Author: valdesfraost

The Ketogenic Diet & Your Gains: Study Shows Body Comp. Benefits (Fat ↓), but Decreased Muscle Gains, However…

Unfortunately, the authors do not report what exactly (foods) the subjects ate.

I am pretty sure you will already have seen the results of Salvador Vargas’ recent study in the Journal of the International Society of Sports Nutrition elsewhere, there are good reasons for me to still address what the authors claim was the first study to determine “if following a KD hypercaloric diet would promote greater gains in fat free mass and fat loss during a hypertrophic training period in resistance-trained men” (Vargas 2018) in an individual post – not just, but also because the scientists were unable to confirm their hypothesis, that a “KD with caloric surplus in combination with RT in trained men would have a positive impact” on both body fat and lean body mass (LBM).

Learn more about and related to low-carbohydrate diets in previous SuppVersity articles:

Protein Oxidation an Issue W/ High PRO Diets?

CHO ↓ = Perfor-mance ↓ – What about Avg. Joes?

More Protein ≠ More Satiety, Study Shows

Is Low Carb Even Crossfit Compatible?

Coffee Promotes Ketosis Despite High Carb Intakes

Keto Diet per se for Superior Weight Loss?

From a methodological perspective, the randomized, parallel arm, controlled, prospective study looks solid – even though the exclusion of anyone who consumes dietary supplements and the neither physique-, nor performance-based inclusion criteria of having more than 2 years of continuous experience in overload training may not necessarily represent what the average gymrat would think of when he/she hears about “resistance-trained individuals” – with an average age of 30 ± 4.5 years, a body weight of 76.7 ± 5.7 kg at a height of 177 ± 3.4 cm (BMI = 23.4 ± 2.2 kg/m²) and a body fat percentage of 15 and 17% in the NKD and KD group, respectively (the difference was statistically non-significant), the subjects came much closer to this concept than the average “trained” study participant who is, often in spite of having trained for years, both weak and fat… accordingly, it’s not totally surprising that the control group, who continued on their self-designed programs and kept their regular non-ketogenic eating habits, gained almost as much lean mass as the NKD group.

Figure 1: Overview of training protocol. WK: Workout (microcycle); UL: Upper-Limb; LL: Lower-Limb; R: Rest; 30X: 3 s of eccentric contraction and explosive movement concentric (Vargas 2018).

Something similar can be said about the subjects’ workout routine. As you can see in Figure 1, the subjects trained four times a week in form of a repeated upper-/lower-body split using a selection of classic resistance training exercises that ranged from bench presses to triceps dips (UL-day) to squats and machine calf raises (LL-day).

In combination with the three rest days, the 32 workouts all subjects performed over the course of the 8-week study triggered the expected improvements in body composition (=an improvement of the lean-to-fat-mass ratio) in all subjects irrespective of whether they had been randomized to the control diet, the ketogenic diet (KD), or the non-ketogenic diet (NKD).

Macronutrient composition of the ketogenic and non-ketogenic diets.

What did the diets look like? The participants were randomly assigned to a KD group (n = 9), non-KD (NKD) (n = 10) group, and control group (CG) (n = 5). Once energy expenditure was determined, together with their weekly training load, a moderate energy surplus was established for experimental groups. To guarantee a hyperenergetic condition, a daily energy intake of ≈39 kcal/kg/d was used in all subjects, with ca. 20% of this energy, i.e. 8 kcal/kg/d (= 2g protein per kg), coming from protein in both, the KD and the NKD group, all subjects should have gotten enough energy and protein to optimize muscle anabolism during and after the 3-6 recommended meals.

The use of a hypercaloric diet + resistance training is imho a novelty in the realms of low-carb research. Accordingly, it’s all the more disappointing that methodological short-comings limit the significance and hamper the interpretation of the results. What am I talking about? Well, neither the levels of ketones that were eventually measured with keto-sticks from week two onward, nor the macro-composition of the “control” diet were adequately reported… and, more importantly, the actual energy and macronutrient intake of the subjects wasn’t even tested – an important short-coming in view of the hunger-quelling effects of ketogenic diets (Gibson 2005; Bellissimo 2015).

A closer look at the actual study results does yet also show significant inter-group differences for both, the individual gains in lean mass and reductions in fat mass in the NKD and KD study groups:

Figure 2: Changes in parameters of body composition over the 8-week study on KD, NKD or control diet (Vargas 2018).

If we do the math, the diverging increases in lean and decreases in fat-mass amount to a higher (albeit not significantly) increase in body composition if the latter is defined by the subjects’ body fat %, I calculated based on the absolute changes in body weight and fat mass.

There are things you should be aware of before jumping to conclusions

The first thing doesn’t even require looking beyond the results of the study at hand: (1) the overall effect of the workout + diet combinations are marginal or small, (2) only the increase in lean mass in the NKD and the decrease of fat mass in the KD group were statistically significant with p < 0.05, and (c) the study which must be considered a small scale pilot clearly suffers from the lack of dietary control. The latter is particularly problematic because previous studies have observed significant appetite reducing effects with ketogenic diets. In the absence of rigorous dietary control, both, the increased fat loss and the decreased muscle mass could well be a result of the subjects’ non-compliance with the standardized energy target of 39kcal/kg/d.

Figure 3: According to the scientists’ calculation of effect sizes even the statistically significant effects of the KD on body fat and the NKD on lean mass were only “small” – an observation that’s not uncommon in trained individuals.

What I think is yet even more important, though, is that using DXA, the alleged “gold standard” for body composition standards, in studies that involve one or multiple transitions from regular high-carb to ketogenic diets and vice versa are prone to yield unreliable results. I’ve discussed that at length in my dissertation to Wilson’s often-criticized keto-gains study, a study that used a virtually identical KD as the study and hand and still yielded fundamentally different results… because Wilson et al. decided to (carb-)refeed their subjects before the final measurement. Whether that was a deliberate mistake, or not has not just been debated more than often enough, it’s also irrelevant when it comes to the significance of the results of the study at hand.

What is relevant, however, is that comparing DXA data from high- vs. low-carb phases is akin to comparing apples and oranges; and this is particularly true if the standard 2-compartment model is used (cf. Toombs 2012 | note: the study at hand didn’t report which method Vargas et al. used, but if they’d used the more accurate but still not infallible 4-component- aka 4C-model, I am sure the scientists would have highlighted that).

The visceral fat data isn’t more reliable.

A note on the 100g loss of visceral fat in the KD group: I am not aware of any studies investigating the effect of glycogen and body water on DXA measured visceral fat levels, but in view of the general tendency to observe increases in body fat in response to glycogen repletion it is not unlikely to assume that the visceral fat advantage Vargas et al. observed in the KD group (check out the figure on the left) could have been a measurement artifact, too.

The small decrease in lean mass and, to a certain degree, the increased loss of body fat may thus be nothing but artifacts the measurement method generates when it’s used on subjects on a diet that has repeatedly been shown to trigger both significant water- and glycogen-reductions (Nana 2012Burke 2017) and thus physiological changes of which the researchers have highlighted previously that they could explain the “substantial changes in [DXA-based] estimates of body composition over the course of the day” Bone & Burke observed in previous studies (Bone 2016).

Figure 4: Relative changes in leg lean and fat mass vs. baseline following glycogen depletion and glycogen loading with and without creatine (Bone. 2017) – this particular figure was initially published in a SuppVersity article from 2016.

As highlighted in a 2016 SuppVersity Article, Bone and Burke observed highly significant increases in lean and fat mass within only 3 days when they fed well-trained cyclists a high(er = 2x more than baseline) carbohydrate diet (see data in Figure 2 | Bone 2017); the exact opposite, i.e. statistically significant and, if you falsely take them at face value, practically relevant reductions in both lean and fat mass, was observed by Bone & Burke as a result of the initial glycogen depletion in the same study.

