Protein Supps + Synthesis After 'Cardio': Milk (Natural 2:8 Whey:Casein) Protein is Best! Plus: 40g May Be Ideal Dose

Protein Supps + Synthesis After 'Cardio': Milk (Natural 2:8 Whey:Casein) Protein is Best! Plus: 40g May Be Ideal Dose

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Even though the study at hand has been conducted in an endurance training scenario, there's no reason to believe that the superiority of milk protein, the natural mix of whey and casein would be a "cardio-specific" thing. In fact, evidence to the contrary has been discussed previously, here and here.

Whey, casein, soy or the rarely used alternative, milk protein, what's best to kickstart the protein synthetic machinery even after endurance workouts? The absorption kinetics of the different proteins, the effects of which a group of scientists from Japan recently re-assessed would suggest that the answer is clear: whey protein, it's the fastest of the four proteins, contains the highest amount of BCAAs (esp. the mTOR- and MPS promoter leucine) content and has been repeatedly shown to rapidly cause significant hyperamonoacidemia (=extremely elevated amino acid levels in the blood | Boirie. 1997; Dangin. 2001; Norton. 2009).

In spite of the fact that whey is also the most insulinogenic of these proteins, it is yet also the one that has been shown to "maximize" amino acid oxidation, thereby contributing to a reduction in nitrogen retention (Boirie. 1997; Dangin. 2001). On the other hand, ingestion of CA causes slower but prolonged aminoacidemia and it has the best leucine net balance during the postprandial period (Boirie. 1997; Dangin. 2001), I've discussed in previous articles, such as "Protein Wheysting".

This is not an anti-high-protein article. It is one arguing in favor of "treating your protein right"

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This is where micellar casein (not sodium or calcium caseinate which are fast-, but slower-than-whey-absorbing "damaged" forms of casein, though) comes in. While casein does not produce the same rapid increase in serum amino acid levels it has been shown to cause moderate but prolonged muscle protein synthesis - the exact opposite of whey protein.

Figure 1: Fractional myofibrillar protein synthesis (A), plasma leucine (B) and plasma insulin (C) levels in young men after ingesting 0.3g/kg whey, casein or a protein-free control drink (Reitelseder. 2011)

The data from Reitelseder et al. (2011) illustrates the link between the time course of the myofibrilliar protein synthesis and a protein's digestion speed, the rate of appearance of leucine (Figure 1, B) in the blood and the protein's insulinogenic (Figure 2, C) effects quite nicely. It is thus only logical to assume and has in fact been shown that the co-ingestion of whey and casein, either mixed or as milk protein is superior to soy protein (SP) [22,23], but also to whey alone, even if the latter is "enhanced" with extra BCAAs and glutamine (learn more!)

Figure 2: As a SuppVersity reader you will rememeber that a previous study showed that whey + casein is profoundly more anabolic than whey that is combined with extra BCAAs and glutamine (Kerksick. 2006)

As the Japanese authors of the study at hand point out, these benefits are likely due to casein's ability to "contributes amino acids that have a prolonged protein-synthetic effect across the leg" - or, put more simply: whey pumps up the AA levels fast, so fast that your body gets wasteful; casein, on the other hand, provides them at a rate that's much more suitable for direct incorporation into the muscle.

Whey (open triangles) increases leucine +protein oxidation vs. casein (closed circles) in man (Boirie. 1997).

Thinking about the perfect mix: Wouldn't it make more sense to have more whey right after a workout and reduce the amount of casein? If that's what you are thinking right now, I have to warn you: As previously pointed out, there's a point of diminishing returns, when excess amino acids as you would increase them by increasing the amount of whey are oxidized and end up as "waste", namely ammonia (and after recycling urate) in your system. The increased leucine oxidation with whey (open triangles) vs. casein (filled circles), as it was observed by Boirie et al. 19 years ago in healthy subjects even though the subjects consumed 43g of casein and only 30g of whey to standardize the leucine content, attests to that. Needless to say, testing a 50:50 or even 60:40 ratio would be something for follow-up studies.

