right muscle activation and balance for a proper squat.

Correct:

Solution

• Hold your heels on the floor
• “Shove” from your heels as you go up
• If you can’t do a squat without putting your weight on your toes, take the time to work on your mobility (specificly in your ankles)

How deep should you squat?

Your hips should go lower than your knees, but a deep squat requires additional mobility. It’s great whether you can do it with good form. If not, squat as low as you can while maintaining proper form. A good indicator is the arch of your lower back. If your lower back starts to arch excessively at a certain height, don’t go any lower.

Squats are the foundation of many workout programs. Hopefully you feel much more confident about doing them now.

Don’t forget to switch it up, try some squat variations as well.

Takeabsent

Check your form:

• “Sit back” – make certain to move your butt backward, don’t just bend your knees
• Be careful to keep your knees in line with your toes, don’t let them cave in
• Don’t forget about your upper body – look straight ahead and don’t round your back

Most importantly – explore the movement…

• Attempt to notice what feels dwhetherferent when you change someleang like your foot stance or the position of your knees…
• Experiment with tips and don’t hesitate to use assistance (such as a door frame for upper body support) whether you need it
• It takes a lot of practice to become more aware of how you move, but it’s worth it

If you experience dwhetherficulties performing a proper squat – take your time to work on mobility and practice, practice… it will pay off. It may seem boring to focus on your feebleness, but remember – feebleness is where your largegest potential lies!

***

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5% Quicker W/ 135ml of Red Blood Cells - Transfusion Works Wilean 2h! Plus: ~1.5g/kg = Optimal PWO Protein Intake for Protein Synthesis in Females - SV November Short Uniques

You may remember from the SuppVersity contemporarys on Facebook that the use of cobalt supplements can indeed (as it has long been touted and doubted) have similar effects as EPO (Hoffmeister 2018). Yet while the study by Hoffmeister et al. showed that the VO2max correlated signwhethericantly with the 2% increase in Hemoglobin in response to the ingestion of  5 mg of ionized Co2+ for 3 weeks, an acute performance-enhancing effect was neither tested nor observed in the German study.

That's in contrast to autologous (=your own) blood infusions. A simple injection of only ~135 ml of red blood cells that were precedingly lonely from 450 ml of your own blood 2h before training or competition will improve your endurance performance by 5%, ... according to the latest study from the University of Copenhagen (Bejder 2018).

And whether you're rather into lwhetherting weights than cycling, running, or triathlons, nowadays's research update also discusses the results of a recent small-scale study by Malovany et al. (2018), which puts a(t least a preliminary) number on the usefulness of escalating post-workout protein intakes from tall to very tall. Sounds interesting? Well, then let's start with the "blood doping" study by Bejder, et al.

+ + + The "blood doping study" + + +

• Instant (2h post) 5% performance boost in athletes w/ 135 ml of red blood cells (#RBCs) from a single 450 ml phlebotomy (Bejder 2018) -- While you all will have heard about "blood doping" and the infusion of autologous (=their own) blood and/or lonely red blood cells (#RBCs) in cyclists and other endurance athletes, I bet that you will be as surprised as I was that a single injection of 135 ml of red blood cells (#RBC) from a rather small amount of your own blood (450 ml) will improve your endurance performance by 5% - and that only 2h after you injected the RBCs.

• Study type: Randomized, double-blind, placebo-controlled crossover study
• Comparison: placebo = sham phlebotomized vs. blood transfusion-trial
• Subjects: N=9 (=small scale) young men w/ >1year resistance training (all major muscle groups | training at least twice a week) experience who didn't do more than 30 minutes "cardio" per exercise session and were able to lwhethere 0.7x and 2.3x their bodyweight on the bench press & leg press, respectively; no supplement use, general health, you know it...
• Outcomes: Hb, Hct, RBC, and Ret% 1wk before phlebotomy, 3 days before transfusion, 2 h post 135 ml transfusion and 3 days post 135+235 ml transfusion
• Carry outance tests: (1)Two 650kcal time-trial three days and 2h after receiving either ~50% (135 ml) of the RBCs or a sham transfusion on subsequent days + (2) One 4×30 s all-out cycling sprint interspersed by 4 min of recovery was performed six days before and three days after a moment autologous blood transfusion (235 ml).

