Making HIIT a Hit Part I/II: The Quest for the Optimal Interval to Rest Ratio for Your Type & Goals - Warming up: Selected Studies + Individual Take Home Messages to Set the Scene

This series will not readdress the "HIIT and/or LISS debate", but simply try to do what the title says: Help you to determine the "ideal" form of HIIT for your type & goals.

After posting yet another article about the benefits of high intensity interval training (HIIT) training on Wednesday, I thought it may be a good idea to take a look at the pertinent literature to get a better grasp of what exactly high intensity interval training actually is... "What it is? What do you mean?" While almost everyone appears to recommend you do at least some amount of high intensity interval training, these days, the definition of both the "high intensity" and the "intervals" which are more than just eponymous of this type of training are usually pretty wooly. The two questions this article is supposed to answer are therefore: How long should the intervals and rest periods be and at which intensity should they be performed.

Attention, this article turned into a two part series: I must warn you, this "quest" turned out to be hell lot of work and way more than I had expected. So I will have to split it up into a two-part series. With today's first part discussing exemplary "success stories" and the subsequent follow up on next Sunday providing a more comprehensive overview and general conclusions one may draw based on the picture that emerges.

Part I: Success stories - learning from the "best"

I decided that it may be a good idea to initially compile some examples of which you could say that they are examples of a successfully implementation of high intensity interval training. In that, I will put an emphasis on "old" studies that have not yet been discussed on the SuppVersity. This means, if you want more examples before next week's 2nd installment with a more general overview, you can simply click through the archive of articles that are marked with the keyword HIIT - either as HTML or RSS (I recommend the latter if you do not intend to read all of them anyway; opens in all good browsers without a reader).

Untrained participants and non-athletes

• 5min on, 2min off HIIT to increase fitness (VO2max) alternated with 40 min steady state cardio for 4 + 5 weeks (Hickson. 1981) -- Hard to believe but it's more than 30(!) years ago that Hickson, Hagberg and Ehsani were able to show that a combination of high intensity interval training with 6x5min cycling at 90-100% of the VO2max and 2-min at 30%-50% active rest between intervals on day one and 40 min of steady state "cardio" on a treadmill on day 2 (6 workouts per week) yielded profound increases in VO2max:
  

  

  Figure 1: Adaptation to combined HIIT + steady state protocol in "occasionally active" but not "regularly" trained men (n=8) and women (n=1) in the Hickson study (Hickson. 1982).

  For our purpose, the most significant finding of this study may however be that the t_1/2, i.e. the amount of time it takes for 50% of the adaptations to take place is only 10 days (on this intense protocol).
  
  Take home message: If VO2Max and overall conditioning is your goal you should up the intensity every three weeks, to make sure you continue to make progress. If you go by VO2max, this would be an increase in the speed you run or bike - not (!) the duration of the intervals and / or their number.

• 2 series of 5s sprint cycling (8-13x) with 55s of active rest increase force production and rids subjects of "useless" type IIb fibers (Linossier. 1993) -- The 10 students (8 men, 2 women; age 22y; VO2max = 51.2ml/kg/min, everything below 55 is still considered ) in the Linossier study performed 4 HIIT only workouts consisting of 5s all-out sprints on a cycle ergometer interspersed by 55s of active rest cycling at a heart rate of 130-140bpm per week. The number of sprints in each of the two sessions on a single training day (15 min of rest between) were increased from 8 to 13 sprints over the 7-week study period. The main results were improvements in both peak performances +25%  and in the 30-s total work +16%.
  
  

  

  Figure 2: Unexpected shift in muscle fiber type distribution (Linossier. 1993)

  What's also relevant, though not directly performance related is the 19% increase in phosphofructokinase and a 20% increase in lactate dehydrogenase, both are glycolytic enzymes and are indicative of improvements in the glycolytic pathway, which goes to show you that you don't have to be afraid of the fiber type changes hampering either your ability to handle glucose or your strength - I mean +29% in maximal force production in the sprint tests are everything else but "weak".
  
  Take home message: Shorter sprints appear to be a valid means to hammer and improve the glycolytic pathway and get rid of the useless type IIb fibers, of which not endurance athletes, but bodybuilders have the lowest amount and sedentary controls the most (cf. figure 1 in the overview of the Intermittent Thoughts on Building Muscle). To actually build muscle the 1% increase in muscle weight the scientists observed, is yet not sufficient enough.