A fair comparison using DXA data would require normalizing the groups’ glycogen levels

In that, it is worth noting that Bone’s results deviate from a previous study by Rouillier et al. who observed a smaller increase in body fat (compared to lean mass) and thus an overall decrease in body fatness in response to 3 days on a high carbohydrate diet in their 2015 study. Whether and to which extent the differential effects on the subjects’ measured (not real) fat mass can be explained by methodological differences such as the lack of intense training and/or differences in the subjects’ athleticism between the studies cannot be said for sure at the moment.

Figure 5: Let’s be clear here, I don’t advocate super-compensation strategies as they were used in Wilson’s 2017 study week 11, as this would skew the data in the opposite way(s), i.e. exaggerate the lean mass gains on a ketogenic diet.

What we can say with reasonable confidence, though, is that you shouldn’t put too much confidence into the accuracy/objectivity of the DXA data from the study at hand. Gold standard or not. DXA is so prone to be skewed by changes in glycogen and body water that t would require a glycogen normalization intervention before the final DXA scan – one that does not provide an unfair advantage to the keto group, though (see the previously discussed study by Wilson et al.)…

What? Oh, no, this does not mean that all previous studies on the effects of ketogenic diets on body composition are bunk. In view of the fact that >90% of them are weight loss trials, the vast majority of this study will have a certain degree of muscle glycogen depletion in both the keto and the control diet simply due to the lack of total energy. This is in contrast to the study at hand, where the non-ketogenic and the control diet were not just significantly higher in carbohydrates, but, in view of the lack of dietary control and the repeatedly observed appetite suppressant effects of ketogenic diets, probably also significantly higher in total energy intake. Against that background, it is reasonable to assume that any glycogen-/water-related differences in DXA-based estimates of body composition would be exasperated compared to studies that used high vs. low carb diets for weight loss purposes.

Re-read my analysis of Wilson’s 2017 study that epitomized the influence of muscle glycogen on DXA data.

Don’t get me wrong: I don’t say the study results are bunk. I do however want you to keep in mind that DXA is very sensitive to changes in glycogen (and water) levels:

Now, if the overall carbohydrate intake of subjects is reduced, this will necessarily affect the skeletal muscle glycogen stores and hence any DXA-based estimation of the subjects’ body composition; and it will do so in a way that we haven’t studied sufficiently in the context of a supposedly hypercaloric diet as it was applied in the study at hand.

Against that background and in view of the fact that the appetite suppressive effects of ketogenic low-carb diets could well have messed with the scientists’ intention to overfeed their subjects, only a fool would use the study at hand as “proof” of the pro-fat loss and/or anti-muscle-gain effects of ketogenic diets (needless to say that only a fool would consider a single small-scale study, in isolation, reliable “proof” of anything 😉 | Comment on Facebook!


  • Bellissimo, Nick, and Tina Akhavan. “Effect of macronutrient composition on short-term food intake and weight loss.” Advances in Nutrition 6.3 (2015): 302S-308S.
  • Bone, Julia L., et al. “Manipulation of muscle creatine and glycogen changes dual x-ray absorptiometry estimates of body composition.” Medicine & Science in Sports & Exercise 49.5 (2017): 1029-1035.
  • Bone, Julia, and Louise M. Burke. “DXA estimates of body composition and carbohydrate loading.” Annals of Nutrition and Metabolism 68.3 (2016b): 228-229.
  • Burke, L. “Dual X-Ray Absorptiometry (DXA) for measurement of body composition in athletes: Experiences that underpin the importance of optimising the reliability of measurement.” Journal of Science and Medicine in Sport 20 (2017): 76.
  • Gibson, Alice A., et al. “Do ketogenic diets really suppress appetite? A systematic review and meta‐analysis.” Obesity Reviews 16.1 (2015): 64-76.
  • Nana, Alisa, et al. “Effects of daily activities on dual-energy X-ray absorptiometry measurements of body composition in active people.” Medicine & Science in Sports & Exercise 44.1 (2012): 180-189.
  • Nymo, Siren, et al. “Timeline of changes in appetite during weight loss with a ketogenic diet.” International Journal of Obesity 41.8 (2017): 1224.
  • Rouillier, Marc-Antoine, et al. “Effect of an acute high carbohydrate diet on body composition using DXA in young men.” Annals of Nutrition and Metabolism 66.4 (2015): 233-236.
  • Toombs, Rebecca J., et al. “The impact of recent technological advances on the trueness and precision of DXA to assess body composition.” Obesity 20.1 (2012): 30-39
  • Vargas, Salvador, et al. “Efficacy of ketogenic diet on body composition during resistance training in trained men: a randomized controlled trial.” Journal of the International Society of Sports Nutrition 15.1 (2018): 31.

The Ketogenic Diet & Your Gains: Study Shows Body Comp. Benefits (Fat ↓), but Decreased Muscle Gains, However… syndicated from


How We Help Our Kids Eat Healthy

Helping your children eat healthy has it’s challenges. However, the return you get in their well being, attention, and sleep is well worth it! We want to set our kids up for success, and the best way to do that is to help them eat healthy. Plus, I’ll also share some areas where we need to improve.

1. Offer Them Healthy Choices First

By no means are we restrictive with our children’s food choices. However, we do make it a point to offer healthy choices first.

I’m thankful my kids like to eat a variety of foods, but I do invest a good amount of time making sure they have the chance to make healthy choices.

It wasn’t until my husband and I began introducing a more holistic approach to nutrition that I really scrutinized the ingredients listed on packaged “food.” Yikes. Now, I’m so much more cognizant of what is going into their little bodies.

2. Let them help in the kitchen

I have to admit, I can do so much better in this area. Yes, it’s faster and MUCH cleaner to do it on my own, but I want them to take ownership for their healthy choices.

My kids love to select their morning and afternoon shake flavors. They prepare them on their own too: scoop, ice, water, blend, and done. Perfectly balanced macro and micronutrient meal.

They come up with some pretty delicious combos. Other times, I have to guide them a bit! And, I feel so relieved that I am filling the nutritional gaps in their diet that our whole foods are missing these days.

3. Educate them so they can understand WHY we are fueling this way.

While we let our kiddos enjoy treats occasionally–well probably more than occasionally–we also try to use words like “strong, energy, and nutritious,” not words like “bad vs. good,” or “diet.”

We remind them that the food we choose helps us feel strong, or have energy to perform well in say, gymnastics, or focus for school.

We notice a marked difference in their behavior when they get dense nutrition in their bodies and adequate sleep. They are simply happier kiddos which helps all of us!

Areas to improve

There are several areas I still need to work on. One being using food as a reward. I’m guilty of giving them a snack just to keep them busy, so I can get something accomplished.

Snacks are fine! Now, I’m making a point to offer fresh fruit, veggies, or a protein bar first before resorting alternatives.

Another area to consider, is eating meals as a family. This is really rare for us. Not to make excuses, but my husband’s job keep him on the road or working long hours a majority of the year.

The times we do get to spend together as a family, we make a point of verbalizing how happy we are to be together. Seriously, the coach-wife life makes your grateful for the smallest moments.

How do you help your kids make healthy choices? Please share!


The post How We Help Our Kids Eat Healthy appeared first on Blonde Ponytail.

