Showing posts with label lactic acid. Show all posts
Showing posts with label lactic acid. Show all posts

Wednesday, July 23, 2014

Beta Alanine + Bicarbonate = Synergistic Internal + External Muscle H+ Buffer With Disappointing Real-World Benefits

No matter what this study says, I am pretty sure that the combination of bicarbonate + beta alanine would rule for Tour de France cyclists - at least during the dreaded time-trials.
In a recent study researchers from the Victoria University and the Queensland University of Technology observed that the combination of the carnonsine pre-cursor beta alanine and sodium bicarbonate will elevate the buffering potential of skeletal muscle in eight apparently healthy, recreationally active men (26.2 ± 1.9 year; 79.8 ± 2.11 kg; 179.0 ± 2.2 cm; VO2peak 51.0 ± 2.5 ml/kg/min) by increasing muscle carnosine and blood bicarbonate levels, respectively.

So much for the good news, the bad news however is that the performance increases on a repeated sprint test were non-signficant and the expected additive effects of beta alanine and baking soda (sodium bicarbonate) during a 110% cycling capacity test were non-existing.
You can learn more about beta alanine & bicarbonate at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

BA + Bicarb are Synergists

Bicarb Buffers Creatine

Beta Alanine Fails to HIIT Back
The trial participants were asked to complete 2 exercise tests, over consecutive days, at the end of each of the four co-supplement periods (see fig.  1).
Figure 1: Design of the study. Each trial consisted of two exercise tests performed over consecutive days. A total of 12 weeks between trials 2 and 3 was implemented to ensure adequate supplement washout time participants randomised to ingest β-alanine during the initial chronic supplementation. MRS Magnetic resonance spectroscopy, RSA repeated sprint ability test, CCT 110 %cycling capacity test. Solid  arrows depict crossover between acute supplementation (Pl and SB). Dotted arrows depict crossover between chronic supplementation (BAl and Pl; Danaher. 2014)
During the double-blind supplementation periods, the subjects consumed capsulated β-alanine (4.8g/day for four weeks, 6.4g/day for two weeks) or the placebo calcium carbonate (CaCO3). To investigate the superimposition of NaHCO3 (baking soda) with β-alanine, the acute administration of NaHCO3 occurred following each of  the 6-week periods of β-alanine and placebo supplementation.
Figure 2: The non-existing increases in peak and average performance with beta alanine and - with the exception of one outlier - bicarbonate supplementation is disappointing; value expressed relative to placebo trial.
This required two trials of either 300 mg/kg body weight sodium bicarbonate or a not wisely chosen "placebo", i.e. CaCO3 (While I have seen this repeatedly, I am asking myself how smart it really si to use calciumcarbonate as a placebo for a bicarbonate, if the carbonate will form HCO3 as soon as it is cleaved from the calcium ion?) , that was administered only once 90 min prior to the exercise bouts of the respective trials and was split into 6 equal doses over the first 50 min of the 90-min pre-exercise period.
Figure 3: Time to exhaustion, blood pH values during repeated sprint & cycling capacity @110% test (Danaher. 2014)
Bottom line: This is not the study to support the usefulness of bicarbonate and beta alanine supplementation for power athletes. It may be a study to support the usefulness of bicarbonate supplementation for Tour de France Trials, but it's also another study to show that the ergogenic effects of "buffers" outside of long(er) duration high intensity work like Tour de France time trials may be generally overrated.

With the study being underpowered, not 100% controlled in terms of the nutritional circumstances of the individual trials and questionable with respect to the use of calcium carbonate as a placebo supplement for sodium bicarbonate and beta alanine, I would be hesitant to discard the use of bicarb and beta alanine and a possible synergy. on the basis of the study at hand, though. Previous studies yielded different results.
Reference:
  • Danaher, Jessica et al. "The effect of β-alanine and NaHCO3co-ingestion on buffering capacity and exercise performance with high-intensity exercise in healthy males." Eur J Appl Physiol (2014) 114:1715–1724