• 7 sessions of 10x4 min cycling at 90% with 2 min rest ramp up skeletal muscle fat metabolism in young women (Talanian. 2006) -- The 8 healthy recreationally active women (22 yr old, 65.0 kg body wt) who had previously engaged in 2-3 just-for-fun sessions of various activities from weight lifting, soccer and cycling to swimming, or walking, participated in no more than 7 HIIT sessions within 2 weeks (1 day on, 1 day off) which consisted of 10x 4min sprints at 90% of their individual VO2max with two minutes of rest in between.
  
  

  

  Figure 3. Changes in substrate utilization during standardized 60 min LISS test at 60% of the VO2Max (Talanian. 2006)

  Contrary to the previously discussed studies, the scientists were in this case less interested in the performance than in the metabolic benefits, which were - as the data in figure 1 show - surprisingly significant given the short duration of the study. The increases in fat oxidation and decreases in the respiratory ratio (the ratio of glucose to fatty acid oxidation) during a standardized 60min light intensity (60% VO2max) test that was performed at the beginning and end of the study, were a consequence of increases in citrate synthase and beta-hydroxyacyl-CoA dehydrogenase (beta -HAD) activity.
  
  Take home message: In view of the important contribution of beta-HAD to the beta oxidation of (esp. medium-chain) fatty acids, the fact that an upregulation of this enzyme has been observed in response to the long duration intervals, but neither light intensitsy exercise (even w/ 2h per day, 5-6 times per week; cf. Phillipps. 1996), nor during a similar 2-week sprint training protocol (30s all-out on cycle ergometer, 4 min rest; cf. Burgomaster. 2005) points towards "long" duration intervals when mitochondrial adaptations that favor fatty oxidation and thus subsequent increases in fat loss with light activity are concerned. 

Highly trained participants and pro-athletes
 

• 3 sessions of 10 intervals at 96% VO2Max with 60-180s rest increase running economy and relative fatty oxidation during subsequent steady state exercise test (Zavorsky. 1998) -- Twelve highly trained endurance athletes volunteered for this study, four of them qualified for the 1996 Canadian Olympic Trials, and one subject was a Canadian record holder in triathlon. On three different occasions the subject ran 10 x 400-m sprints with active recovery periods of 60, 120, 180s (randomly assigned). 10 min before and afterwards standardized running economy tests were performed.
  
  

  

  Figure 4: Respiratory exchange ratio in RE test before and after the sprinting protocol (Zavorsky. 1998)

  During these running economy tests, which consisted of 2 x 5 min running on a treadmill at 12km/h or 16km/h (5 min total rest in between), the subjects exhibited, much contrary to the research hypothesis, by the way, an increase in the running economy (RE, a measure of how efficiently a person uses oxygen while running at a given pace) and - probably of greater interest for most of you an increase in fatty acid oxidation, as evidenced by the reduced respiratory exchange ratio (RER, figure 4). The latter was particularly pronounced in the "low intensity" RE test at 12km/h.
  
  As far as the differential effects of the rest intervals is concerned, significant effects were observed for the rates of perceived exertion (60s: 17.7; 120s: 16.1; 180s: 14.4), but not for the performance related measurements velocity, and the time it took the athletes to run the 400m sprints (actually the latter should be self-evident with identical velocities).
  
  Take home message: Doing ten short sprints (if you are not an athlete, shorter ones will suffice) before you go jogging (or do any other type of steady state cardio) won't hamper your running economy. And since the study at hand suggests that the relative increase in fatty acid oxidation is specifically pronounced in the lower intensities (this is supposedly even more the case if you jog at 10km/h), the combination of sprints + steady state cardio appears to be an ideal "cardio" only day, when you are trying to lose body fat.

• 8x all-out (100% VO2max) 2.5min intervals with 4 min of active rest increase VO2Max, peak aerobic power and 5k time trial performance regardless rest between sessions (Gross. 2007) -- With the unique twist with respect to the training frequency this study is somewhat unique. While other studies report similar benefits in highly trained collegiate cyclists (13 men, 4 women; VO2Max at baseline 62ml/kg/min) or other endurance athletes, this is one of the few that investigates whether it makes a difference if the athletes implement the 3-days per week HIIT regimen as a block or interspersed by one day of rest into their regimen.
  