How We Help Our Kids Eat Healthy syndicated from

Cyclists & Asthma? ~20% Increased Protein Synthesis W/ Salbutamol, Another Reason its Abuse Cannot be Ignored

Even if it is medically indicated, there’s more and more evidence that using beta-2-agonists (esp. but not exclusively orally) could provide an unfair advantage to athletes: increased protein synthesis, increased mitochondrial neogenesis, established ergogenic effects,…

If you’ve been following the news, you will be aware that the Tour de France Champion Chris Froome who has been busted with elevated levels of the beta-2-agonists Salbutamol in his blood (learn more). Now, we could debate forever about whether the green light Froome just got is a case of double-standards or not, but that’s not the purpose of this article, anyway. Rather, I want to explain why the claim that salbutamol, officially an asthma medication, wouldn’t be a worthwhile doping agent is bullshit.

Learn more about Clen– / Albuterol and safer ways to get jacked at the SuppVersity

Albuterol Can Improve Glucose Metabolism

The Myostatin <> Clenbuterol Connection

Higenamine Useful “OTC Clenbuterol”?

Out of question: β2-Agonists = Doping Agents

β2-Agonists Build Muscle: 1kg (DXA) in 4 Wks

Albuterol+Coffee – Science-based fat burner?!

I’ve addressed the (ab-)use and positive side effects of beta-2-agonists in previous articles. Next to proven ergogenic effects in cycling (see “Albuterol / Salbutamol Doping Works!” | read it) these agents have also been shown to have a direct beneficial (=lowering) effect on the protein synthesis brake myostatin (read more). In today’s follow-up I want to address a related study, a study in trained men and a study that adds another item to the list of benefits of “having asthma” (and being prescribed clenbuterol, albuterol, salbutamol, etc.) as a cyclist.

Figure 1: From increased protein synthesis to boosted mitochondrial biogenesis the (ab-)use of regular amounts of beta-2-agonists has been shown to have various benefits that would warrant their ban in drug-controlled sports.

In said study, researchers from the Department of Nutrition, Exercise and Sports at the University of Copenhagen (Hostrup 2018) investigated the effect of beta2‐adrenoceptor stimulation on skeletal muscle protein turnover and intracellular signalling – a previously “[, in humans, ] insufficiently explored, particularly in association with exercise” (Hostrup 2018).

The study was a randomized placebo‐controlled crossover study with 12 trained men, in which the Danish researchers probed the effect of beta2‐agonist (6 × 4 mg oral salbutamol) on protein turnover rates, intracellular signalling, and mRNA response in skeletal muscle was investigated 0.5–5 h after quadriceps resistance exercise. In order to standardize the treatment and generate reliable results, …

“[…e]ach trial was preceded by a four‐day lead‐in treatment period. Leg protein turnover rates were assessed by infusion of [13C6]‐phenylalanine and sampling of arterial and venous blood as well as vastus lateralis muscle biopsies 0.5 and 5 h after exercise. Furthermore, myofibrillar fractional synthesis rate (FSR), intracellular signalling and mRNA response were measured in muscle biopsies.” (Hostrup 2018)

So, there’s no reason to doubt the practically relevant 20% increase in myofibrillar FSR for salbutamol compared to placebo [0.079(±0.007) vs. 0.066(±0.004)% × h−1](P < 0.05) – with both, the relative increase and the net leg phenylalanine balance 0.5–5 h after exercise, i.e. 3.6(±2.6) nmol × min−1 × 100 g, being highly relevant for an athlete, especially in view of the previous observation that benefits are additive and significant gains over time can be expected for at least a few weeks before an already less likely (vs. clenbuterol) beta-2-receptor downregulation occurs.

Figure 2: Hostrup et al. found a practically relevant, statistically significant increase in protein synthesis not just in response to the administration of 6x4mg of salbutamol, but also a baseline effect in response to the 4-day preload at only 4x4mg of the asthma medication – a dosage that is used quite certainly year-round by athletes around the world (Hostrup 2018).

In contrast to what the actually relevant outcome, the increase in protein synthesis, would suggest, the scientists did not observe a relevant decline in myostatin. In fact, the protein that acts as a protein synthesis brake and is meant to limit the domain sizes in skeletal muscle to maintain full functionality increased significantly both 0.5 and 5h after the intervention (see Figure 3):

Figure 3: The changes in regulatory gene expression do not necessarily predict an increase in protein synthesis, but the increase in PGC-1alpha, for example, will also come handy for any endurance athlete (and everyone trying to build a more potent metabolic engine by increasing mitochondrial adaptation to exercise | data from Hostrup 2018).

Even though this adds a question mark after the previously voiced hypothesis that a decrease in myostatin (which has btw. only been observed with clenbuterol, the much longer acting cousin of salbutamol | more), it does not negate that as little as 24mg of salbutamol (in the four days before each trial, the subjects consumed only 16mg/d) and hence less than the recommended maximal daily dose (=8×4 mg per day | for the treatment of asthma triggered a(n over time) performance-relevant increase in protein synthesis in all but two outliers (see Figure 2).

Yes, inhaled beta-2-agonists are less ergogenic than oral drugs, but the same research group has previously demonstrated successfully that the “[d]aily inhalation of terbutaline in near‐therapeutic doses induces skeletal muscle growth” (Jessen 2018 | learn more).

It is thus hardly useful to keep citing Kindermann’s 2007 opinion piece stating that ergogenic effects are unlikely to occur, whenever another athlete is busted with elevated levels of beta-2-agonist. The latter is particularly true in view of the fact that Kindermann focussed on inhaled beta-2-agonists, which shouldn’t even show up on a blood test as the post-administration serum concentrations tend to be significantly lower than what you’d see after the administration of salbutamol and co in pill form (oral tablet, as it was used in the study at hand).

The poor endurance athletes are most likely to suffer from asthma. Incidentally, those who are treated are also significantly more likely to be among the Olympic medalists… crazy coincidence, right (data from Fitch 2008)?

Data on exactly how many “poor” athletes suffer dearly from asthma and how many of them take the convenient pills 4-8x a day is unfortunately not available. What we do know from the few studies that investigated the (ab-)use of asthma medications showed a prevalence of 16.7% for Olympic athletes (Weiler 1998) – and, among those, no one was as likely to suffer as the group of cyclists (see Figure 4, left)… those poor dudes 😉

Suggested read for non-asthmatic athletes: Specific timing may change the body composition effects of whey protein, 2018 study suggests.

Let’s not be unfair, but let’s be realistic: In view of the fact that scientists have long speculated that the constant exposure to particulate matter from exhaustive fumes, etc. has long been suspected to contribute to the increased asthma rates in cyclists, it would be unfair to place cyclists with pharmacologically treated asthma under general suspicion. The way officials and now the sports tribunal sweep their abuse under the carper, on the other hand, is clearly unwarranted – the evidence for practically (not just statistically) significant effects on exercise performance and training adaptation (VO2, muscle mass, etc) is there.

And, said research is accumulating quickly and in a way that darkens the shadow the abuse of beta-2-agonists by athletes has been casting for years on the extraordinarily high prevalence of asthma, especially, but not exclusively among elite athletes in endurance sports | Comment!


  • Fitch, Kenneth D., et al. “Asthma and the elite athlete: summary of the International Olympic Committee’s consensus conference, Lausanne, Switzerland, January 22-24, 2008.” Journal of allergy and clinical immunology 122.2 (2008): 254-260.
  • Hostrup, Morten, et al. “Beta2‐adrenoceptor agonist salbutamol increases protein turnover rates and alters signalling in skeletal muscle after resistance exercise in young men.” The Journal of Physiology (2018).
  • Weiler, John M., Teresa Layton, and Margaret Hunt. “Asthma in United States Olympic athletes who participated in the 1996 Summer Games.” Journal of Allergy and Clinical Immunology 102.5 (1998): 722-726.

