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In general, you have to count and limit your weekly HIIT sessions. Doing as much as humanly possible, could yet make sense, when youre preparing for Olympia 2016 and realize 5 weeks before the event that you have been lingering for too long ;-)

I think as a SuppVersity reader you know by now that "more wont yield more" - no matter if we are talking about supplements or exercise. Now, while weve had countless examples of the "more aint more" principle thats also at the heart of the "Three Simple Rules of Supplementation" (read article) for supplements (e.g. zinc, chromium, etc.) and the simple notion that eating less wont always result in greater weight loss, evidence for the pro-anabolic / adaptive effects of exercise in general, and non-steady state cardio, in particular is scarce. Against that background its all the more important for us to cherish the publication of a paper from the Norwegian University of Science and Technology and the St Olav University Hospital in Trondheim Norway, Roy told me about by messaging me via the SuppVersity Facebook Page.

"More HIIT doesnt help more, either"

I guess the above would be the elevator pitch for the mythical "turbo lift" in Star Trek. For someone like yourself who has learned never to swallow "expert" wisdom just like that, the statement "more HIIT doesnt hep more, either" obviously wont be satisfying.

Figure 2: Illustration of the training in the low frequency (LF) and high frequency (HF) group.

If you look at the illustration above, you will already know somewhat more about the "more" in the previous sentence. As you can see, the parameter that has been modified is not the volume, its the frequency!  - and thus one of the parameters of which many gymrats think that it could hardly be high enough (AM + PM training, 7 days a week - does that ring a bell?). What this people ignore is the simple truth that ...

... adapatation takes time and training more often does not accelerate this process!

In the end, I am actually quite surprised to see that the net VO2 "gain" the scientists measured in the subsequent detraining phase (see Figure 2) was identical. Or, more explicitly, that packing 24 training sessions into three weeks did not blunt the mitochondrial adaptation processes that are responsible for the increase in VO2max, altogether.

Figure 2: VO2max and heart rate values of the 16 healthy subjects before / after high vs. low frequency HIIT (Hatle. 2014)

If we are brutally honest, though, there is obviously an advantage for the 24 sessions in 8 weeks version of this training protocol (see Figure 3, as well). The VO2max scores were after all identical only in the "catch-up" up period in week 11 and due to the rapid decline after week 12 the benefits faded equally rapid in both groups when the 19 healthy, normalweight, but non-athletic subjects returned to their usual laziness (detraining = not training at all).
References:

• Hatle H, Støbakk PK, Mølmen HE, Brønstad E, Tjønna AE, et al. "Effect of 24 Sessions of High-Intensity Aerobic Interval Training Carried out at Either High or Moderate Frequency, a Randomized Trial." PLoS ONE 9(2). (2014): e88375. doi:10.1371/journal.pone.0088375

Brain builders and muscle builders are similarly effective DNA protectors in the elderly.

As a SuppVersity reader you wont be surprised to hear that Bernhard Franzke and his colleagues from the University of Vienna were able to confirm that resistance training can improve the resistance of human DNA to H2O2 damage in institutionalised elderly. What may be news to you, though, is that very similar effects can be achieved by cognitive training in form of coordinative or cognitive tasks that were performed only two times per week by the 105 institutionalised elderly women and men (aged 65–98 years) the scientists recruited from five different senior residences in the area of Vienna (Franzke. 2014).
In the recent Austrian study, the subjects had been randomized to three groups. The previously described cognitive training group, which also served as a "control", as well as two resistance training groups.