  

  

  Percent change in TT5k velocitym TT5k power output VO2peak, and peak aerobic power output in cyclists trainin on consecutive vs. non-consecutive days (Gross. 2007)

  Interestingly enough, neither the performance outcome on the pre- and post tests, i.e. increases in VO2Max (+5.7%), peak aerobic power (+7.2%), 5k time trial performance (+6.9%), nor the actual performance during each of the workouts the subjects performed in the course of the 3-week study period suffered from doing the HIIT sessions back to back. These results refute previous speculations that doing HIIT as a block would trigger greater metabolic adaptations, specifically in athletes (e.g. Padilla. 2000). Even more, though the changes were not statistically significant, the data in figure 5 shows that - with one for endurance athletes important exception, namely the VO2Max - training on non-consecutive days produced marginally better results.
  
  Take home message: While it appears as if it would not make a difference whether you perform your HIIT workouts blocked or within your training week. The non-significant differences in figure 5 could suggest that endurance athletes intending to improve their already high VO2Max even further would be better off with the blocked training. Everybody else has the choice and I would pick the interspersed variety, whenever my schedule allows me to do this - my personal experience told me that this works better for me... apropos, take another look at figure 5 you see the narrow bars indicating the standard deviations? This goes to tell you that it is very likely that not just the personal preferences, but also the actual outcome will vary from trainee to trainee, which supports the notion that you will have to experiment to find what works best for you.

That's it for the "success stories"! Don't forget to come back next Sunday for part II and in case you have not done so already, just browse the previous SuppVersity posts on this matter, either as HTML version, post by post, or from the RSS overview (works in every modern browser, yet not in Google spyware ;-). I know you are smart enough to draw your own conclusions. And what's more, this may yield some cognitive input for the comment area of this article, where you can post questions. I will try to tackle those I can answer in the next installment.

References:

• Burgomaster KA, Hughes SC, Heigenhauser GJF, Bradwell SN, Gibala MJ. Six sessions of sprint interval training increase muscle oxidative potential and cycle endurance capacity in humans. J Appl Physiol. 2005; 98: 1985–1990.  
• Gross M, Swensen T, King D. Nonconsecutive- versus consecutive-day high-intensity interval training in cyclists. Med Sci Sports Exerc. 2007 Sep;39(9):1666-71.
• Hickson RC, Hagberg JM, Ehsani AA, et al. Time course of the adaptive responses of aerobic power and heart rate to training. Med Sci Sports Exerc 1981; 13: 17-20.
• Linossier MT, Denis C, Dormois D, Geyssant A, Lacour JR. Ergometric and metabolic adaptation to a 5-s sprint training programme. Eur J Appl Physiol Occup Physiol. 1993;67(5):408-14. 
• Padilla S, Mujika I, Orbañanos J, Angulo F. Exercise intensity during competition time trials in professional road cycling. Med Sci Sports Exerc. 2000 Apr;32(4):850-6.
• Phillips SM, Green HJ, Tarnopolsky MA, Heigenhauser GJ, Grant SM. Progressive effect of endurance training on metabolic adaptations in working skeletal muscle. Am J Physiol Endocrinol Metab. 1996: 270: E265– E272, 1996
• Talanian JL, Galloway SD, Heigenhauser GJ, Bonen A, Spriet LL. Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women. J Appl Physiol. 2007 Apr;102(4):1439-47. 
• Zavorsky GS, Montgomery DL, Pearsall DJ. Effect of intense interval workouts on running economy using three recovery durations. Eur J Appl Physiol. 1998; 77: 224-30.

The Female(?) Athlete Triad - Part III/III: Road to Recovery! Step #1 = "Increase Your Energy Intake"! Plus: Learn How to Calculate Your Resting Energy Expenditure (BMR)

You don't have to eat Burgers and French fries all day, but it's almost certain that you got to eat MORE than before. In this installment we will thus take a look on how much you'd minimally to function in your regular everyday life.

I have to admit I did underestimate the workload that would be associated with the SuppVersity Female(?) Athlete Triad Series. When I wrote the first part of this series, I originally did not even plan to have a second, let alone third part. Now, I've reached Part III and have to realize that the simple question "how much do I have to eat" can become pretty hairy. Not the least, because I personally have never been an advocate of meticulous calorie counting and yet cannot ignore the fact that I have to give you something you can start from... to cut a long story short, also to avoid falling victim to the aforementioned "bloggers triad", I will tackle the rest of this series, the "Road to Recovery" as I called it in as many steps as it will take: No renumbering just Step #1, Step #3, Step #3, ...