Cyclists & Asthma? ~20% Increased Protein Synthesis W/ Salbutamol, Another Reason its Abuse Cannot be Ignored syndicated from

NAC Lowers DOMS, Initially, but on Day 5-6 it Makes Things Worse | Plus: Putative Performance Benefit is Negligible

In the long run, choking the exercise-induced fire too much is going to negate all the cherishable benefits of working out.

As a SuppVersity reader, you know what hormesis is and are aware that the proinflammatory assault of exercise, is an essential stimulant to musculoskeletal adaptation – a number of human and dozens of animal experiments show: if you quell the production of pro-inflammatory reactive oxygen species with high doses of vitamin C and E the growth and health response to exercise will be impaired. And vitamin C + E are not the only radical scavengers with this side effect.

In 2013, I wrote about a study that clearly demonstrated how N-acetyl-l-cysteine aka NAC “Reduces Inflammation, Muscle Injury & Cytokine Expression, but Impairs Anabolic Signaling, Satellite Cell Activity and Recovery” (re-read it) – keep that in mind before getting overly excited.

Read about exercise- and nutrition-related studies in the SuppVersity Classic Articles

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Hence, NAC supplements shouldn’t be used chronically. To control the inflammatory response to a workout and be able to return to the grind earlier, however, many people still rely on its noticeable ability to reduce early onset of DOMS (deep onset muscle soreness – learn more).

Is taking NAC ever a good idea for athletes?

Well, the good news for NAC lovers is: When used during a short competition, sportsmen and -women can actually benefit from the anti-DOMS effects, a recent study from the University of Auckland (Rhodes 2018) confirmed when it investigated…

“whether NAC supplementation decreases muscle soreness and enhances performance in a semi-elite sport setting [as well as] adverse effects and the tolerability of oral NAC supplementation” (Rhodes 2018).

The bad news is that using NAC for that very purpose won’t just impair long-term gains, it would also backfire in terms of the what one could call a delayed DOMS response (if DOMS wasn’t already delayed onset muscle soreness, obviously) on day 5-6 of the recovery period.

Figure 1: Schematic overview of the experimental design. Preliminary YYIRT-L1 performance measures were taken during preseason training, and post-supplementation performance measures were performed on days 5 and 6 of supplementation (NAC or placebo). Side effects and subjective muscle soreness were monitored through a daily TXT message during the supplementation period. NAC = N-acetylcysteine (Rhodes 2018).

That’s at least what Rhodes’ et al’s observation that the initial “likely protective effect” (−19% ± 27%) on subjective muscle soreness of the 28 semi-professional, semi-elite male rugby players (age = 20.4 ± 0.9 yrs, height = 182.3 ± 7.4 cm, weight = 103 ± 12 kg, Yo-Yo Intermittent Recovery Test Level 1 [YIRT-L1] = 17.14 ± 1.73 level) who participated in the study, turned out to be reversed after 5-6 days of supplementation with 1g of NAC to when the authors observed a “very likely harmful effect” (71% ± 59%).

Figure 2: Running times (lower = better) and subjectively measured muscle soreness before during and at the end of the 6-day intervention with 1g of NAC in 28 semi-professional, semi-elite male rugby players (Rhodes 2018).

The effects on the actual exercise performance during the shuttle-run, on the other hand, were negligible – yes, this means you can safely ignore them. Everbody can tell that by looking at the running times in Figure 2, … and yes, I don’t care that the results of the “sportsci” parallel group trial spreadsheet (Hopkins 2015) suggest a “likely beneficial performance effect on maximum shuttle sprint time (2.4%; 90% confidence limit ± 4.8%)”.

Whether more helps more is not clear! What is clear, though, is that 2 and more grams of NAC are more prone produce side effects in form of diarrhea, nausea, vomiting, and headache. You should furthermore remember that hormesis is all about managing the exercise stress – not annihilating. If you’re using NAC, using the lowest effective dose should thus always be your goal.

To be fair, I should point out that the authors refrain from claiming to have a found a practically relevant performance benefit, when they write that…”this study was unable to demonstrate a clear effect of 1 g NAC on total time to complete a broken bronco exercise protocol” – that this was due to the low dosage of NAC, which is what they claim right after the cited passage, though, sounds a bit biased; and that despite the quoted results from a 2011 study by Cobley et al. (Cobley 2011), who gave their participants a higher dose of 50 mg/kg/day and observed an increase in YYIRT-L1 performance over time, with the greatest performance enhancement seen on the last testing session (three sessions in total).

When it comes to choosing whether and at which dose to use NAC (or vitamin C and vitamin E) you must consider hormetic dose-response relationship between stress exposure (X-axis) and adaptational response (Y-axis). Stimulatory effects occur in the low-dose region at the left of the no-observed-effects-level (NOAEL), whereas adverse effects occur in the high-dose region at the right of the NOAEL – The higher your baseline stress the more likely you’ll benefit from antioxidants by reducing the background noise and enhancing the signal:noise ratio (Agathokleous 2018)

Overall, we need more research before we can – with some confidence – advice athletes to consume (high dose) NAC supplements during phases of intense competition; and that is particularly true for the purported recovery- and performance-enhancing effects semi-elite athletes are supposed to experience during exercise sessions with a high turnaround rate.

Learn more about hormesis

Taking NAC right before or during a meet or competition may still make sense — I wouldn’t totally exclude that there is a dosage effect, though, accordingly higher dosages (5g vs. 1g) should be recommended to those who want to (ab-)use NAC strategically during what Rhodes et al. aptly describe as “periods of anticipated high energy turnover with limited recovery time, such as during tournaments, competitions, or back-to-back hard training sessions” (Rhodes 2018).

During the training/off-season, however, it would be madness to interfere with ROS formation and IL-6 release as they have been found to be the real drivers of the adaptive response you’re training for… ah, and by the way: To write “I take my NAC away from my workout” in the comments, will only expose your lack of knowledge about the way(s) your body functions. It’s not going to help you soothe your conscience and make you feel good about a habit (=takig your NAC supplements religiously) that’s almost certainly going to impair your gains | Comment!


  • Agathokleous, Evgenios, Mitsutoshi Kitao, and Edward J. Calabrese. “Environmental hormesis and its fundamental biological basis: Rewriting the history of toxicology.” Environmental research 165 (2018): 274-278.
  • Cobley, James N., et al. “N-Acetylcysteine’s attenuation of fatigue after repeated bouts of intermittent exercise: practical implications for tournament situations.” International journal of sport nutrition and exercise metabolism 21.6 (2011): 451-461.
  • Rhodes, etal. “Acute Effect of Oral N-Acetylcysteine on Muscle Soreness and Exercise Performance in Semi-Elite Rugby Players”. Journal of Dietary Supplements (2018).

NAC Lowers DOMS, Initially, but on Day 5-6 it Makes Things Worse | Plus: Putative Performance Benefit is Negligible syndicated from

Ketone Esters a Smart Supplement? | Pure Nitrate vs. Beets | Caffeine Muscle Recruitment, Power and Performance

Time for a new installment of the supplement short news.

I think it’s about time for another installment of the short news, i.e. an article that consists of several brief write-ups on very recent papers. Today’s topics are: (1) the question whether it is a smart move to consume ketone esters on top of Gatorade or similar products before your workout; (2) the difference in physiological effects of potassium nitrate and beetroot juice; and (3) how caffeine improves muscle recruitment and hence endurance performance.

You can learn more about beetroot juice at the SuppVersity

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Nitrate Drugs Work, But Are Not Safe

Win the Super Bowl w/ Beet- root Juice!

140ml of Beetroot Juice That All it Takes!