"The RT groups (RT and RTS) performed two sessions of RT per week, supervised by a sport scientist, conducted on two non-consecutive days. Training attendance was recorded every session. The only equipment used was exercise bands and a chair. [...] The main part consisted of 10 exercises for the main muscle groups (legs, back, abdomen, chest, shoulder and arms). One training session started with 10 min of warm-up, continued with 30–40 min of strength training and ended with a 10-min cool-down. To keep the training stimulus high enough, the exercise program was adjusted to the participants’ individual needs, by either adapting the resistance of the elastic band (shorter or stronger band) or by modifying the exercise, by means of performing a more diffiult version. In the initial phase (4 weeks) one set of 15 repetitions was performed in order to learn the correct form of each exercise. From the fifth week on, the intensity and volume were progressively increased from two sets of light exercises to two sets of heavy resistance. If the participants could easily perform two sets of 15 repetitions they were told either to take more resistance or to perform a more difficult version of the exercise" (Franzke. 2014).

In contrast to the RT group, which did "nothing", but the previously described resistance training regimen, the subjects in the RTS group consumed a multi-ingredient supplement every morning, as well as directly after each training session. Said supplement consisted of 20.7g protein [56 energy (En) %, 19.7g whey protein, 3 g leucine, >10 g essential amino acids], 9.3 g carbohydrates (25 En%, 0.8 BE); 3.0 g fat (18 En%), 1.2 g roughage (2 En%), 800 IU (20 ?g) of vitamin D, 250 mg calcium, vitamins C, E, B6 and B12, folic acid and magnesium (one portion FortiFit, Nutricia with a total energy content per drink of only 150 kcal).

Figure 1: Changes in parameters of DNA damage and antioxidant enzyme expression (Franzke. 2014).

In spite of the fact that the intake of the nutritional supplement was controlled at breakfast as well as after the training sessions, it did not provide significant additional benefits on top of the regular resistance training protocol.

We should keep in mind, though, that (a) non-significant benefits were visible for the formamidopyrimidine DNA glycosylase (FPG) and the expression of superoxide dismutase and that (b) the actual benefits of protein supplements would have become visible only if the scientists had accessed the changes in body composition, as well.
References:

• Franzke, B. et al. "The impact of six months strength training, nutritional supplementation or cognitive training on DNA damage in institutionalised elderly." Mutagenesis (2015):147–153.

The advantage of HDL is its stability that reduces the risk of plaque build-up in the intestinal wall, which is clogged by the remnants of oxidized LDL and causes heart disease & co.

First things first: We are not talking about "hard experimental evidence" as you could generate it in a randomized controlled trial in a metabolic ward. The data I am reporting today is from a cohort with 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year - an epidemiological study that used stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.

Interestingly, this is the first study with a quality data-set that determined the association between specific dietary micronutrients with HDL-C, HDL-2, HDL-3, and apoA1, and how these dietary associations differ across the various measures of HDL - not just one.
To identify the HDL-promoters in the diet, the scientists use demographic and clinical variables in the base model. What they found was that numerous dietary intakes increased total HDL-C variance.
The results of their stepwise linear regression model in Table 1 indicate - probably for some people much surprisingly - that all alcohol intake levels were positively associated with HDL-C.

"In addition, magnesium, folate, and the saturated fat, myristic acid (14:0), were all positively and independently associated with HDL-C. Carbohydrate intake, iron, and % of fat derived from animal sources were each negatively additive for HDL-C." (Kim. 2014)

Similar effects from dietary intakes were observed for HDL-2, of which we know that it is decreased in women with rheumatoid arthritis (Arts. 2012) and individuals with other inflammatory diseases (including metabolic syndrom) and associated with a slightly higher reduction in acute myocardial infarction risk than "regular" HDL in several studies (Salonen. Salonen. 1991; Stampfer. 1991; Buring. 1992; Gaziano. 1993) for all alcohol intakes, magnesium, folate, and myristic acid (14:0), eicosapentaenoic acid (20:5, a ?-3 EPA), all of which were positively and independently associated with HDL-2 levels.

Table 1:  Best-fit model from stepwise linear regression predicting HDL-C levels using dietary intake data (Kim. 2014)

The opposite was the case for arachidonic acid (20:4, an ?-6 ARA), carbohydrate and iron intakes, which were both negatively associated with HDL-2 (see Table 1).

Dont forget to put things into perspective!