In view of the fact that each of those steps should contain at least one thing you can actually do, we will start out right with the single most important change you will have to make in order to escape the self-perpetuation vicious circle I've been outlining in the last installment of this series.

Step 1: Increase your energy intake! But how much do you need?

Figure 1: Dose-dependent effects of restricted energy availability on LH pulse amplitude (squares, top) and frequency (triangles, bottom) in subgroups of women with luteal phases of exactly 11 days and >11days.  Effects are relative to values at 45 kcal/lean body mass (Loucks. 2003)

If you take a look a the way the luteinizing hormone secretion becomes impaired, when your energy intake goes below a critical threshold of roughly 30kcal/kg (for men you will see propably see your T-levels plummet if you go below this level - diet or not!), it should be obvious that your first step towards recovery is to increase your basal energy intake, i.e. the amount of energy you consume irrespective of your daily energy expenditure, above this critical threshold.

For a 25-year old woman with a body fat percentage of 20% and a total body weight of 65kg this would imply that your daily energy intake must never be lower than 0.8 x 65kg x 30kcal/kg = 1560kcal - even when you are dieting.

Despite being based on empirical evidence, going solely by LH abnormalities is probably not the best way to estimate your energy requirements. Therefore, I have picked two practical alternatives for you to chose from:

• The standard equation to calculate the basal metabolic rate independent of your daily activity levels, i.e. the Harris-Benedict equation reads (the values are in kg, cm and years, for weight, height and age, respectively)
• REE (women) = 655.1 + 9.5663 x weight in kg + 1.85 x height - 4.676 x age
• REE (men) 66.5 + 13.75 x weight  + 5.003 x height - 6.775 x age

• 

  Active (wo-)men need more than their REE (img sheknows.ca)

  Multiplied with the "correct" Acitivity Level Factors these REE values will also yield an estimation of your overall daily energy expenditure which is 1.53x, 1.76x and 2.25x higher than your REE depending on whether you are sedentary or lightly active (1.53x), active or moderately active (1.76x) or vigorously active (2.25x), with the latter being the category approx. 90% of those who are trapped in the athlete triad still belong to.
• Probably more accurate since developed and tested with an athletic population, but reliant on way more information would be a recently proposed equation by Oshima et al., which reads
• REE (men & women) = 2.3 x bone mineral weight + 4.5 x adipose tissue weight + 13 x skeletal muscle weight + 54 x rest weight*
  *(brain, liver, kidney, glands, skin, etc.)
• It is easy to see that this equation has been developed to be used in professional studies. After all, the majority of people won't even know that there is a profound difference between both your fat mass and your total adipose tissue mass, as well as your "lean mass" and the amount of skeletal muscle tissue you are effectively carrying around.

* * *

While the calculation of your resting energy expenditure with the Harris-Benedict equation should actually be pretty straight forward and yields

Daily REE (Harris-Bendict) = 655.1kcal + 9.5663kcal/kg x 65 kg
+ 1.85kcal/cm x 170cm - 4.676kcal/year x 25 years = 1474.51kcal

the same cannot be said of the more sophisticated equation Oshima et al. proposed. Not because it was more complicated to plug the figures into a calculator, but rather because you are unlikely to have the respective data handy.

How to use the Oshima equation without DXA data - An example

Since this is at least in my experience the parameter most of you will be missing, I base the following example calculation on the assumption that we don't have the quantitative data on Mrs Jane Average's bone mineral density and are thus not able to estimate the corresponding bone mass (in kg) by multiplying the bone mineral density (in g) by x 1.85 / 1000.