Monday, April 7, 2014

Not All Artificial Sweeteners Are Created Equal: New Studies on Aspartame, Acesulfame-K & Combination of Saccharin + Neohesperidin Dihydrochalcone

It was about time for an artificial sweetener update, wasn't it?
Alright, I have to admit I am not following the artificial sweetener scene closely enough to have heard about SUCRAM, an artificial sweetener that is composed of saccharin (a classic) and neohepseridin dihydrochalcone, the new kid on the blog, which is yet not officially approved by either the FDA or it European equivalent o be used in the processed junk, most people call "food", these days. If we put some faith into the latest study investigating the effects of this agent, which is apparently already heavily used in animal feeds in Europe it does yet "dramatically reduce enteric disease" and "enhance growth performance in early-weaned piglets." (Daly. 2014)

Whether and to which extent these beneficial effects on gut health are mediated by changes in the gut microbiome is yet still uncertain; and since "uncertain" is a word scientists don't like, Kristian Daily and his colleagues from the University of Liverpool conducted a study to find out, whether the non-negligible health benefits would be brought about by AI <> gut interactions.
You can learn more about this topic at the SuppVersity

Food Gut Interactions

Macrobiotic MaPi2 What's That?

Sweet But not Innocent?

Sucralose is for Diabetics Not

Stevia: Much More Than Sweet

Sweeter Than Legal
To this ends, the scientists employed a DNA-based pyrosequencing technology to investigate the changes in the intestinal microbiota of piglets weaned to a diet supplemented with either a natural sugar, lactose or said artificial sweetener (SUCRAM)
Figure 1: Total and lactobacillus OTU4228 concentrations in piglets on hydrolzysate carbohydrate diet without sweeteners, with lactose or SUCRAM diets and corresponding concentration of lactic acid in the caecal contents (Daly. 2014)
As you can see in Figure 1, both, the addition of lactose and the saccharin/NHDC mix lead to dramatical increases in the caecal Lactobacillus population and could well explain the previously reported "pro gut health" effect of SUCRAM in piglets (Vente-Spreeuwenberg. 2004; Pierce. 2006)

But that's obviously not all that's news-worthy!

I did after all promise you news on products you may be using, as well - aspartame and acesulfame-k, to be precise. Now, while the former is a constant target of public (mostly broscientific) criticism, the latter has been a thorn in my side ever since I have started investigating artificial sweeteners.

Lean more about the "Gut Type Diet" - No Fad, Guaranteed!
And while previous studies only suggested that the effects of acesulfam-k on the pancreas could have pro-obesogenic consequences, a recent model experiment from the Louisiana State University appears to finally prove that acesulfam-k may actively promote the deposition of body fat in the presence of insulin resistance.

Ok, the results have been derived in a Caenorhabditis elegans, a "worm", but one that has long and actually surprisingly successfully been used as a "model for studying the basic biology of obesity" (Jones. 2009) - I know, I am not convinced either, but if the results do actually translate to humans, this would be major (bad) news for the food industry.

In view of the fact that most companies have been pulling acesulfame-k from their products over the past years, anyway, I would not discard the findings Jolene Zheng et al. present in their latest paper in Chemico-Biological Interactions as meaningless, not despite, but rather because a scientists from PepsiCo was part of the research team which observed these significant increases in intestinal fat (=visceral fat of the worm) when the critters were fed with acesulfam-k sweetened coke.
Cheating? Why would be using artificial sweeteners cheating? In spite of the fact that there is no credible evidence for a causal relationship between the consumption of artificially sweetened foods and obesity (there is a correlation that could well be the result of reverse causation), there is some concerning evidence that the extreme sweet taste and the way people appear to escalate the dosages reduce your bodies ability to control its energy balance by thwarting with its mostly sugar-based first-line energy intake sensor.
What I would not recommend either, though, is to (ab-)use aspartame-containing diet coke as a "weight loss beverage": It's certainly ok to sooth your sweet tooth, when you're dieting and I am not saying that you must not drink one or another Diet Coke or Pepsi on the weekend. What I am saying, though, that I don't believe that the consumption of copious amounts of this stuff will result in a similar body fat reduction (see Figure 2) in you, where compensatory mechanisms, your sweet tongue and a whole host of other things complicate weight and even more so fat loss compared to C. elegans.