And just to make sure, I dont get angry emails from bulletproof coffee drinkers: Your coffee is fine, the content of the only "good" saturated fat, i.e. myristic acid, happens to be especially high coconut oil (41%; Sodamade. 2013) and relatively high in butter (12% independent of whether its grass-fed or not; Couvreur. 2006) - surprised? Not really, I guess. As a SuppVersity reader you are by now aware that the bad reputation coconut oil and butter have for being mostly saturated fats is no longer supported by contemporary scientific evidence (Dias. 2014).

And with respect to the total animal fat intake - for the average Westerner thats a good measure of how much processed meat he / she eats, so I would not overrate the small negative association (1/80 of the one of having a ton of carbohydrates in your diet!) the scientists found in the study at hand.
References:

• Arts, Elke, et al. "High-density lipoprotein cholesterol subfractions HDL2 and HDL3 are reduced in women with rheumatoid arthritis and may augment the cardiovascular risk of women with RA: a cross-sectional study." Arthritis Res Ther 14.3 (2012): R116.
• Buring, J. E., et al. "Decreased HDL2 and HDL3 cholesterol, Apo AI and Apo A-II, and increased risk of myocardial infarction." Circulation 85.1 (1992): 22-29.
• Couvreur, S., et al. "The linear relationship between the proportion of fresh grass in the cow diet, milk fatty acid composition, and butter properties." Journal of dairy science 89.6 (2006): 1956-1969.
• Dias, C. B., et al. "Saturated fat consumption may not be the main cause of increased blood lipid levels." Medical hypotheses 82.2 (2014): 187-195.
• Gaziano, J. Michael, et al. "Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction." New England Journal of Medicine 329.25 (1993): 1829-1834. 
• Kim et al. "Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants." Nutrition & Metabolism 2014, 11:44.
• Leon, ARTHUR S., and OTTO A. Sanchez. "Response of blood lipids to exercise training alone or combined with dietary intervention." Medicine and science in sports and exercise 33.6 Suppl (2001): S502-15.
• Salonen, Jukka T., et al. "HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men." Circulation 84.1 (1991): 129-139. 
• Sodamade, A¹, and O. S. Bolaji. "Fatty acids composition of three different vegetable oils (soybean oil, groundnut oil and coconut oil) by high-performance liquid chromatography." Chemistry and Materials Research 3.7 (2013): 26-29.
• Stampfer, Meir J., et al. "A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction." New England Journal of Medicine 325.6 (1991): 373-381.

Compared to liquid beverages, gels have the advantage of causing lower GI stress, when significant quantities of CHOs are consumed during exercise. Bars, can be held in the cheek pouch and chewed during critical phases of a race.

The headline gives it away. Todays SuppVersity article is a brief review of the (mostly sponsored) literature on Gatora.... ah, I mean carbohydrate supplementation during exercise. The headline also implies that the usefulness and efficacy of carbohydrate supplements depends on exercise duration and the type of exercise.

As a seasoned student of the SuppVersity you will know that certain paradox involved with regard to the duration / type of exercise. Short exercise durations, for example, shouldnt require large CHO boluses, long duration exercise, on the other hand, is fueled mostly by fat - so why should you supplement with carbohydrates, anyway?
I promise to answer this and other questions in the following paragraphs, but before I do so, I would like to point out that there is as of now no evidence that the much-praised "fat adaptation" increases the exercise performance to an "Olympia" level. Carbohydrate supplements, on the other hand, are still part of the regular supplementation regimen for the 99% of the top athletes.

That being said, the human physiology dictates that the use of carbohydrate supplements during aerobic workouts that last less than 60 minutes is useless, because muscle glycogen is generally not limiting to performance when exercise durations are less than ~60 minutes.