Figure 2: The individual contribution of the body compartments (based on Oashima. 2011 & Taguchi 2011) in the Oshima equation relative to total body weight in 57 male and 93 female athletes can serve as a basis to estimate your resting energy expenditure. The text provides an example how this is done for a 25y-old, 170cm, 65kg woman with 20% body fat. The same can be done for men & women from other "weight classes", the values are yet probably not representative of live-long sedentary individuals

For Jane Average, the athletic woman from our previous example, who had a total body weight of 65kg and a body fat percentage of 20%m we can still estimate all the parameter we need by extrapolating values from the data in figure 2 (don't tell me that's not accurate, you will be surprised ;-):

Do not count each salad leaf! As mentioned in the introduction, already, I have never been a fan of calorie counting. Part of the problem of the athlete triad is however that once you are in it, you have no baseline you could tweak by following my usual advise of logging your food intake for 1-2 weeks, taking stock and going from there. Likewise you can (for the reasons I explained in the last installment) not go by your appetite / hunger, simply because you have long "starved it away". If you really want to return to normalcy, however, you must not start to count the energetic value of each and every salad leaf, tomato, piece of broccoli or single rice corn you put into your. Therefore, the things you will count are ...

• meats, eggs, fish, dairy, etc.
• rice, (sweet) potatoes, oats, pasta, bread, etc.
• coconut oil, olive oil, butter, ghee, sauces, etc.
• any form of treat / fast and convenient food or caloric beverage
• food supplements, e.g. protein shakes or bars

You will also count pieces of fruits and veggies with a caloric value similar to carrots, but whenever you catch yourself cutting off half of the asparagus spear you were just about to eat, eat at least another two + buttery Sauce Hollandaise on top ;-)

• assuming that the body height of our woman is 1,70cm, she would have a BMI of 22.5 kg/m² and therefore fall into the middle category in figure 2
  
• accordingly her bone mineral weight would be ~7% of her body weight, which allows us to estimate her total bone mineral weight to be 4.55kg
• her total fat mass, which is ~85% of the total adipose tissue weight would be 20% of her body weight, i.e. 13kg; we need to multiply that by 1.18 in order to accommodate for the non-fat part of the adipose tissue and get a total adipose tissue mass of 15.3kg

Since the weight of the "other organs" (including brain, liver, kidney, skin, etc.) is subject to lower inter-individual differences, than the exact amount of skeletal muscle, we will use the purple 30% "rest / organ mass" value from figure 2 (remember with a BMI of 22.5 our exemplary woman falls into the middle category) instead of simply relying on the  common yet incorrect assumption that the skeletal muscle mass was was more or less identical to the difference of total body and fat mass:

• to determine the weight of the metabolically highly active organs (compare the coefficients to those of the "purported fat burner" skeletal muscle - at rest, brain, liver, kidney, but also ovaries & co consume 4x more energy than muscle!) in the Oshima equation we  multiply the total body weight with0.3 (=30%) and get a a "rest weight" of 19.5kg
• eventually we determine the skeletal muscle weight by simply subtracting all the values we have from the total body weight - viola, our exemplary woman has a skeletal muscle weight of 25.65kg

All that's left to do now, is to plug those values into the Oshima equation, which will then look like this:

Daily REE (Oshima) = 2.3kcal/kg x 4.55kg + 4.5kcal/kg x 15.3kg
+ 13kcal/kg x 25.65 kg + 54kcal/kg x 19.5kg = 1465.77kcal

So, assuming that I did not hit the wrong buttons on my calculator, this result is actually almost identical (8.74kcal/day) to the estimation the Harris-Benedict equation yielded. This in turn, goes to show you that within the "normal zone", into which Mrs. Jane Average certainly would fall, simple standard equations such as the often criticized, yet still widely used Harris-Benedict equation appear to be pretty accurate. At least, when we are talking about the minimal requirements of someone who's not doing much more than walk from the bed, to the fridge, to the car, to the table in his office, back to the car and ... you know what the average white-color worker does these days.

Extraordinary individuals have extraordinary energy requirements - and you are extraordinary!

Fortunately, you are none of those office "triseathletes" whose athletic triad consists of exhaustive in your office chair idling, extreme stressed in the car sitting and lazy on the couch lying... right? I thought so! And this is why there is no way that the ~1,500kcal will suffice to break out of the vicious circle of a real athlete's triad. 

On the contrary, it is however "as sure as eggs is eggs" that falling short of those minimal energy requirements is the single best recipe to fall victim to the very same triad.