Table 1: Amino acids in milk (MP), caseinate (CA), whey (WP) and soy (SP) protein (Kanda. 2016).

What exactly the ideal ratio of whey to casein protein may be will still have to be determined (probably it'll depend on when you take your protein shake), but the 2:8 ratio, meaning 20% whey protein and 80% casein that was used in the study at hand is "nature's standard formula" and thus what your average milk protein will have. A protein, by the way, of which Kanda et al. wanted to confirm in their latest experiment that it "causes a prolonged increase in muscle protein synthesis compared to WP [whey protein]or CA [casein] alone" (Kanda. 2016).

In contrast to "the average" study, the Kanda et al. did so in the presence of an endurance, not a strength or no training stimulus at all and used both, the milk-derived proteins caseinate (CA | faster absorbing, non-micellar form of casein), whey (WP) & milk protein (MP) to soy (SP). You can review the individual amino acid composition of all four in Table 1 on the right and will notice that "technically speaking", i.e. judged based on its BCAA content, soy is the "worst muscle builder", whey the "best".

Time for the convenient, but annoying truth(s)!

Truth #1: It's a rodent study! That's convenient for the scientists, because using rodents is cheap and easy, but annoying for us, because rodents are a good model for humans, but only that - a model - and by no means the best one. Since we cannot switch the subjects, though, we have to live with the fact that the subjects in the study at hand were Sprague-Dawley rats with a bodyweight of approximately 150 g (at least there were many | n = 237) who were subjected to a swimming exercise protocol during which they swam for a whopping 2h.

You should care about postworkout protein synthesis! While previous studies had suggested that the FSR / MPS response to training and supplementation would not, a more recent study I discussed in detail, last week, clearly demonstrates that FSR / MPS does matter. Read it!

Now, where there's shadow, there's also light: The good thing about rodent studies (bad for the rats, though) is, after all, that, much in contrast to humans, rats can be sacrificed after an experiment like that and will thus allow researches to assess the effects of exercise and supplementation with the aforementioned proteins much more accurately than a single or even multiple muscle biopsies.

Table 2: Macronutrient profile of test proteins; milk (MP), caseinate (CA), whey (WP) and soy protein (SP | Kanda. 2016)

That does not fully compensate for truth #2, though, which is that the scientists made the mistake of using caseinate (Fonterra Co-operative Group, Ltd., Auckland, New Zealand), instead of the more expensive and slower/-est digesting (due to its micelle structure, which gels during the digestion process) molecularly intact micellar casein, of which one could expect that it may have postponed the peak in fractional protein synthesis (FSR) that occurred after 120 minutes with the caseinate even more (Figure 3, left).

Figure 3: Time course of the fractional protein synthesis after endurance exercise with all four proteins (left) and corresponding AUC values (~net protein influx, right | Kanda. 2016).

The previous hypothesis is obviously merely speculative and eventually irrelevant. I mean, micellar casein, or not, it is very unlikely that the overall AUC, i.e. the incremental area under the FSR curve and thus the net influx of protein into the muscle, would have been increased to a level that would top that of milk protein (black bar in Figure 3, right), which had a measurable, but not statistically significantly more pronounced effect on the protein influx than any other of the four proteins.

Bottom line: Yes, it's rodents, but eventually the study at hand simply extends previous studies (A, B) in humans, where the combination of whey + casein likewise outperformed the competition...

FSR during dose escalation study; the human equivalent dose (HED) of 3.09g/kg, the 100% dose, in rats is ~0.5g/kg in man and thus ca. 30-50g milk protein, depending on your body weight. (Kanda. 2015)

And when we are talking about "extending the existent research", it may be worth mentioning that the researchers also provide new evidence in regards to the "ceiling" or "muscle full"-effect that occurs when ingesting more protein won't yield any extra increases in protein synthesis. In the study at hand, this effect was reached at a human equivalent dosage of ca. 0.5g per kg body weight (that's the 100% dose in Figure 4) or ~ 40g which is - initially surprisingly - more than the often touted 20-30g (depending on the human study you cite). In view of the 20:80 mix of whey and casein, the lower leucine content and slower absorption of the latter, it is yet actually logical to need more milk protein vs. whey to "reach the ceiling" | Comment!