That being said, I would be inclined to know, when and if SUCRAM is going to be available as a food additive for humans. It does after all sound quite nice to do your tummy a favor while you're "cheating", right? Although,... when I come to think about it, we actually don't need a "new" sweetener to mess up our gut microbiome. As I already hinted at in a related SuppVersity Classic Article Series with the telling title "Sucralose, Hazardous or Innocent?" (Part I, Part II, Part III), Payne et al.  (2012) have already identified fructose, mannitol and d-tagatose as promoters of lactobacillus growth and sucrose as their primary enemy (learn more about the interaction in Part II of the series).
References: 
  • Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." Obesity Reviews 13.9 (2012): 799-809.
  • Pierce, K. M., et al. "The effect of lactose and inulin on intestinal morphology, selected microbial populations and volatile fatty acid concentrations in the gastro-intestinal tract of the weanling pig." ANIMAL SCIENCE-GLASGOW THEN PENICUIK- 82.3 (2006): 311.
  • Jones, Kevin T., and Kaveh Ashrafi. "Caenorhabditis elegans as an emerging model for studying the basic biology of obesity." Disease models & mechanisms 2.5-6 (2009): 224-229.
  • Vente-Spreeuwenberg, M. A. M., et al. "Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets." Livestock Production Science 86.1 (2004): 169-177.

Saturday, July 23, 2011

Electrical Stimulation Improves Clearance of Lactic Acid After Anaerobic Activity in Collegiate Athletes. EMS Turns Out to Be as Effective as 'Traditional' Massage Therapy.

Image 1: The EU-940 EMS device the
scientists used in their study to activate
the vastus medialis and lateralis (high-
lighted in the image) of their subjects, is
very different from the average EMS based
"abdominal toner" advertised on TV.
Even here, at the SuppVersity, news on ergogenics, i.e. things that improve (athletic) performance, are usually about a pill, a fancy plant extract or another 'superfood'. Today's news, however is about a much more "physical" means to improve anaerobic exercise performance, decrease lactate accumulation and improve regeneration: Electrical Muscle Stimulation (EMS).

EMS? Now, many of you will probably remember those TV spots, where you were told that "Abmaster" & Co would transform your pot-belly into a "six-packed" attractant for the opposite sex, if you did not miss this "unique" opportunity and bought one of those electro-shockers no sane fitness professionals would voluntarily substitute his/her good old sit-ups and leg raises for. Yet, while these battery-powered torture instruments did, or I should say, were intended to electrically stimulate muscles (in fact in many of the obese buyers of these products, the abs were probably covered by a layer of fat that was way too thick for actually "stimulation" of the abdominal muscles to occur), both the devices, as well as the EMS protocol Seo et al. (Seo. 2011) employed in their double-blind randomized controlled trial at the Sports Science Research Laboratory of Kyungwoon University in Korea were a little more sophisticated.
Did you know? The fatigue index is a concept used in the study of fatigue during anaerobic activities. It is the ratio of power decline to the length of the time interval in seconds between peak power and minimum power. This means lower fatigue indexes equate lower declines of exercise intensity per time unit. When looking at the data in figure 1, you may want to keep in mind that higher starting values / greater overall workloads will entail greater declines in anaerobic power per time unit and thus present with higher fatigue indexes
During and after 3 all out intervals on an ergometer (resistance: 0.8 x body weight Nm; active rest between intervals: 10 seconds) verbal feedback on perceived fatigue, fatigue indexes in W/s, mean power/weight, total work and lactic acid values (from serum drawn before, after and at 15 min and 25 min post exercise) were recorded in a group of 24 randomly selected collegiate Taekwando athletes (age: 19.8yrs, height; 177cm; weight: 66kg, training experience: 5yrs; mean values with non-significant differences between groups).
Figure 1: Fatigue index, mean power (primary axis) and total workload (secondary axis) during Wingate ergometer test
(data adapted from Seo. 2011)
Immediately after the exercise bout, eight athletes, each, received one of the following treatments:
    Table 1: Outline of the massage
    protocol the  athletes in the massage
    group received after having performed
    an exhaustive anaerobic Wingate
    ergometer test (according to Lee. 1998)
  • The control group received no regenerative treatment at all. 
  • The massage group was subjected to a massage protocol which had been shown to effectively improve exercise recovery in a previous study by the same authors (Lee. 1998).
  • The EMS group was attached to an interferential current unit (EU-940, ITO CO., LTD, Tokyo, Japan), which applied an interferential current with a carrier frequency of 4kHz and a pulse duration of 125µs via four vacuum electrodes (vacuum pressure: 60ppm) to the vastus medialis and the vastus lateralis of the subjects.*
    * "The current  intensity was set within the range of the minimum visible contraction of the quadriceps femoris muscle", so that the muscle of the quadriceps were maximally stimulated, while the current was not so intense that cross-over effects to neighboring muscle groups would occur.
Seo and his colleagues found "significant differences in the lactic acid concentrations in the blood among the three groups [...] at 15 min and 25 min after exercise".
Figure 2: Relative reduction in lactic acid concentration after a wingate performance test followed by massage or EMS therapy compared to untreated control (data adapted from Seo. 2011)
As the data in figure 1 shows, massage and EMS promote the clearance of lactic acid to a similar degree (+17-18% vs. control). So, if you are a professional athlete you should either make good use of your already existing six pack and attract a significant other who is a massage therapist or save some bucks and get yourself a reasonably professional EMS device, in case you intend to be a gold medalist at the 2012 Olympics in London ;-)