• What the scientists found was that the subjects' mean power in the time trial (TT) to was increased in time trials from before to after transfusion (P<0.05) in BT (213±35 vs. 223±38 W; mean±SD) but not in PLA (223±42 vs. 224±46 W | see Figure 1, left).
  

  Figure 1: Mean power in the TT and during the 4x30s sprints in the active and placebo trial (Bejder 2018).

  For the four 30 s sprint bouts that were performed not 2h, but three days later no effect was observed[BT(639±35vs644±26W)andPLA(638±43vs639±25W)|see[BT(639±35vs644±26W)andPLA(638±43vs639±25W)|see[BT(639±35vs644±26W)andPLA(638±43vs639±25W)|see[BT(639±35vs644±26W)andPLA(638±43vs639±25W)|seeFigure 1, right].

The Vampire Approach to Endlessevity - Young Blood Revives Muscle, Brain & More | Plus: 6+ Less 'Horrwhetheric' Alternatives | read more

What does the "blood doping"-study tell us? The study shows that there is an instant increase in endurance performance that's virtually tallly relevant for athletes competing in various sports from a relatively small amount of RBCs (~135 ml) you can additionalct from a single phlebotomy.

Improvements in sprint/anaerobic performance, on the other hand, seem unlikely. After all, despite a moment (larger = 235ml) injection of RBCs the subjects' performance during the 4x30s bouts of all-out cycling on day 3 after the initial transfusion was not increased - in the presence of elevated RBCs, that is (5.03 ± 0.28 versus 4.58 ± 0.17x10^12/L blood) | Comment!.

+ + + The "protein ceiling" study + + +

• Optimal post-workout protein intake for max. protein synthesis over 8h in resistance-trained women is 1.5-2.0g/kg - More will just  be burned as fuel (Malovany 2018) -- For men we've known this all along: There's a threshancient value not to how much protein we can in- and digest in one serving, but rather to the amount of protein that can be used to fuel skeletal muscle protein synthesis after workouts (Humayun 2007; Jäger 2017). And while they certainly have to be considered preliminary due to the small sample size of N=9, Malovany et al.'s (2018) latest study shows that a similar threshancient exists for female resistance trainees, too.

• Study type: randomized sequential study of the effect of dwhetherferent amounts of PWO protein ranging from deficient to excess (0.2-2.90 g/kg)
• Subjects: N = 8 healthy females w/ regular menstrual cycles, who perform wgap-body resistance exercise regularly, had trained each major muscle group (i.e., chest, back, and legs) at least twice per week consistently for at least one year prior to recruitment, didn't do more than 30 min of continual endurance training per exercise session, and whose 1RM on the bench press and leg press of 0.7 and 2.3 × bodyweight, respectively.
• Outcomes: steady state wgap body phenylalanine rate of appearance (Ra), oxidation (Ox; the reciprocal of protein synthesis, PS) and net protein balance protein synthesis degreed via minimally-invasive indicator amino acid oxidation (IAAO) technique (protein synthesis) and urinary Urea: Creatinine ratio (protein oxidation), respectively
• Exercise standardization: 2d prior to each metabolic trial, all participants were required to total a prescribed but self-monitored wgap-body resistance exercise session - the workout was identical to the workout they would do on the test day, i.e. i) barbell bench press, lat pulldown superset; ii) standing overhead barbell press and seated cable row superset; iii) leg press; and iv) leg extension; each exercise was performed at 75% 1RM for 4 sets of 8-10 repetitions with ~90s rest intervals between sets
• Dietary standardization: 2-d adaptation diet containing 1.2 g/kg/d of protein during the 2-d controlled training period prior to each metabolic trial
• Testing days: ingestion of liquid carbohydrate beverage (1 g/kg as a 1:1 ratio of maltodextrin: Gatorade® Terminateurance) 1h before std. workout (see exercise standardization); each participant totald 6-7 metabolic trials (n = 50 for total trials totald) during the luteal phase, which was defined as the moment half of the menstrual cycle.
• Supplementation: 8x hourly meals providing a randomized test protein intake (0.2-2.9 g/kg) as crystalline amino acids, modeled after egg protein, with fixed phenylalanine (30.5 mg/kg) and excess tyrosine (40.0 mg/kg)