References:

• Boirie, Yves, et al. "Slow and fast dietary proteins differently modulate postprandial protein accretion." Proceedings of the National Academy of Sciences 94.26 (1997): 14930-14935.
• Dangin, Martial, et al. "The digestion rate of protein is an independent regulating factor of postprandial protein retention." American Journal of Physiology-Endocrinology And Metabolism 280.2 (2001): E340-E348.
• Kanda, Atsushi, et al. "Effects Of Whey, Casein, Or Milk Protein Ingestion On Muscle Protein Synthesis After Endurance Exercise." MEDICINE AND SCIENCE IN SPORTS AND EXERCISE. Vol. 46. No. 5. 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA: LIPPINCOTT WILLIAMS & WILKINS, 2014.
• Kerksick, Chad M., et al. "The effects of protein and amino acid supplementation on performance and training adaptations during ten weeks of resistance training." The Journal of Strength & Conditioning Research 20.3 (2006): 643-653.
• Norton, Layne E., et al. "The leucine content of a complete meal directs peak activation but not duration of skeletal muscle protein synthesis and mammalian target of rapamycin signaling in rats." The Journal of nutrition 139.6 (2009): 1103-1109.
• Reitelseder, Søren, et al. "Whey and casein labeled with L-[1-13C] leucine and muscle protein synthesis: effect of resistance exercise and protein ingestion." American Journal of Physiology-Endocrinology and Metabolism 300.1 (2011): E231-E242.

Tribulus Boosts Testosterone (+12%), IGF-1 (+20%), Sheds 2kg (7%) Body Fat and Maintains Lean Mass in 12 Wk RCT

Tribulus Boosts Testosterone (+12%), IGF-1 (+20%), Sheds 2kg (7%) Body Fat and Maintains Lean Mass in 12 Wk RCT

andropause build muscle gains lose fat male health testosterone testosterone booster tribulus tribulus terrestris TRT

Could a high dose of purified saponin tribulus extract as it was obviously used in the study at hand actually be a valid TRT alternative or even option? 

No, this is not the 2015 study in trained boxers that found similarly surprising, because impressive benefits from tribulus terrestris (TT) supplementation (read it). It's a new study from the Jerzy Kukuczka Academy of Physical Education in Katowice, Poland (Wilk. 2016) that has no direct link to the previously discussed study from the  Shanghai University of Sport Affiliated School of Sports in China.

And even though, the aim, i.e. to determine the effects of steriodal saponins from tribulus terrestris on the blood concentration of testosterone (T), GH and IGF-1 was similar, the overall design of the study was significantly different.

Don't forget to work out - Without exercise you're not going to get lean and jacked, bro!

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While the previously discussed study by Ma et al. (2015) was conducted with young athletic individuals, Wilk et al. deliberately chose 14 men between the age of 45 and 60 years, i.e. exactly those years in a man's life over the course of which the natural hormone production starts to decline significantly.

Table 1: How to recognize your T-levels are declining (from Matsumoto. 2002).

Over twelve weeks, the subjects who were normal-to-overweight with a body mass index of 25–33, and body fat content between 23–30%, received either...

• experimental group: steroidal saponins (TT) - for the first six weeks three capsules (900 mg) per day in split doses (2x capsules were ingested in the morning on an empty stomach, 600 mg, and one at bedtime, 300 mg) and twice the dose, i.e. 6 capsules (1,800 mg) were ingested per day in split doses (4x capsules in the morning on an empty stomach, 1,200 mg, and 2x capsules at bedtime, 600 mg), or 

What's the use of the "front load", i.e. taking more in the AM vs. PM? That's a question I just received from Peter via Facebook. Good question, but one the scientists do not answer. So I'd have to speculate that they may have intended to mirror the natural 24h (=circadian) rhythm of testosterone which peaks in the AM and declines over the day to re-increase over night and peak again in the AM. What is particularly interesting about this rhythm, by the way, is that it - or rather the peaks in the AM, are lost as you age (see Figure on the left | Bremner. 1983).