Edit (26 July): The lactate & Lactic acid confusion

After I posted this piece of information an interesting discussion around the physiological role of lactic acid broke lose on Facebook and I do not want to deny you the great information my buddy Sean Casey from CasePerformance brought to the table. So, here is what he had to say:
Lactic Acid is an interesting thing....During the 1970-1980’s various studies found lactic acid impaired strength and contraction velocity in samples of isolated muscle tissue (1). Based off these early findings, many researchers evaluated ...post workout recovery modalities on their ability to remove lactate from muscle tissue post workout. Similarly, coaches and athletes started employing post workout techniques aimed at removing lactate from muscular tissue. For instance, our high school track coach used to have us lie on our backs and rest our legs on an elevated surface w/ respect to our body. Usually we'd lie on the floor next to a wall & place legs on wall. The theory was that acid would “drain” out of our muscle tissue, allowing our legs to be fresher for the following day’s workout. (I know, a very bro-science approach; , but mentally felt good and you'd always get a cool tingly sensation when you set your legs down and the blood rushed back into them!)

Interestingly, it turns out that lactic acid may not be the best form of measurement with respect to evaluating the effectiveness of a PWRM [post workout recovery measures]. As pointed out by Cairns SP, it may have a much smaller effect on muscle fatigue than was previously hypothesized(1). Thanks to advances in technology, scientists are now able to study muscle tissue closer to physiological temperatures (old studies were completed at muscle tissue held at cooler temperatures, 50-68ºF). As shown by Westerblad et al., acid had little effect on contraction velocity when completed on muscle tissue held at 89ºF (2). On the other hand, a 2006 study by Knuth et al. did indicate that lactic acid decreased muscle contractile power even at warmer temperatures(3). 

Although the lactate question is still being debated amongst scientist, athletes must ask themselves if the research is even applicable to their post training recovery protocol. Although lactate may induce muscular fatigue, its quickly metabolized within the body (1/2 life: muscle- 9.5 minutes; blood- 15 minutes), and eliminated from our system 90 minutes after an exercise session has been completed (4)(5). Thus, exercise induced lactic acid from one workout is likely not even present during a subsequent workout depending on when you complete it.