Nitrate + Caf = Ergogenic Sledgehammer

Beet Every Personal Best W/ Beets!
  • Ketone esters may be smart to consume on top of carbohydrate supplement before and during high-intensity exercise (Evans 2018) — This is at least what you can assume based on the observations Evans & Egan made in their latest study.

    The researchers had N=11 male team sports athletes (mean±SD: age, 25.4±4.6 y; height 1.80±0.05 cm; body mass, 78.6±5.3 kg; VO2max 53.9±2.2 mL/kg/min) perform the same Loughborough Intermittent Shuttle Test (Part A, 5×15 min intermittent running; Part B, shuttle run to exhaustion) twice. Once with and once without extra 750 mg/kg of ketone esters (KE) in the 6.4% carbohydrate-electrolyte solution that was consumed before and during exercise.

    Figure 1: 15 m sprint times (A), and shuttle run time to exhaustion (B) during each trial. Data are presented as mean values, with error bars representing 95% confidence intervals (Evans 2018)

    In spite of the fact, that the provision of the supplement significantly increased plasma βHB concentrations from ~1.5 to 2.6 mM during exercise (P < 0.001), and notwithstanding the fact that plasma glucose and lactate concentrations were lower during KE compared to PLA (moderate-to-large effect sizes), neither the heart rate (HR), rate of perceived exertion (RPE), or 15 m sprint times differed significantly between trials. In fact, even “the run time to exhaustion was not different (P = 0.126, d = 0.45) between PLA [(mean (95% CI); 268, (199, 336) sec] and KE (229, (178, 280) sec]” (Evans 2018).

    What did differ – and that may actually surprise you, were the number of incorrect responses in a multi-tasking test increased from pre- to post-exercise in PLA [1.8 (−0.6, 4.1)] but not KE [0.0 (−1.8, 1.8)] (P = 0.017; d = 0.70) – an observation about which the scientists write:

    “The primary physiological role of ketogenesis as a survival mechanism during low carbohydrate availability is providing a substrate to the brain in the presence of diminishing blood glucose concentrations. Cognitive benefits and a neuroprotective role are established for exogenous ketones in non-exercise contexts. Notably, in a short-term (5 day) feeding study, rats supplemented daily with KME were 38% faster at completing a radial maze task, and made more correct decisions before making a mistake during the test” (Evans 2018).

    An issue the scientists still have to solve, though, is that several participants experienced incidences of GI symptoms. Hence, future studies should evaluate the dose-response effect in order to minimize both, dosing and GI stress in athletes.

  • NO-ergogenic? Beetroot juice works, pure potassium nitrate doesn’t! (Thompson 2018) — In their latest paper Christopher Thompson et al. describe an important experiment. While previous studies on different nitrate sources always focused on the acute effects of the intervention, the scientists from the Sport and Health Sciences Department at the University of Exeter, evaluated “the physiological and exercise performance adaptations to sprint interval training (SIT)” (Thompson 2018) in a 4-week study.
    Figure 2: Results of new meta-analysis of studies investigating the effect of nitrate (both from juice and supplements) on exercise performance; top – trained individuals vs. bottom untrained individuals – the comparison shows: trained subjects benefit less, mechanism probably anti-fatigue effect (Van de Walle 2018)

    To test if different types of NO3− supplementation evoke divergent physiological and performance adaptations to SIT, the authors compared the effects of 4-wk SIT with and without concurrent dietary NO3− supplementation administered as either NO3−-rich beetroot juice (BR) or potassium NO3− (KNO3) – and here’s what they observed in their thirty recreationally active subjects

    • During severe-intensity exercise, V̇o2peak and time to task failure were improved to a greater extent with SIT + BR than SIT and SIT + KNO3 (P < 0.05).
    • There was also a greater reduction in the accumulation of muscle lactate at 3 min of severe-intensity exercise in SIT + BR compared with SIT + KNO3 (P < 0.05).
    • Plasma NO2− concentration fell to a greater extent during severe-intensity exercise in SIT + BR compared with SIT and SIT + KNO3 (P < 0.05).
    • There were no differences between groups in the reduction in the muscle phosphocreatine recovery time constant from pre- to postintervention (P > 0.05).

    The scientists believe that this result is a direct consequence of “greater NO-mediated signaling in SIT + BR compared with SIT + KNO3” (Thompson 2018) – an assumption that seems somewhat unlikely, the NO2- levels did, after all, plummet faster in the beetroot vs. control and KNO3 groups. Accordingly, one may at least speculate that the ergogenic effects depend on other substances in the beetroot juice, such as betalain which has a track record of significantly improving athletic performance (Van Hoorebeke 2016; Montenegro 2016).

  • More activity = higher performance – Caffeine’s performance benefits may indeed be, at least partially, mediated by increased “muscle recruitment, which enables greater work done above critical power and a greater degree of end-exercise decline in quadriceps twitch force during a 4-km cycling time trial” (Felippe 2018).

    Now, what is interesting is that this result of a recent study on the influence of caffeine on the total work done above critical power (CP) during a 4-km cycling time trial (TT) and the subsequent consequence on the development of central and peripheral fatigue is that the improvements come at a cost in form of greater locomotor muscle fatigue. 

  • In the study, nine cyclists had performed three constant-load exercise trials to determine CP and two 4-km TTs ~75 min after oral caffeine (5 mg/kg) or cellulose (placebo) ingestion. Neuromuscular functions were assessed before and 50 min after supplementation and 1 min after TT. Oral supplementation alone had no effect on neuromuscular function (P > 0.05). Compared with placebo, caffeine increased mean power output (~4%, P = 0.01) and muscle recruitment (as inferred by EMG, ~17%, P = 0.01) and reduced the time to complete the TT (~2%, P = 0.01). Work performed above CP during the caffeine trial (16.7 ± 2.1 kJ) was significantly higher than during the placebo (14.7 ± 2.1 kJ, P = 0.01). End-exercise decline in quadriceps twitch force (pre- to postexercise decrease in twitch force at 1 and 10 Hz) was more pronounced after caffeine compared with placebo (121 ± 13 and 137 ± 14 N vs. 146 ± 13 and 156 ± 11 N; P < 0.05). There was no effect of caffeine on central fatigue. 

When timing seems to matter: “Protein-Timing & Fasting: Fasted Sprints & the Remarkable Muscle↑, Fat↓ Effect of Timing Whey With vs. Between Meals” (read it)

So what’s the verdict then? (A) Keep drinking your pre-workout coffee, unless you have a gene-test showing that you are a slow metabolizer and feel no performance increase or even a decrement when taking caffeine before workouts. (B) No matter what your source may be: nitrates are currently a hype supplement but the effect size is small, relevant mostly for untrained individuals and probably significantly more pronounced in its natural form, i.e. from beetroot juice vs. potassium nitrate. (C) For your muscles the extra-ketones you may be consuming alongside your Gatorade may be overkill (hence no performance benefits), but your brain may thank you for the extra fuel | Comment!