Resting metabolic rate and real-life energy requirements

If you take another look at figure 1, the corresponding LH-based energy intake rule of thumb, I derived from the data by Loucks et al., as well as the coefficients (the factors in front of the parameters) in the Oshima equation, it should actually be obvious that those basal energy requirements are more or less "hard-wired" into our hypothalamic energy control system. With 54 out of 74kcal/kg body weight (73%) being used simply for the maintenance of organ functions, alone (!), there is not much room to conserve energy other than eating up the organs, the bones and the skeletal muscle and of course shutting down such superfluous organs as the ovaries or testes, and... hold on, aren't that all the symptoms of the athlete's triad?

Figure 3: Mean, median and minimal energy intake (in kcal/kg) in eumenorrheoic vs. amenorrheoic female athletes (data calculated based on an overview in Manore. 2002)

Against that background it is no wonder that my statistical makeover of the stats from a list of studies that was included in a 2002 paper by Manore, already suggests that the 1,500kcal are in fact an absolute minimum for the real light-weights among female athletes. Only in one of the 15 studies with datasets from 138 women on which the values in figure 3 are based, were the ~30kcal/kg body weight sufficient to prevent onset of amenorrhea. And when I am telling you that this group of female athletes also happened to be the group who consumed the highest amount of carbohydrates relative to their overall calorie intake per kg of body weight, I am actually already touching on the topic of the next installment, in which we are going to take a look on how you should distribute your overall energy intake across the macronutrient spectrum.
 
A pros pos, while you are waiting for the next installment of this series you should stop counting asparagus spears, calculate your resting metabolic rate and see where you are standing, in terms of your current caloric intake! And though I personally doubt both the quantitative validity of the activity level factors Harris and Benedict provide, you should not forget that chances are slim if not non-existent, that you will recover, if you don't aim for a 1.76x higher energy intake than your RMR calculations would prescribe on workout days.

References:

• Harris JA, Benedict FG. A biometric study of basal metabolism in man. Publ no 279. Washington, DC: Carnegie Institution, 1919.
• Loucks AB, Thuma JR. LH pulsatility is disrupted at a threshold of energy availability in regularly menstruating women. J. Clin. Endocrinol. Metab. 2003; 88: 297–311. 
• Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med. 2002;32(14):887-901.
• Oshima S, Miyauchi S, Kawano H, Ishijima T, Asaka M, Taguchi M, Torii S, Higuchi M. Fat-free mass can be utilized to assess resting energy expenditure for male athletes of different body size. J Nutr Sci Vitaminol (Tokyo). 2011;57(6):394-400.
• Taguchi M, Ishikawa-Takata K, Tatsuta W, Katsuragi C, Usui C, Sakamoto S, Higuchi M. Resting energy expenditure can be assessed by fat-free mass in female athletes regardless of body size. J Nutr Sci Vitaminol (Tokyo). 2011;57(1):22-9.

Maximal Intra- & Post-Workout Fat Oxidation With Pause or 90min LISS Between 2x40min Incremental Exercise Bouts?

Image 1: You better don't even think about losing fat, while you cycle!

As a regular reader of the SuppVersity  you know that I don't believe in the idea of "working out to lose fat", at least not if that implies that you would actually try to burn the fat while you are working out ... yeah, right! I am talking about the hilarious concept of the "fat burning zone". I was still amazed, when I came across a paper that's scheduled for the October issue of Journal of Applied Physiology Nutrition and Metabolism (thanks to my friend Sean Casey from CasePerformance, who helped me out on this one) and investigates the effects of two different modes of what initially looked like a novel torture method and then turned out to be somewhat of a comparison of a twice-a-day cardio-workout, as you could perform it during a contest preparation to make weight and it's evil twin brother.

Train insane... and for nothing?

Enough of those metaphors, let's take a closer look at what the 15 healthy, moderately trained male subjects (age 27.4 +/-1; BMI 23.1; body fat 14.4%; fat free mass 63.7kg) were put through (note: all subjects performed both protocols in random order; see figure 1):

Figure 1: Outline of the study protocol; the two trials differed only with respect to the medial part, where the heavy group kept on working out, while the "light" group waited for their second incremental exercise trial.

I guess I don't have to tell you that the upper path, with the additional light intensity steady state exercise in-between was the "evil twin", while the lower one with "only" two bouts of exercise to the anaerobic threshold (when the respiratory ratio RER reaches RER=1) was the lullaby version.

Image 2: Train hard, but make it smart!