All this being said, don't misinterpret my comments and think that I'm trying to put down the role of EMS. I've had to use one a fair amount due to various issues and have found it to be effective. Anything that can get a muscle contracting and increase blood flow is always a good thing ;-) 

References

1 Cairns SP. Lactic acid and exercise performance: culprit or friend? Sports Med. 2006;36(4):279-91.

2 Westerblad H, Bruton JD, Lännergren J. The effect of intracellular pH on contractile function of intact, single fibres of mouse muscle declines with increasing temperature. J Physiol. 1997 Apr 1;500 ( Pt 1):193-204.

3 Knuth ST, Dave H, Peters JR, Fitts RH. Low cell pH depresses peak power in rat skeletal muscle fibres at both 30 degrees C and 15 degrees C: implications for muscle fatigue. J Physiol. 2006 Sep 15;575(Pt 3):887-99. Epub 2006 Jun 29.

4 Karlsson J, Saltin B. Oxygen deficit and muscle metabolites in intermittent exercise. Acta Physiol Scand 1971; 82: 115-22.

5 Barnett A. Using recovery modalities between training sessions in elite athletes: does it help? Sports Med. 2006;36(9):781-96.
The only thing I would like to add to Sean's insightful dissertation is a criticism of the indiscriminate use of lactate, which is sort of 'recycled' muscle fuel, and lactic acid, which is its ugly 'degraded' relative. With the ever increasing H+ levels as they can be observed in the course of a long distance race, for example, more and more lactate gets degraded into lactic acid and thus works like a buffer similar to the beta-alanine derived intramuscular H+ buffer carnosine. Now it is no wonder that with H+ release being a measure of muscular exertion and lactic acid being a measure of H+ buffering, Faude et al. (Faude. 2009) found in what is one of the most recent reviews on the role of lactate in exercise metabolism that
[t]hirty-two studies evaluated the relationship of LTs with performance in (partly simulated) endurance events. The overwhelming majority of those studies reported strong linear correlations, particularly for running events, suggesting a high percentage of common variance between LT and endurance performance.
And, after all, it does not really matter in how far the established performance increases from massages and EMG therapy are related to their ability to accelerate lactate clearance, or more generally to their ability to increase blood flow and thus nutrient delivery and waste clearance in the respective tissue - does it?

Tuesday, November 23, 2010

L-Arginine @5g/Day Reduces Lactate Levels in Male Athletes

While the NO-hype of the last years unquestionably is/was a scam, l-arginine, the amino acid that does not build muscle via increased NO-production, transpires to be ergogenic via very different mechanisms.

Scientists from Iran (Mozezzaneh. 2010) have now found that 5g of supplemental l-arginine significantly decreased the blood lactate levels of athletes (N=30) in the course of a 3 week supplementation period, but failed to induce consecutive or concurrent increases in VO2 max (a direct marker of exercise capacity):
Blood lactate level was significantly decreased in the L-arginine group compared to the placebo one. There was no significant difference between the two groups in VO2max at anaerobic threshold. Only in the L-arginine group, VO2 max at anaerobic threshold was significantly increased. In addition, there was no significant difference in VO2 max at anaerobic threshold for the placebo group.
If you remember the previous news on arginine, you may understand that I will repeat my advice not to flush your good old pre-workout down the toilet. Even if it was just for the cosmetic pump and the decrease in lactic acid, this is probably more than some newer and probably fancier products will provide.

Thursday, September 2, 2010

4g L-Carnitine Per Day do not Increase Muscle Carnitine and/or Exercise Performance

Only 2 days ago, you read at the SuppVersity about L-Carnitine being a costly, but ineffective ingredient in many weight loss supplements. Today's news is about a study on the effect of 14-day l-carnitine supplementation (4g/day) on muscle and blood carnitine fractions, and muscle and blood lactate concentrations, during high-intensity sprint cycling exercise. The results observed in 8 subjects were unambiguous:
L-carnitine supplementation had no significant effect on muscle carnitine content and thus could not alter lactate accumulation during exercise.
The increase of plasma carnitine, on the other hand, is insufficient to bring about the ergogenic effects carnitine supplements are advertised for. So if you can't get it into the cell, you could as well dump it into the toilette - or better just don't buy it ;-)