  • Evans, Mark & Egan, Brendan. “Intermittent Running and Cognitive Performance after Ketone Ester Ingestion.” Medicine & Science in Sports & Exercise: June 25, 2018 – Publish Ahead of Print
  • Leandro Camati Felippe, Guilherme Assunção Ferreira, Sara Kely Learsi, Daniel Boari, Romulo Bertuzzi, and Adriano Eduardo Lima-Silva. “Caffeine increases both total work performed above critical power and peripheral fatigue during a 4-km cycling time trial.” Journal of Applied Physiology 2018 124:6, 1491-1501.
  • Christopher Thompson, Anni Vanhatalo, Stefan Kadach, Lee J. Wylie, Jonathan Fulford, Scott K. Ferguson, Jamie R. Blackwell, Stephen J. Bailey, and Andrew M. Jones. “Discrete physiological effects of beetroot juice and potassium nitrate supplementation following 4-wk sprint interval training.” Journal of Applied Physiology 2018 124:6, 1519-1528.
  • Montenegro, Cristhian F., et al. “Betalain-rich concentrate supplementation improves exercise performance and recovery in competitive triathletes.” Applied Physiology, Nutrition, and Metabolism 42.2 (2016): 166-172.
  • Van De Walle, Gavin P., and Matthew D. Vukovich. “The Effect of Nitrate Supplementation on Exercise Tolerance and Performance: A Systematic Review and Meta-Analysis.” The Journal of Strength & Conditioning Research 32.6 (2018): 1796-1808.
  • Van Hoorebeke, Justin S., et al. “Betalain-rich concentrate supplementation improves exercise performance in competitive runners.” Sports 4.3 (2016): 40.

Ketone Esters a Smart Supplement? | Pure Nitrate vs. Beets | Caffeine Muscle Recruitment, Power and Performance syndicated from

#RedMeat for Your #Heart: 500g/Week = Nothing but Healthy for Myocardium and Arteries if it’s Lean + Unprocessed

This is the degree of processing that’s tolerable 😉

Fat, ground, burnt, and adulterated with steroids, antibiotics, nitrates, sulfites, and chemical preservatives – that’s how the average Westerner “likes” his meat (’cause it’s cheap, you know).

No wonder that the majority of epidemiological studies (you know that’s the branch of science, where people invent explanations for observations) “shows”: red meat kills!

As a SuppVersity reader, you know from previous articles that experimental evidence suggests otherwise… at least for lean, properly prepared meats from appropriately reared animals (those are the animals that don’t make taking extra steroids and antibiotics obsolete).

Learn more about meat at the SuppVersity

You May Eat Pork, too!

Body Fat > Meat for CVD

Meat & Prostate Cancer?

Meat – Is cooking the problem

Meat Packaging = Problem?

Grass-Fed Pork? Is it Worth it?

With the publication of Lauren E O’Connor’s, Douglas Paddon-Jones’, Amy J Wright’s and Wayne W Campbell’s latest paper the number of studies that support the notion “that lean, unprocessed red meat can be incorporated into healthy eating patterns to improve cardiometabolic disease (CMD) risk factors” (O’Connor 2018)” has increased by +1 and provides a link that even (or, rather, especially) people who trust in epidemiology cannot ignore: the Mediterranean Diet link.

In an investigator-blinded, randomized, crossover, controlled feeding trial, 41 overweight or obese [BMI (kg/m²) 25–37], aged 30–69 y [representing middle-aged adults and adulthood life stage groups of the Dietary Reference Intakes (Trumbo 2002)] were provided with a Mediterranean Pattern diet for two 5-wk interventions separated by 4 wk of self-selected eating.

What did this “Mediterranean Pattern diet” diet look like? The diet contained ∼500 g [typical US intake (Med-Red)] and ∼200 g [commonly recommended intake in heart-healthy eating patterns (Med-Control)] of lean, unprocessed beef or pork per week. 

Daily macronutrient intakes were targeted at 40% of total energy as carbohydrate, 22% protein, and 40% fat. Daily fat intakes were targeted at 7% of total energy as saturated fat and 20% monounsaturated fat. Med-Red and Med-Control differed predominantly in the amounts of red meat and poultry provided.

Figure 1: Overview of the main characteristics of the dietary intervention in O’Connor 2018

What is important enough to repeat is that even though the amount of red meat differed significantly, the Med-Red and Med-Control diets contained identical amounts of fish and legumes, were iso-energetic and adapted so that they would provide and (within statistical margins) identical macronutrient content. The diets also had in common that…

  • the desired macronutrient ratio was achieved by adding/removing dairy, eggs, and grain products, 
  • sodium, potassium, magnesium, and calcium intakes were targeted to be within ±15% between the Med-Red and Med-Control menus, 
  • each subject’s energy requirement was estimated using sex-specific equations and menus were designed to maintain subjects’ baseline 1 body mass

What? Oh, yes – to mirror the red wine intake of the “true” Mediterranean Diet “the subjects were given the option to consume 150 mL of self-selected dry red wine daily” (O’Connor 2018).

Adherence is key and providing subjects with food makes it easier for them to adhere: In the study at hand, all foods were prepared and provided to subjects during the two Mediterranean Pattern interventions by the NIH-supported Indiana Clinical Research Center Bionutrition Facility at Purdue University. The meats were consumed in mixed heterogeneous dishes. All red meat and poultry provided was lean [<10 g total fat, <5 g saturated fat, and <95 mg cholesterol]. All red meats and poultry underwent no further preservation processing beyond refrigeration or freezing, i.e., no smoking, curing, salting, or the addition of chemical preservatives.

Subjects weighed in and met with study staff weekly to monitor body mass and promote compliance, respectively. Subjects completed daily (and returned weekly) menu check-off lists to track self-reported deviations from the provided Mediterranean Pattern. Dietary intake and compliance were measured from the menu check-off lists of 3 d during the last week of each intervention.

Baseline and postintervention outcomes included fasting blood pressure, serum lipids, lipoproteins, glucose, insulin, and ambulatory blood pressure.

The raw data were adjusted for age, sex, and body mass at each time point, the level of significance was set at P < 0.05 and the results… (I know you’ve been waiting for them) were unambiguous:

  • Figure 2: Changes in lipids and lipoproteins after consuming a Med-Red or Med-Control diet for 5 wk. Results are presented as LS means ± SEMs (n = 41). Data were analyzed using a doubly repeated-measures ANOVA adjusted for age, sex, and body mass at each time point. *Nondifferential change over time. †Differential response between Med-Red and Med-Control when intervention × time P value < 0.05. ‡Intervention-specific change over time indicated by intervention × time P < 0.05.

    Med-Red decreased total-C 3% more than Med-Control,

  • LDL cholesterol and ApoB decreased by 8% and 6%, respectively, with Med-Red, but did not change with Med-Control, 
  • the significant reduction in cholesterol, and LDL were more pronounced in the red meat group (see Figure 2),
  • total-C:HDL cholesterol, triglycerides, CRP, glucose, insulin, and HOMA-IR score did not change with Med-Red or Med-Control,
  • fasting and ambulatory blood pressure parameters improved with both Mediterranean Patterns, except during sleep, independent of red meat intake amount.

Moreover, there were no differences between postintervention values of Med-Red and Med-Control for any CMD risk factors, and no difference between males and females in Mediterranean Pattern-induced cardiometabolic changes were found, independent of red meat intake amount. However, …

“When considering baseline and intervention drink-equivalents as a covariate, there were still greater reductions in total-C with Med-Red, and reductions in LDL cholesterol with Med-Red but no changes with Med-Control, but the overall time effect and intervention-specific effects on ApoB diminished” (O’Connor 2018).

The most fundamental message of the study at hand does therefore remain: Red meat, if it’s unprocessed and sufficiently (<10g of fat) lean is not unhealthier (rather the opposite) than poultry… no matter what epidemiologists will tell you.

Table 1: Unadjusted means, SD, and n, at each time point of Med-Red and Med-Control (O’Connor 2018).

What? Oh, yeah. I hear them. The vegans are crying “fraud”, because – obviously – the control diet should have included no meat at all. True that. An additional group using a completely meat-free (like lacto-ovo-vegetarian) version of the Med Diet would have been a nice add-on but its omission is not a shortcoming of a study that was specifically designed to test the hypothesis “that the amount of red meat consumed would not influence Mediterranean Pattern-induced improvements in CMD risk factors of adults who are overweight or obese” (O’Connor 2018) – to test this was, after all, exactly what the study accomplished.