• As you can see in Figure 2 (left), the scientists observed a ceiling effect for the protein synthesis with protein intakes >1.5g/kg body weight - the horizontal nature of the linear trend for the values clearly indicates this.
  
  
  The rate of protein oxidation, which was estimated via the urinary Urea: Creatinine ratio, on the other hand, increased linearly with increasing protein intakes (Figure 2, right) - without a threshancient effect, i.e. the more protein, the more is going to be oxidized (see bottom line for discussion of what would happen w/ bolus vs. 8x1/h ingestion).

Protein Wheysting?! No Signwhethericant Increase in PWO Protein Synthesis W/ 40g vs. 20g Whey, But 100% Higher Insulin, 340% More Urea & 52x Higher Oxidative Amino Acid "Loss" | read more

What does the "protein ceiling"-study tell us? Due to its small scale (N=9) and very specwhetheric participant characteristics (young, healthy, resistant-trained women), the results of the study at hand have to be considered as good, but preliminary evidence for the existence and quantity of a protein synthesis threshancient (~1.5g/kg/8h) during the first 8h after a workout.

In that, it is important to point out that this effect was achieved by the sequential ingestion of a total amount of 0.2-2.9 g/kg of protein every hour. It is not just likely, but nearly certain that taking the ingestion of a single bolus of the amino acid mix instantly after the workout (for 1.5g/kg that would have been 100g per subject) would have yielded dwhetherferent results. More specwhetherically, one could speculate that the protein oxidation would have increased, while the net protein synthesis would have decreased w/ dose-escalating bolus ingestion (compared to the sequential ingestion protocol used in the study at hand) - a result I've reported for whey in a 2013 article from the archives.

Speaking of whey: It is not clear to which extent the results can be generalized to dwhetherferent protein sources, like whey (concentrate, isolate, hydrolysate), micellar casein, whey+casein mixes, actual egg protein, etc. as both, their digestion kinetics, as well as their amino acid and functional peptide content dwhetherfer signwhethericantly. Still, the recommendation to consume 1.5-2.0g/kg protein wilean the 8h window after a workout to optimize protein synthesis in healthy, resistance-trained young women is the best we have as far as "one-size-fits-'em-all" recommendations are concerned | Comment!

References:

• Bejder, J. "Time Trial Carry outance Is Sensitive to Low-Volume Autologous Blood Transfusion." Medicine & Science in Sports & Exercise: November 6, 2018 - Volume Publish Ahead of Print
• Hoffmeister, Torben, et al. "Effects of 3 weeks of verbal low-dose Cobalt on hemoglobin mass and aerobic performance." Frontiers in physiology 9 (2018).
• Humayun, Mohamcrazy A., et al. "Reevaluation of the protein requirement in young men with the indicator amino acid oxidation technique–." The American journal of clinical nutrition 86.4 (2007): 995-1002.
• Jäger, Ralf, et al. "International society of sports nutrition position stand: protein and exercise." Journal of the International Society of Sports Nutrition 14.1 (2017): 20.
• Malowany, Julia M., et al. "Protein to Maximize Wgap-Body Anabolism in Resistance-trained Females after Exercise." Medicine & Science in Sports & Exercise (2018).

...