• control group: placebo (CON) - in the form of gelatin capsules using the same supplementation protocol as it was prescribed in the experimental group 

And even though all subjects participated in a physical activity program over the 12 week study period, the workouts the scientists describe as follows,...

"Get leaner, more muscular and hornier than ever before" - That's probably the promise on the T-booster someone will release after reading this SuppVersity Classic article and sourcing an inferior Shilajit extract on Alibaba. Is that going to be a waste of time - just as the majority of the tribulus products on the market, which are lightyears away from providing grams of pure saponines on a multiple serving per day basis | learn more.

"4 training sessions per week, with 2 sessions directed at the improvemnt of anaerobic power (resistance exercise), while 2 consisted of aerobic endurance exercise. Aerobic training was performed on a stationary cycle ergometer, starting with 30 minutes of continuous exercise at an intensity of 70–75% of maximum heart rate (HR max). Every two weeks, the work volume was increased by 5 minutes in order to reach 60 minutes in the last two weeks of the experiment. Strength training had a holistic aproach, involving all major muscle groups (the back, chest, abdomen, arms and lower limbs). For the first four weeks, exercises were performed in 3 sets of 8–12 reps with the resistance equal to 60–70% of 1RM and 2 min rest periods between sets. During the experiment, the number of sets of each exercise increased from 3 to 4 sets in weeks 5–8, and respectively to 5 sets in weeks 9–12 for each exercise," (Wilk. 2016)

was of course not the same as the one in the previously discussed Chinese study. In conjunction with the standardized isocaloric (same energy content) mixed diet containing 55% carbohydrate, 20% protein, 25% fat, the workouts are still an important means of standardizing / reducing inter-group differences that could otherwise arise due to personal exercise and / or diet preferences.

Figure 1: Relative changes in blood lipids, GH, IGF-1 and testosterone (Wilk. 2016).

The results of the scientists' two series of laboratory tests (independent tests were conducted at the beginning and after 12 weeks of the intervention), revealed a statistically significant effect of the intervention on the following variables: T-Ch (η2 = 0.542), HDL-Ch (η2 = 0.522), LDL-Ch (η2 = 0.587), T (η2 = 0.603), IGF-1 (η2 = 0.512) and GH (η2 = 0.621).

Figure 2: Relative changes in body composition; effect sizes and p-values (Wilk. 2016).

Effects of which you will probably pleased to hear that they went hand in hand with significant decreases in total body fat (TBF) total body mass (BM) and borderline significant effects on the fat-free mass (muscle, organ and bone mass) of the subjects - an observation of which the scientists say that it "indicate[s] that treatment or supplementation of individual hormone deficiencies can be a successful form of counteracting the aging process" - an aging process that is evidenced by increasing body fat levels, decreasing amounts of fat-free mass and concomitant deterioration of blood lipids and blood glucose (the latter was unfortunately not measured in the study at hand).

Wtf!? What kind of tribulus was that? I wish I could tell you that, but a brand name or other specifics are not mentioned in the publicly financed study from Poland.

Make no mistake about it, the impressive increases in free T in Brown's often miscited 2001 study from which I took this figure were due to a combination of the prohormone androstenediol with tribulus and other herbs. To ascribe the T-increase to TT is idiotic.

What I can tell you is that the results are in line with a 2009 study by Milasius, et al. who used food a commercial supplement Tribulus from Optimum Nutrition, USA, and observed positive effects on the acid-base equilibrium after short-term, high intensity anaerobic exercise in competitive athletes. The study at hand apparently used a more pruified steroidal saponin supplement, however, and observed similar effects as Brown et al. (2001), who supplemented tribulus alongside 300mg of the prohormone androstenediol and found - not to anyone's surprise, probably a significant effect on serum testosterone concentration in both young and older men (see Figure to the right).