Mediation analysis suggests: It’s not the amount of Cantonese Roast Pork Belly (recipe) you eat that increases the level of inflammation in your body, but the belly you get if you eat too much of it or non-red/processed meat foods | read #SVClassic

Bottom line: The study at hand adds to the already existing experimental evidence that the link between red meat and heart disease (and metabolic syndrome, as tested in previous studies) is not a mechanistic one … or, let’s be more precise: It’s not a link that’s mediated by the “red” in the meat, but rather by the fat (probably eventually the total calories), the nitrite-forming nitrate salts and its chemical cousins that are sprinkled on and injected into processed meats.

Speaking of which, it’s the nitrates your bacon has been “cured” with that “uncure” (=make you sick)… that’s especially problematic if you put the bacon in a pan and fry it – a process that gives rises to a plethora of well-known carcinogens, but it’s not exclusive to fried bacon 😮

The same sh*t happens upon exposure to stomach acid (Fine 1977) and whenever protein and nitrates are exposed to a highly reactive environment. Now, the industry is smart, no? Well, at least they believe so and add other additives to… yes, you guessed it: to counter the ill effects (=nitrosamine formation) of the previously added additives – well, unless you live in the Mediterranean and cherish Prosciutto di Parma which has been nitrate free (again) for >25 years, already… but I am getting off topic – nitrates and cancer are not heart disease and when it comes to the latter you better don’t buy any meat product that was processed with anything but a knife.

What? Oh, no grinding your bee is perfectly ok, if it’s kept cool during the process and grounding is actually the only process it undergoes … needless to say that the latter this is no longer the case since the lobbyists from Kraft Foods and others have “convinced” the FSIS to (re-)allow sodium benzoate, sodium propionate, and benzoic acid as anti-bacterial agents | Comment!


  • Fine, David H., et al. “Formation in vivo of volatile N-nitrosamines in man after ingestion of cooked bacon and spinach.” Nature 265.5596 (1977): 753.
  • Glória, M. Beatriz A., James F. Barbour, and Richard A. Scanlan. “Volatile nitrosamines in fried bacon.” Journal of Agricultural and Food Chemistry 45.5 (1997): 1816-1818.
  • Micha, Renata, Georgios Michas, and Dariush Mozaffarian. “Unprocessed red and processed meats and risk of coronary artery disease and type 2 diabetes–an updated review of the evidence.” Current atherosclerosis reports 14.6 (2012): 515-524.
  • O’Connor, Lauren E., et al. “A Mediterranean-style eating pattern with lean, unprocessed red meat has cardiometabolic benefits for adults who are overweight or obese in a randomized, crossover, controlled feeding trial.” The American Journal of Clinical Nutrition.
  • Trumbo, Paula, et al. “Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids.” Journal of the American Dietetic Association 102.11 (2002): 1621-1630.

#RedMeat for Your #Heart: 500g/Week = Nothing but Healthy for Myocardium and Arteries if it’s Lean + Unprocessed syndicated from

Maximizing Training-Induced Cellular Adaptation: Training Low, Carb Cycling, Altitude & Hypoxia Training for Athletes

The mitochondria are the cell-constituents where the most relevant aspects of (endurance-)exercise-induced adaptations take place, and hence the main, but not the only target of the strategies highlighted in these assorted “cliff notes”.

Usually, I am not a fan of writing about review papers (without attached meta-analysis) but in view of popular demand, I am going to give it a try and provide you with the “cliff notes” on the latest review of the theoretical background and practical implications of training with a goal the authors of the paper call “Maximizing Cellular Adaptation to Endurance Exercise in Skeletal Muscle (Hawley 2018).

Cliff notes, if you will on surpassing “barriers to [human] performance” – including the 2h mark for a marathon.

High-protein diets are for endurance athletes too… if they’re higher in carbs than in protein 😉

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Protein Oxidation = Health Threat

Protein Timing DOES Matter!

More Protein = More Liver Fat?

In order to keep it both comprehensive and clear, I will draw on a modified version of the original paper’s structure with what I consider the main implications as headlines. In that I will start with something people tend to forget or rather to push far back in their heads:

World class athletes are both born and raised

I know, it sounds unfair, but even the “American Dream” in its original formulation by Truslow Adams doesn’t guarantee equal chances for everyone, but rather a “better and richer and fuller [life] for everyone, with opportunity for each according to ability or achievement” (Adams, republished in 2017) – never forget that: more often than not, it is after all not a lack of achievement, motivation, or the amount of work you have been investing that’s to blame for your inability to become an NFL-quarterback, a world-cup winning soccer player, or a box champion – It’s your damn genes PLUS the ways you cultivated them from your earliest days on.

Note: We don’t have the “endurance athlete”-geneset, yet! While many companies offer services that will allegedly tell you what kind of sport you would excel in, the guys running the companies must have constructed a time machine if they can indeed provide you with reliable information, because as of 2018, we haven’t discovered this geneset, yet!
Figure 1: VO2 curve of “fittest” athlete in a scientific study, an Olympic gold medalist cross-country skier (Burtscher 2011)

Keywords in this context are: Extreme VO2max values (the current record amounts to the 90.6 mL/kg/min scientists measured on an Olympic gold medalist cross-country skier Burtscher et al. observed in 2011, see Figure 1) maximal metabolic flexibility, optimal ATP management, highly efficient handling of oxidative stress, and a resilience to fatigue that goes way beyond “being able to tough it out”.

Accordingly, the most important and, in fact, the only practical implication, here, is: Accept that not everyone is meant to be a world-class athlete in whatever sport it is you want to excel in.

Train low, compete high – Carbohydrate cycling

This is one of the many strategies I’ve written about. The corresponding articles discuss papers showing that:

  • Cutting carbs after your HIIT training for 7 days before competition may significantly up your time-trial performance (in a carb-replete state) – Read article
  • “Sleeping Low” (not recharging glycogen stores after PM workouts) may lead to game-changing performance gains within only 3 weeks of training | read article

The exact underlying mechanisms are too complicated to be elaborated within these cliff notes, let’s just say they are part of an interaction of training-induced responses and nutrient availability that is behind many of the practical implications discussed today.

Figure 2: Skeletal muscle signaling responses after a single bout of endurance exercise are amplified in the face of low glycogen availability (Hawley 2018); AMPK and PGC-1 are the best-known motors of this process.

If you go low-carb for one, two or three weeks, or rather cut out carbs after or before training seems to matter relatively little; in fact, the (at best almost full) depletion of glycogen seems to be the main modulator of the desired adaptational response, as it signals your muscles that they have to improve their ability to burn fat (without compromising the ability to burn glucose, as high-fat diets would).

Post-workout carb fasting and glycogen depleted cardio in the morning | more.

Train low, compete high – How is it done?  Lower your carb intake temporary to train with low(ish) glycogen levels to trigger increases in the mitochondrial building protein PGC1-alpha and build a bigger metabolic engine. “Temporary” can be a continuous low-carb diet for 1-2 weeks in the offseason (don’t expect to see great performance benefits before you return to training with well-stocked glycogen stores, though), or by the means of intermittent carbohydrate fasting (e.g. after working out in the PM). As with the previously suggested method, you cannot expect performance improvements while you’re still “training low” – to see the full benefits of your efforts, you will have to up your carb intake again.

Train high, compete low – Altitude training (LLTH & LHTL)

It’s almost an old hat and, above all, one whose beauty in terms of its efficacy has long been overestimated… and still, there is as Hawley et al. point out, effective for both, professional athletes, as well as anyone else who seeks to maximize his training response.