Parenteral, ... ah I mean SuppVersital Advisory: Please don't take any of the results or the whole discussion here as an incentive to perform either of these protocols on a daily basis for the rest of your life - especially if the only thing you are allowed to consume during and in between the trial which started at 7-8AM fasted is water (it should be said that this was an experimental necessity here, as everything else would have skewed the results). If you do, I can guarantee that you will be joining the rest of the pack who's sitting in your Dr's complaining about low thyroid, chronic fatigue, or whatever other self-diagnose people who don't want to admit to themselves that they are overtraining will be en vogue then.

So what do you expect the outcome did look like? No, wrong. None of the subjects collapsed... or at least the scientists don't mention that. And let's be honest it's not impossible. I know a couple of people who still believe they had to exercise the fat away who follow a similar protocol ;-) That said, let's see if that's even worth it - I mean do you really burn fat at all when you exhaust yourself like that?

Figure 2: Fat oxidation during the 40min incremental exercise bouts on the cycle ergometer at the beginning (Incr 1) and end (Incr 2) of the trial (data based on Chenevière. 2013)

As the data in figure 2 shows, the answer is straight forward: YES! You do. And surprisingly much, in fact. This is by the way partly mediated by the surprising effect the 90min of LISS had on the "fat max" exercise intensity which is now, in the 2nd incremental exercise trial (Incr 2) 60.9 % of the VOmax, while it is in the "low intensity" trial with the 90min PAUSE instead of LISS at 56.9%. This may sound bad at first, but if you can go faster without shifting to glucose as your preferred fuel this does obviously allow you to burn more fat - and that's exactly what the subjects did during the heavy trial: They derived 9% more of their total energy expenditure from fat and burned 34% more total fat minute per minute - that this would have been meager 8g even if they had been cycling at that high intensity for the whole 45min incremental exercise bout is yet further evidence of the futility of trying to "exercise the fat away"...

So if you can't burn it while you train, what can you do to burn more after you train?

By now, I guess I will have convinced all of you that you won't get ripped by burning an additional 8g of fat while you work out, but what about this EPOC thingy... I mean that "burn fat after you workout concept", what about that? Does it make sense to literally run around all do to make use of that?

Figure 2: Respiratory exchange ratio (lower values = higher percentage of fatty acids oxidized), lactate and heart rate after the second incremental exercise bout (Incr 2; data based on Chenevière. 2013)

Well, if we are honest, the post-exercise data collected right after the incremental exercise bout # (Incr 2, figure 1) is even more disappointing. Ok, the respiratory exchange ratio is minimally, yet statistically significantly lower, but the heart rate the exertion and the lactate levels are much higher. Plus, you cannot tell me that any sane individual would keep on fasting after this torture and in the very same moment you start eating your the "RER advantage" will be lost, anyway.

Image 3: These abs were not sculpted in the "fat burning one"! Click here to read the original article I used this image with, the "Fat Loss Support Routine" from the Step By Step to Your own Workout Routine guide.

So what's the bottom line, here? Aside from another primer on the fallacy of trying to do more, more and once again more, instead of simply getting your diet in check and sticking to it, to lose weight, there is actually a take home message you could derive from the results of this study: Let's assume that - hypothetically, of course - you got to make weight fast and still have more than enough time to recover after this quick weight loss fix before your performance must be back to it's usual heights. In a situation like this, and only as a short time intervention, the additional total energy expenditure during the 90min of LISS and the increased fat oxidation, combined, would make the "evil twin" protocol, with its 2x incremental exercise regimen interspersed by 90min of relatively light cycling in the fasted state, an option, you could even  improve on by replacing the 2x 45 min bouts with 2x20min of HIIT + 2x10min cool-down and guzzling some non-gluconeogenic BCAAs (max. 10g-15g / 45min) while you are putting yourself through this torturous regimen.

References:

• Chenevière X, Borrani F, Droz D, Gojanovic B, Malatesta D. Effects of 2 different prior endurance exercises on whole-body fat oxidation kinetics: light vs. heavy exercise. Appl Physiol Nutr Metab. 2013 Oct;37(5):955-64.

On Short Notice: Insanity vs. TurboFire - What's the Best HIIT Regimen? Plus: USA vs. China, Chews vs. Raisins, Epi-Sesamine vs. Body Fat, Exercise vs. Neurotoxins & More

Figure 1: The latest medal prognosis for Olympia 2013 by researchers at the Department of Economics at the Ruhr-Universität Bochum in Germany (Otten. 2013) - I must admit I am curious how accurate this prognosis will be... what's your take? The US or China? Who's going to take the lead?