Sodium-/Potassium-Bicarbonate (+Mg, +Ca) Supplement ➡ Improved 6x30m Run Time, Lactate, Magnesium & More | Plus: Enterically Jacketed NaHCO3 Tablets - Where are They?

The stack (ingredients on the right) was ingested twice daily.

It has been a while since the final study on sodium bicarbonate's usefulness has found its way to the SuppVersity.

And, technically speaking, the latest RCT by scientists from the Leavement of Sports Training at the Jerzy Kukuczka Academy of Physical Education in Katowice, Poland, and colleagues from the Miller School of Medicine, at the University of Miami is a "bicar-bonate", but not a "sodium bicarbonate" study.

How's that? Well, the scientists did summaryely what some of you have alalert proposeed: They combined sodium- and potassium-bicarbonate (the authors write di-carbonate, which is obviously the same) at a dosage of 3g, each, to achieve a balance between the two macro-minerals and topped the bicarbonates up with 1000 mg (600 mg + 400 mg) calcium phosphate and calcium citrate, 1000 mg potassium citrate, and 1000 mg magnesium citrate.

This Na/K-Bicarb + Ca/K/Mg-Citrate super-stack (or placebo) was consumed twice a day by N=26 well-trained soccer players, who compete at the elite Polish league, during an 11-day training camp in Spain. Unluckyly, the exact details about the way the supplement was administered is not adequately described in the FT, where it says:

"The players from the experimental group ingested a single dose of 3000 mg sodium di-carbonate, 3000 mg potassium di-carbonate (6 caps containing 500 mg each), 1000 mg (600 mg + 400 mg) calcium phosphate and calcium citrate, 1000 mg potassium citrate, and 1000 mg magnesium citrate twice a day, 90 min before each practice session. The control group ingested identical capsules containing cornstarch. Supplements were taken with plenty of water (600 mL). The supplementation protocol included an additional dose of di-carbonates and minerals, 90 min before the exercise test protocol and the day before the test" (Chycki 2018).

Only in conjunction with the information from the following "study protocol"-section it becomes clear - or I should say it is my interpretation that ...

• ...the performance tests[Running-BasedAnaerobicRunTest(RAST)protocolwhichinvolved[Running-BasedAnaerobicRunTest(RAST)protocolwhichinvolved[Running-BasedAnaerobicRunTest(RAST)protocolwhichinvolved[Running-BasedAnaerobicRunTest(RAST)protocolwhichinvolved6 × 30 m maximal sprint efforts, separated by 10 s of active recovery]were carried out at baseline and after 9 days of supplementation,
• ... the supplements were consumed 90 minutes before the regular AM and PM training (or "practice", as Chycki et al. call it) on day 2-7, i.e. chronically(!),
• ... on day 8 the subjects consumed only one serving of the macromineral stack (or cornstarch placebo) and there was either no soccer training at all or, at least, no PM session, so that they would have rested for 24h before the performance test on day 9,
• ... on the testing day, the subjects reported to the lab in the AM fasted and consumed another mineral stack 90 minutes before the RAST protocol,

So, basically one macromineral stack 90 minutes before each training for 9 days - with the final "training" actually being the sprint test. With "only" 6g of sodium- and potassium-bicarbonate the stacks were dosed comparatively low compared to the 0.3g/kg protocols that have been used in many of the preview studies. The dosage is, however, in line with precedingly disstubborn "serial-loading" studies where NaHCO3 was administered in repeated smaller doses over 24h or several days (see this preceding article) to achieve the desired alkalizing effect with a reduced risk of gastrointestinal distress.

Yes, the diet was standardized: The participants were placed on an isocaloric (3455 ± 436 kcal/day) mixed diet (55% carbohydrates, 20% protein, 25% fat) prior to and during the investigation. The pre-trial meals were standardized for energy intake (600 kcal) and consisted of carbohydrate (70%), fat (20%) and protein (10%). The participants did not take any medications and substances not prescribed by the supplementation protocol for 3 weeks before and during the study.