It should not work for short duration exercise, but it still does

Interestingly, 16 out of 23 studies, Trent Stellingwerff and Gregory R. Cox from the Canadian Sport Institute-Pacific and the Australian Institute of Sport reviewed for their recent paper in Applied Physiology have found that carbohydrate supplementation and/or oral (mouth) exposure to carbohydrate can improve performance of tasks less than 1 hour in duration:

You wont fully deplete your muscular glyocogen levels during short duration resistance training (Haff. 2003)

"In 2004 a seminal paper was published showing that a carbohydrate mouth-wash (swirling 25ml of a 6% CHO beverage (only ~1.5g of CHO in 25ml [6.4% maltodextrin solution (CHO)]) around in the mouth for ~10 sec, every 7.5min) significantly improved time trial (TT) performance [in seven male and two female endurance cyclists] by ~3% (Carter et al. 2004a)." (Stellingwerff & Cox. 2014)

This effect of CHO mouth-washing to improve performance in events from 30-60min has now been replicated in several other performance studies (10 of 13 studies) using both cycling and running interventions and with both sweet (sucrose) and non-sweet (maltodextrin) caloric CHO sources,as compared to 5 non-caloric artificial sweetener placebo trials showing no performance enhancing effects.

Figure 1: Hard to believe, but true - In 2010 Pottier et al. observed that CHO mouth-rinsing, but not CHO ingestion increases the 1h high intensity time-trial performance in trained subjects.

 "All these findings have been mechanistically supported with a functional magnetic resonance brain imaging study showing that CHO mouth-washing from both sweet tasting glucose and non-sweet maltodextrin can stimulate the brain areas of the insula/frontal operculum, orbitofrontal cortex and striatum, which are involved with brain centers responsible for reward and motor control (Chambers et al. 2009). Interestingly, if the mouth (oral receptors) and GI tract is by-passed by CHO infusion straight into the blood stream then 1h cycling TT performance was unaltered as compared to no CHO supplementation (Carter et al. 2004b)." (Stellingwerff & Cox. 2014)

Studies evaluating the effects on perceived exertion (Fares et al. 2011) found similar benefits all of which support the idea that the effect does not occur in the musculature, but rather in the head.
It should be obvious that the physiological, or rater intra-muscular benefits of carbohydrate supplements increases with the exercise duration.

CHO supplementation during exercise that lasts 60 minutes or longer

In view of the fact that it is 100% logical and well established by studies by Coyle et al. (Coyle 1992a; Coyle 1992b) that the intake of carbohydrate (glucose alone, and glucose + fructose blends) can significantly improve prolonged endurance capacity and performance (>60min of exercise (Jeukendrup 2010)).

Figure 2: Overview of the performance increases in the 50 studies Stellingwerff & Cox reviewed (2014)

Against that background I will not bother you with another overview of the results, but focus on the efficacy of different carbohydrate supplementation strategies and types of carbohydrate supplements for exercise durations beyond the "magical" hour.

Glucose + fructose - the combination advantage

As a SuppVersity reader youve previously heard about the benefits of combining glucose and fructose in your intra-workout beverage. It is thus only logical that most commercially available formulas are mixtures  glucose + fructose (GLU:FRU) or maltodextrin + fructose - so-called "multi-transportable CHOs". The advantage of using both glucose and fructose is that the carbohydrates will be absorbed via SGLT1 and GLUT5 intestinal transporters.

Specifically during long(er) duration exercise, when the carbohydrate consumption can exceed 60g/h there is a significant performance increase with multi- vs. single source carbohydrate supplements (Stellingwerff & Cox. 2014)

An advantage that has been scientifically established among others by Jeukendrup et al. (2010) who found that this pattern of CHO ingestion results in ~20 to 50% higher CHO oxidation rates compared to the ingestion of a drink that contains nothing but glucose or maltodextrin.


Now an increase in carbohydrate oxidation alone does not sound like something you would aim for as an endurance athlete. In practice, increases in carbohydrate oxidation have yet been shown to increase the performance during prolonged exercise bouts compared to isocaloric glucose-only beverages. (Currell et al. 2008; Triplett et al. 2010; OBrien et al. 2011; OBrien et al. 2013).
Needless to say that there is still research to be done with respect to individual influencing variables of carbohydrate requirements. The currently available evidence, for example, is largely based on results from runners and cyclists. Two other factors / issues that come to mind are...