Since no such effects were observed in the often cited study by Neychev, et al.  (2005) in allegedly much younger subjects, the question future studies will have to answer is whether that's due to an (subject-)age- or dosage / otherwise supplement-related difference between the high dose of (probably) pure saponins used in the study at hand and the relatively low dose of Bulgaria TT (200mg/day) with 60% saponins that was used by Neychev, et al. in 2005 | Comment!

References:

• Bremner, William J., Michael V. Vitiello, and Patricia N. Prinz. "Loss of Circadian Rhythmicity in Blood Testosterone Levels with Aging in Normal Men*." The Journal of Clinical Endocrinology & Metabolism 56.6 (1983): 1278-1281.
• Brown, Gregory A., et al. "Endocrine and lipid responses to chronic androstenediol-herbal supplementation in 30 to 58 year old men." Journal of the American College of Nutrition 20.5 (2001): 520-528.
• Matsumoto, Alvin M. "Andropause clinical implications of the decline in serum testosterone levels with aging in men." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 57.2 (2002): M76-M99.
• Milasius, K., R. Dadeliene, and Ju Skernevicius. "The influence of the Tribulus terrestris extract on the parameters of the functional preparedness and athletes’ organism homeostasis." Fiziol Zh 55.5 (2009): 89-96.
• Neychev, Vladimir Kostadinov, and Vanyo Ivano Mitev. "The aphrodisiac herb Tribulus terrestris does not influence the androgen production in young men." Journal of ethnopharmacology 101.1 (2005): 319-323.
• Wilk, Michał, et al. "Endocrine Responses to Physical Training and Tribulus Terrestris Supplememtation in Middle-Age Men." Central European Journal of Sport Sciences and Medicine 13.1 (2016): 65-71.

Important Insights into Muscle Growth: Muscle Breakdown & Protein Synthesis Balance Determines Your Muscle Gains

Important Insights into Muscle Growth: Muscle Breakdown & Protein Synthesis Balance Determines Your Muscle Gains

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MyoPS - muscle damage = gainz - It's as easy as that, but this simple equation gets complicated by decreases in both...

You will remember from previous SuppVersity articles that the assumption that an acute increase in myofibrillar protein synthesis (MyoPS) you measure after a workout would necessarily translate into "muscle gains" is oversymplistic. In fact, a correlation between muscle hypertrophy and acute MPS has been shown not to exist (learn more).

In the introduction to their latest paper, Felipe Damas et al. (2016) highlight our lack of understanding of the different mechanisms that eventually determine t he hypertrophy response to resistance training.

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To investigate how muscle hypertrophy is modulated through RT, Damas et al. "measured day-to-day integrated myofibrillar protein synthesis (MyoPS) using deuterium-oxide ingestion and assessed muscle damage at the beginning (T1), at 3wk (T2), and 10wk of RT (T3)" in a study that involved ten young men (27(1) y) who had muscle biopsies (vastus lateralis) taken to measure integrated MyoPS and muscle damage (Z-band streaming and indirect parameters) before and 24h and 48h post-resistance exercise (RE) at T1, T2 and T3.

Figure 1: Experimental design. RE: resistance exercise; D2O: deuterated water; MVC: maximal voluntary isometric torque; SOR: muscle soreness; T1: 1st week of resistance training (RT); T2: 3rd week of RT; T3: last week of RT (Damas. 2016).

The analysis of the data from the subjects who had prior experience in lower limb RT, before they trained their lower limbs (bilateral 45° leg-press exercise and leg extension) for 10 weeks in the study at hand (twice a week, totaling 19 workouts), but who had not engaged in lower limb RT for at least 6 months prior to the study and did not use vitamin supplements or anti-inflammatory medications chronically were recruited, provided some interesting insights.