Figure 3: Effects of altitude/hypoxic training vs. sea-level training on RBC (10^5 cell/μl) – with average levels of 4-6 million cells the increases range from < 5% to >50% with some researchers claiming only athletes with initially low(ish) RBC counts will see significant benefits – a hypothesis others see very skeptical, though (Park 2016).

Most researchers still believe that the increase red blood cell count in altitude/hypoxic training vs. sea-level training is the most relevant factor contributing to the beneficial effects of training high, competing low (and/or sleeping high and training low).

The masks are no alternative for altitude training; they will – at best train your inspiratory muscle which is yet not a bottleneck to performance.

As early as in the 1970s, scientists from the GDR (yes, those who also beat everyone else when it came to doping) found that the effects occur after only a few weeks of training and become observable only after returning to sea levels (hence “train high, compete low”). Even for this strategy, though, it is still too early to make definitive recommendations as to the intricate details of the “ideal” protocol. It’s not even clear if athletes should prefer LLTH or LHTL, i.e. live low and train high or live high and train low protocols.

What is 100% clear, however, is that masks like the one on the right are a waste of money (unless you want to train your inspiratory muscle).

Training in hypoxia – What to expect from altitude training? If you want to learn more about altitude training and take a look at the performance increases in a bunch of studies, I suggest you take a look at the free FT of Baker’s and Hopkins’ paper “Altitude training for sea-level competition” in Sportscience Training & Technology here!.

Train hot, compete cool – Heat acclimatization training

While the adaptation-augmenting effects of training in the heat are partly mediated by the same fundamental mitochondrial building protein as both previously discussed training strategies (PGC-alpha), the triggers belong (supposedly) to a series of aptly named “heat shock proteins”. While it has become clear that they’re not expressed exclusively in response to heat stress, their elevation seems to be responsible at least for the chronic adaptational effects.

Figure 4: Thermoregulation is an important part of exercise performance (Wikipedia).

Heat acclimatization does yet have both, chronic and acute effects endurance athletes can benefit from. Especially, if they know that their next competition will take place in the heat, heat acclimatization in the classic sense of getting accustomed to working out in the heat is both important and, as studies like James et al. (2018) have shown only recently.

Time to fatigue during a cycling bout at 85% Vo2max. Before the time trial, subjects exercised for 30 minutes at 45%Vo2max and performed 15 × 3 to 8-minute intervals at 75%Vo2max interjected with 15 × 3 to 8-minute active recovery periods at 45% Vo2max. Following this 180-minute sequence, subjects cycled to fatigue at 85% Vo2max. Equal boluses of each supplement were provided at 10-minute intervals over the 180-minute period before the fatigue test (as published in Kerksick & Roberts 2010).

Which supplements do really work? I know it’s not popular, these days, but there’s simply absolutely no doubt that carbohydrates (2:1 glucose:fructose) are the #1 performance enhancing supplement for endurance athletes… and that does not refute the previous claim that intermittent carbohydrate reductions can augment the adaptational response to exercise.

The only supplement that comes at least close to carbs in terms of the amount and quality of research is caffeine at doses of 3-6 mg/kg.

The effects of additional protein (see Figure on the left) has been investigated thoroughly recently; preliminary evidence clearly supports that adding protein to cho supplements will improve endurance performance.

That’s in contrast to one of the new hype-supplements, i.e. dietary nitrates or supplemental nitrate salts, which appear to yield measurable benefits only in untrained individuals, yet not athletes. In a similar vein, the often-recommended antioxidants have almost no scientific back-up when it comes chronic performance improvements in athletes. In fact, it seems as if there were short-term benefits and long-term reductions in the adaptational response (keyword: hormesis).

Beta-alanine and, even more so, sodium bicarbonate have their value as intra- and extracellular pH buffers (Carr 2011; Christensen 2017). Another buffer, but one that buffers your PCr reserves does also have some, but not ample evidence of its benefits on endurance performance: creatine (Indranil 2016)! Only very conflicting results are yet available for ketone supplements with some studies, such as Cox et al. (2016) showing beneficial, while others, such as O’Malley et al (2017) demonstrating significant performance decrements – more studies and comparisons of different types of ketone supplements (salts vs. esters) are necessary to say who will benefit and who won’t. 

Figure 5: Mean (±SD) kilometer split times during the 5-km time trial James et al. used as their subjects in a recent study investigating the effect of heat acclimatization (HA) and pre-cooling (PC) individually and in conjunction  (James 2018).

In their study, the scientists from the University of Brighton used both, a heat acclimatization (HA) and/or precooling (PC) in nine amateur trained runners who completed 5-km treadmill time trials (TTs) in the heat (32° C, 60% relative humidity) under 4 conditions; no intervention (CON), PC, short-term HA (5 days—HA) and STHA with PC (HA + PC). Mean (±SD) performance times were – you can see the results in Figure 5 – and what do you see? Yes, HA works, PC does not and won’t add significantly to the benefits of heat acclimatization significantly, either.

Keep muscle and recover faster – Higher protein intakes

While it is a matter of fact that carbs are the #1 performance enhance for endurance athletes, their protein requirements have long been underestimated significantly. And that’s not necessarily just because of potential muscle loss beyond what’s considered optimal for marathon running and co.

Figure 6: Overview of the potential effects of protein ingestion on supporting the recovery from endurance-based exercise as means to enhance endurance capacity and performance (Moore 2014).

In fact for the skinny endurance runner, the addition of protein usually won’t lead to significant increase in muscle mass, anyway. What the recently emerging pro-protein research does show, though, is that it can accelerate post-workout recovery by (a) speeding up the replacement of lost muscle glycogen, as well as (b) preventing/reducing muscle damage. As Moore et al. point out in their 2014 paper, these benefits seem to be determined (or at least confounded) by protein type, protein amount, and protein timing. In their review, the also summarize the potential mechanisms:

“Potential metchanisms include (i) oxidation of amino acids to be used for hepatic gluconeogenesis and (or) deaminiation, or as a fuel source by skeletal muscle mitochondria; (ii) increases in mitochondrial protein synthesis to enhance substrate metabolism and utilization; (iii) promotion of myofibrillar remodelling to maintain muscle protein quality and function by removing old or damaged proteins; (iv) stimulation of net myofibrillar protein synthesis to enable greater muscle force/power output; and (v) promotion of glycogen resynthesis when co-ingested with carbohydrate (CHO).”

Avid SuppVersity readers will have heard about all of these and way more (high) protein benefits in previous articles, … they’ve also heard about the at least 30g of quality protein per meal rule which is valid for everyone: strength-, figure-, endurance- and non-athletes – especially when you’re cutting  (Hector 2018) or competing at a level (e.g. Tour de France) where you simply cannot eat enough food, gels, bars and what-not to avoid losing weight.

Latest Study Shows that a 3.3 g/kg High-Protein Diet is Safe — And Yes, This Means it Doesn’t Hurt Your Kidney or Liver | more

You run? Eat more protein – Ok, but how much more? If that’s the question you’ve been asking you for years, you’ll be happy to hear that studies like Kato et al. are (2016) contributing to our understanding of how much protein endurance athletes actually need. Based on the metabolism of marker amino acids, the researchers calculated that intakes of minimally 1.65 g/kg body weight and an IMHO very conservative recommendation of only 1.83 g/kg body weight for endurance athletes (using the same technique, researchers found the protein requirements of bodybuilders to be even higher ~20% or 2.2 g/kg, to be a bit more precise) | Bandegan 2017) | Comment on Facebook!


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