• the dose-response relationship, which appears to be capped at 75g/h - at least according to a large-scale multi-center study by Smith et al. (Smith. 2013) who found that their subjects, endurance trained cyclists or triathletes experienced significant performance increases, with increasing amounts of carbohydrates (0, 10, 20, 30, 40, 50, 60, 70, 80, 90, 100, 110 and 120g of CHO/h) during a 2h constant load ride.
  
  

  Figure 3: Mean log time to complete time trial (natural) as function of CHO treatment condition with fitted quadratic curve (with 95% CI of mean curves). Differences 100 represent percent change in performance. The quadratic function relating CHO ingestion rate to time complete time trial for 43% (95% CI = 11%–75%,P= 0.059) of the variation in mean performance score (Smith. 2013)

  The CHO given was a 1:1:1 glucose:maltodextrin:fructose blend. Results indicated incremental performance improvements of 1.0%, 2.0%, 3.0%, 4.0%, and 4.7% at 9, 19, 31, 48, and 78g CHO/h, respectively, with diminishing performance enhancement seen at CHO levels >78g/h.
  
  The optimal amount for performance (+4.7%) was 78g/h, with a range of 68 to 88g/h. However, even at 10g/h, a 1.0% increase in performance was observed, showing even a small amount of carbohydrate has the potential to positively impact performance. 
• the optimal mix of glucose, dextrose, fructose, maltodextrin or other "special" carbohydrates  - needless to say that waxy maize, hydroxypropyl distarches (learn more) or the expensive fast absorbing highly insulinogenic patented carbohydrate source Vitargo come to mind, when we are talking about finding the optimal mix of different carbohydrate sources - a mix, by the way, of which you can safely assume that it will differ according to the physiological demands of the workout and the exercise duration.
  
  One thing we shouldnt forget, though, is that next to optimal performance, optimal GI tolerance, i.e. the absence of bloating, diarrhea & co would be an important criteria the "optimal" carbohydrate blend would have to meet.

• Figure 4: CHO suppl. ameliorates  testosterone reductions in 800m runners (de Sousa. 2010)

  the impact of carbohydrate supplementation on hormonal changes during and in response exercise - several human studies suggest that CHO supplementation attenuates the suppression of the hypothalamic-pituitary-gonadal axis and the rise in stress hormones during periods of intense training; a recent rodent study shows that the provision of carbohydrate supple- ments can prevent / reverse exercise-associated menstrual dysfunction (de Sousa. 2010; Zhao. 2014)

I guess, I could come up with additional research gabs, but in the end, a list of "gaps" is not exactly useful for you. Much in contrast to a conclusion, which I am about to formulate in the bottom line, now.
References:

• Carter,  J.,  Jeukendrup,  A.E.,  Mundel,  T.,  and  Jones,  D.A.  (2003).  Carbohydrate  supplementation  improves moderate and high-intensity exercise in the heat. Pflügers Archiv : European journal of physiology446: 211-9.
• Carter, J.M., Jeukendrup, A.E., and Jones, D.A. (2004a). The effect of carbohydrate mouth rinse on 1-h cycle time trial performance. Medicine and science in sports and exercise36: 2107-11.
• Carter, J.M., Jeukendrup, A.E.,  Mann, C.H., and  Jones, D.A. (2004b). The effect of glucose infusion on glucose kinetics during a 1-h time trial. Medicine and science in sports and exercise36: 1543-50. 
• Chambers,  E.S.,  Bridge,  M.W.,  and  Jones,  D.A.  (2009). Carbohydrate  sensing  in  the  human  mouth:  effects  on exercise performance and brain activity. The Journal of physiology587: 1779-94. 
• de Sousa, Maysa Vieira, et al. (2010). Effects of carbohydrate supplementation on competitive runners undergoing overload training followed by a session of intermittent exercise." European journal of applied physiology 109.3: 507-516.
• Fares, E.J. and Kayser, B. (2011). Carbohydrate mouthrinse effects on exercise capacity in pre- and postprandial States. J Nutr Metab2011: 385962.   
• Pottier, Andries, et al. (2010). Mouth rinse but not ingestion of a carbohydrate solution improves 1?h cycle time trial performance" Scandinavian journal of medicine & science in sports 20.1: 105-111.
• Sawka,  M.N.,  Burke,  L.M.,  Eichner,  E.R.,  Maughan,  R.J.,  Montain,  S.J.,  and  Stachenfeld,  N.S. (2007).  American College of Sports Medicine position stand. Exerciseand fluid replacement. Medicine and science in sports and exercise39: 377-90.
• Smith, JohnEric W., et al. (2013). Curvilinear dose-response relationship of carbohydrate (0-120 g/h) and performance." Med Sci Sports Exerc 45.2: 336-341. 
• Stellingwerff, T., & Cox, G. R. (2014). Systematic Review: Carbohydrate Supplementation on Exercise Performance or Capacity of Varying Durations. Applied Physiology, Nutrition, and Metabolism (2014). Ahead of Print. 
• Zhao, Can, et al. (2014). Effects of carbohydrate supplements on exercise-induced menstrual dysfunction and ovarian subcellular structural changes in rats." Journal of Sport and Health Science 3.3: 189-195.

It was about time for an artificial sweetener update, wasnt it?

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

Whether and to which extent these beneficial effects on gut health are mediated by changes in the gut microbiome is yet still uncertain; and since "uncertain" is a word scientists dont like, Kristian Daily and his colleagues from the University of Liverpool conducted a study to find out, whether the non-negligible health benefits would be brought about by AI <> gut interactions.
To this ends, the scientists employed a DNA-based pyrosequencing technology to investigate the changes in the intestinal microbiota of piglets weaned to a diet supplemented with either a natural sugar, lactose or said artificial sweetener (SUCRAM)

Figure 1: Total and lactobacillus OTU4228 concentrations in piglets on hydrolzysate carbohydrate diet without sweeteners, with lactose or SUCRAM diets and corresponding concentration of lactic acid in the caecal contents (Daly. 2014)

As you can see in Figure 1, both, the addition of lactose and the saccharin/NHDC mix lead to dramatical increases in the caecal Lactobacillus population and could well explain the previously reported "pro gut health" effect of SUCRAM in piglets (Vente-Spreeuwenberg. 2004; Pierce. 2006)

But thats obviously not all thats news-worthy!

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

Lean more about the "Gut Type Diet" - No Fad, Guaranteed!

And while previous studies only suggested that the effects of acesulfam-k on the pancreas could have pro-obesogenic consequences, a recent model experiment from the Louisiana State University appears to finally prove that acesulfam-k may actively promote the deposition of body fat in the presence of insulin resistance.

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

In view of the fact that most companies have been pulling acesulfame-k from their products over the past years, anyway, I would not discard the findings Jolene Zheng et al. present in their latest paper in Chemico-Biological Interactions as meaningless, not despite, but rather because a scientists from PepsiCo was part of the research team which observed these significant increases in intestinal fat (=visceral fat of the worm) when the critters were fed with acesulfam-k sweetened coke.
References: 

• Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." Obesity Reviews 13.9 (2012): 799-809.
• Pierce, K. M., et al. "The effect of lactose and inulin on intestinal morphology, selected microbial populations and volatile fatty acid concentrations in the gastro-intestinal tract of the weanling pig." ANIMAL SCIENCE-GLASGOW THEN PENICUIK- 82.3 (2006): 311.
• Jones, Kevin T., and Kaveh Ashrafi. "Caenorhabditis elegans as an emerging model for studying the basic biology of obesity." Disease models & mechanisms 2.5-6 (2009): 224-229.
• Vente-Spreeuwenberg, M. A. M., et al. "Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets." Livestock Production Science 86.1 (2004): 169-177.