Figure 2: Fibre cross-sectional area (CSA) at the first week (T1), third week (T2) and tenth week (T3) of resistance training. † Significantly different (P < 0.05) from T1 and T2. Values are means (SEM | Damas. 2016)

Firstly, there's the increase in fibre cross-sectional area, which was observed to be significant only when the scientists compared the fcsa at T3 compared with T1 (P =0.017) and T2 (P = 0.027; see Figure 2) - in other words: Significant gains were made only over the latter part of the training period.

Figure 3: (A) Myofibrillar (Myo) fractional synthetic rate (FSR) at rest, 24h and 48h following a single bout of resistance exercise at the first week (T1), third week (T2) and tenth week (T3) of resistance training. * Significantly different (P < 0.05) from rest at T1. # Main acute time effect (24h significantly different (P = 0.003) from 48h independent of training phase). ‡ Main training phase effect (T1 significantly different (P < 0.03) from T2 and T3). (B) Change from baseline in the percentage of fibres that showed any Zband streaming sign following a single bout of resistance exercise at the T1, T2 and T3. ‡ Significantly different (P < 0.05) from T2 and T3. + Significantly different (P < 0.05) from T3 (Damas. 2016).

These increases in the actual muscle size gains (vs. MyoPS) are the related to the second and most important observation, which is, as the highly significant decrease in Z-Band data in Figure 3.b indicates, a result of the improved difference between muscle protein synthesis, which decreased much less than the protein breakdown the scientists approximated by the means of directly assessed muscle ultrastructure changes (Z-band streaming). In other words: the "net gains" increased over time, as the subjects accommodated to the workouts.

In the previous study by Mitchell et al. (2014) there was no correlation between MyoPS / FSR andn the actual increase in muscle size over 16 weeks.

Bottom line: One thing that is important to highlight is the training status of the subjects of whom I previously pointed out that "had not engaged in lower limb RT for at least 6 months prior to the study" (Damas. 2016). This is important, because it is probably the prerequisite for the time-effect. A time effect which is characterized by (a) slightly decreasing protein synthesis from week one to week three (and following) and highly significantly decreasing muscle damage over the first 3 weeks, over which the muscle damage due to the initially unaccustomed exercise declined progressively.

Accordingly, Damas et al. were able to confirm a correlation between MyoPS, i.e. the myofibrillar protein synthesis, and the actual muscle hypertrophy that had not been observed by Mitchell, et al. (2014 | read up on the study in my previous article) only in the latter ~70% of the study when the net muscle gains increased due to the significant decrease in protein breakdown.

That the results of this study which are in disagreement with a previous studies that found "acute increases in MyoPS aligned qualitatively with hypertrophy-related chronic RT outcomes, such as increases in muscle volume and muscle fibre CSA (fCSA)" would be "due to damage to protein structures that would require repair, and therefore a greater increase in protein synthetic response" was the point of departure for Damas et al. in the study at hand. And it is also what the data the experiment generated confirmed: "Despite the lack of correlation between initial MyoPS and muscle hypertrophy, we observed that early (T2) and later (T3) rates of MyoPS, while attenuated compared to initial (T1), were strongly correlated with muscle hypertrophy" (Damas. 2016).

Another related and likewise important important finding of the study at hand is the observation that the subjects' muscle damage, on the other hand, "which was progressively mitigated throughout RT reaching a minimal magnitude at the end of 10wk of RT, did not correlate with MyoPS or hypertrophy at any time point during RT" (Damas. 2016). Eventually, the exercise induced increase in protein synthesis may thus still be considered the determinant factors underpinning RT-induced muscle hypertrophy in - as long, at least, as we are looking at trained subjects doing exercises they have already accommodated to (within ~3 weeks) | Comment on Facebook!

References:

• Damas, Felipe, et al. "Resistance training‐induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage." The Journal of physiology (2016).
• Mitchell, Cameron J., et al. "Acute post-exercise myofibrillar protein synthesis is not correlated with resistance training-induced muscle hypertrophy in young men." PLoS One 9.2 (2014): e89431.

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

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

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

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

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

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

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

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

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

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

Bitter perception (Mennella. 2013).

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

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

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

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

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

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

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

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

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

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

References:

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