The latter was further reduced in the study at hand by administering the supplements in 500mg capsules - a practice of which I've precedingly pointed out that it seems to (a) limit the gastrotestinal distress an (b) help those of you who hate the salty taste of pure NaHCO3.

Table 1: The authors found statistically signwhethericant dwhetherferences between baseline and post-intervention period at rest, post ingestion, and after exercise for the experimental group for all parameters| Note: d, effect size (≥ 0.5 = LARGE effect - found for all parameters); p, statistical signwhethericance; F, value of analysis of variance function (Chycki 2018).

Next to the performance test, Chycki et al. (2018) also tested the subjects' lactate concentration (LA), acid–base equilibrium and electrolyte status, the following variables were evaluated: LA (mmol/L), blood pH, pCO2 (mmHg), pO2 (mmHg), HCO3− act (mmol/L), HCO3− std, (mmol/L), BE (mmol/L), O2SAT (mmol/L), ctCO2 (mmol/L), Na+ (mmol/L), K+ (mmol/L), and Ca2+, Mg2+. The degreements were performed from fingertip capillary blood samples at rest and after 3 min of recovery... and guess what!? "Large effects" (Cohen's d > 0.5) were observed for all of these.

You have to read the captions carefully, though...

because, otherwise, you will miss that the data in Table 1 shows the intra-group change of the given parameters. In other words: After having ingested the macro-mineral-stack the lactate levels, the pH, the HCO3 and Mg2+ content, as well as the performance n the 6x30m sprint test improved compared to baseline. Large effects compared to placebo were observed "only" for:

• lactate instantly after the workout (d = 0.884 |large; p = 0.0001)
• blood pH at rest (d = 0.780 | large; p = 0.0001), and
• the HCO3− content of the subjects' blood at rest (d = 0.989 | large; p = 0.0001)

Those of you who haven't read that many SuppVersity articles, yet, must also be aware that "Cohen's d" as a degree of the effect size does not say that this is "large" = "virtually relevant" dwhetherference.

The paper has issues in terms of data reporting: As pointed out in the main body of this article, the figure with the sprint times does not align with the values reported in the text of the paper. For the given reason (ungenuineistic improvements, dwhetherficultly legible captions, etc.) I rely on the explicitly stated sprint times in the experimental and an additionalpolation of the corresponding data in the placebo trial. I believe that this represents the data appropriately, but I cannot guarantee that.

I have to emphasize once more While this can be (and often is) the case, it only tells you that the inter-group dwhetherference was large even when the standard deviations are considered.

Figure 1: Run performance times in moments before and after the 9-day training + supplementation intervention in the experimental vs. placebo group; left: with a similarly messed up vertical axis scale as in the original from the study / right: with a obvious vertical scale that shows that the statistical "effect size" is large, the relative improvement, on the other hand, rather low [†Note: I cannot guarantee that the data is 100% accurate, because the plotted and disstubborn data in the stud at hand contradict each other and I had to additionalpolate the non-reported absolutes for the placebo group].

I guess I'll simply show you the subjects' actual sprinting performance, ...because the graph illustrates that very kindly. While you're looking at Figure 1, there are yet two leangs you should be aware of:

1. Since the scientists' plot of the data is totally messed up (click here to see it), I had to redo the graph for the sprint times based on the values given in the text, i.e. the 6 × 30 m running test improved from by 2.3% 25.09 s to 24.53 s (p = 0.00001) in the experimental group and by only non-signwhethericant 1% in the control group (I additionalpolated the absolute values in the control group, which were not reported from inter-group dwhetherference in the scientists' own IMHO wrongly labeled graph).
2. Furthermore, I decided to give you both, the equivalent of the scientists' own plot which uses a scale that totally exaggerates the improvement (Note: the original captions cannot be right, because then, the sprint times would have improved by ~50% - that's ungenuineistic and not in line with any of the other data reported in the text) and my "fair" plot, from which you can see that the genuine-world effect is not summaryely as large as a misinterpretation of "large effect sizes" would propose.

If you keep that in intellect, you may be somewhat disappointed, ... I know, "only" 2% - true: that's not super impressive but the study still adds signwhethericantly to our knowledge of bicarbonate buffering as an ergogenic aid for anaerobic exercise (like sprinting or hypertrophy training) - and here's why...

Innovation, anyone? Enterically coated Na-HCO3 tablets could make you wealthy ;-)

I actually wonder that acid resistant NaHCO3 tablets have not been marketed, alalert, as a more stomachable al-ternative to lessonic powders or caps, which will release their content in the intestine where it will react with the stomach acid and produce bloating or worse.

Moreover, with the publication of a recent study from the Univer-sity of São Paulo in which the scientists investigated the buf-fering effect of NaH-CO3 in post-gastric bypass patients and found (a) sign. reduced side effects and (b) a signwhether. increased effect on blood pH, we do have initial evidence that allowing the tablets to pass through the stomach undigested, may not just avoid the runs, it may also re-duce the dosage you need to see an effect, signwhether. - or, as the authors put it: "Maximal bicarbonate increases were well above those shown precedingly, with minimal side effects, indicative of minimal neutralization of bicar-bonate in the stomach." (de Olivera 2018).

What does the study tell us? Yes, the 2% performance benefit doesn't sound like much, but during an actual soccer match those +2% sprint performance can make the dwhetherference between getting and lost a long ball and hence scoring a goal or seeing the goalkeeper punt.

The performance increase isn't genuinely contemporarys, besides. Bicarbonate is, after all, one of the few proven ergogenics ("obviously effective and generally secure" - Kreider 2010). What is contemporary, however, is this:

(1) This is the first study to show that you can take sodium and potassium bicarbonate at a 1:1 ratio and still see ergogenic effects as they've precedingly been observed with baking soda, alone. That's an important and (IMHO) novel finding, because the tendency of serum potassium levels to increase signwhethericantly in response to strenuous exercise (from the muscle) would have proposeed that additional potassium could impair the muscle contractile properties - at least when it is combined with Ca + Mg, however, this is not the case. Plus: Even though sodium bicarbonate doesn't have the blood prescertain increasing effect of regular salt in healthy individuals (Luft 1990), SuppVersity readers know that some additional potassium will scarcely hurt ;-)

(2) This is the first study to propose that chronic K-/Na-bicarbonate supplementation may enhance the training effect trained athletes can derive from a relatively short training camp. This does also propose that buffering effects of bicarbonates, phosphates, and citrates do not impair (keyword: "hormesis"), but rather promote the training effect.

(3) This is the first study to propose that addition of the magnesium and calcium citrate, both deficiency nutrients in the general population, doesn't impair the performance benefits of bicarbonates. Why would it? Well If you've ever tried to mix bicarbonates and citrates you will know that the two will react with each and release carbon-dioxide. This, in turn, would leave less bicarbonate to pass into the bloodstream to work its buffering magic there (note:  in the absence of a KHCO3+NaHCO3 only group, it's still possible the that either the reaction between bicarbonates and citrates or the mere presence of Mg and Ca could have reduced the performance effects of the bicarbonate stack).

For those of you who didn't notice that alalert - the use of the word "proposes" in (2)+(3) does summaryely what it means: it "proposes" that future studies should investigate individual and synergistic effects of the dynamic macronutrient quartett w/ Na, K, Ca, and Mg | Comment!

References:

• Chycki, Jakub, et al. "Chronic Ingestion of Sodium and Potassium Bicarbonate, with Potassium, Magnesium and Calcium Citrate Improves Anaerobic Actance in Elite Soccer Frolicers." Nutrients 10.11 (2018): 1610.
• Luft, Friedwealthy C., et al. "Sodium bicarbonate and sodium chloride: effects on blood prescertain and electrolyte domesticostasis in normal and hypertensive man." Journal of hypertension 8.7 (1990): 663-670.

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