The Queen has officially opened the Olympic Games 2013 and the games have their first doping case - those of you who followed yesterday's advice to subscribe to the SuppVersity Facebook page are already in the know... anyways, this is not the place for one of my hypocrisy rants, but for the weekly installment of "On Short Notice". Still, in the "honor" of the Olympics *rofl* and the spirit of the SuppVersity - which is, as you all know, the place you will get the news first! - I have compiled the TOP15 from the latest medal prognosis by Sebastian Otten, the chair of the Department of Economics at the Ruhr-Universität Bochum in Germany, for you as an appetizer (figure 1). Moreover, I picked more sports and less health, weight-loss, supplementation and nutrition related topics from my ever-growing collection of "On Short Notice" items, which is by the way already so exuberant that there will be another episode of this series either tomorrow or early next week, mostly because otherwise the latest news would come in late... so, let's go for it!

Insanity vs. TurboFire Interval - What's the optimal HIIT regimen?

As part of her recently published master thesis, Sarah A. McGlinchy investigated the differential effects two commercial fitness programs had on the heart rate pulmonary O2 uptake, CO2 output, caloric expenditure and substrate utilization during exercise and recovery, as well as the subjective satisfaction and physical exertion of trained individuals (N=15, four males and 11 females, aged 22.3 ± 1.6 years McGlinchy. 2013).

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  Image 1: Insanity (top) vs. Turbo Fire (bottom) - My HIIT workouts look profoundly different, but this does not mean that those workouts cannot be effective; specifically if you enjoy stuff like this and don't do it alone in front of your TV, but with friends & new friends at the gym. And trust me, I don't even need a study to be able to tell you that a workout you enjoy will be more productive than the "objectively" best workout you hate

  Insanity® Interval Training Protocol - A plyometric cardio circuit workout that is performed after a 9 min warum-up and followed by a 5 min stretch. It revolves around different drills (performed at progressively increasing intensity) that are separated by 30s water breaks, the drills last about 1 min each - the total length of the workout is 41 minutes and 35 seconds (click here to watch a promo video on YouTube)
• Turbo Fire® Interval Training Protocol - The HIIT 30 variety of a series of DVDs that comes from the same company that sells the P90X DVDs includes a 3 min warm-up, a 3 min cool down with stretching and slow movements to get the heart rate back to normal and a series of five drills of which the first four are repeated twice and the last one three times. Drills last about 1 min and are supposed to be performed with maximum effort each is followed by one minute of active recovery (walking, jogging in place, etc.). Water breaks are allowed during the active recovery. The total length of the workout is 30 minutes and 36 seconds (click here to watch a private workout video on YouTube).

I don't know about you, but based on the part of the videos I saw, before I felt I had seen enough, I would probably prefer the Insanity (Ins) over the Turbo Fire (TF) protocol; not so the study participants, though: After having performed both workouts in a randomized order, their "positive engagement" was slightly more pronounced after the TF protocol (see figure 2, left). It should however be mentioned that neither the the pre- to post- nor the inter-workout differences were statistically significant (with a total number of subjects of N=15, the difference could well have been 7/8, had the subjects been asked to pick one or the other).

Figure 2: Physical exhaustion, tranquility and pos. engagement after workouts (left), respiratory exchange ratio at rest and from min. 5-60 (middle), and time (in s) during the workout, when the heart rate was within the given percentages of the calculated personal HR_max(data adapted from McGlinchy. 2013)

My gut tells me that the part of the preference for the TurboFire (TF) protocol could be due to from a) the shorter overall duration and b) the greater exhaustion the subjects in experienced during the Insanity trial -I mean "insanity"? What else do you expect???

Ignore fatty acid oxidation and total calorie expenditure - pick the one you like!

The significantly less pronounced at the end of the TurboFire Intervals stand in contrast to the total the subjects were working out in the 81-90% HR_max, though. With 1000 seconds (vs. 580s) the latter was significantly longer during the Turbo Fire session. Accordingly, the subjects' respiratory exchange ratio (RER), a measure for the relation of glucose to fatty acid oxidation was significantly higher, as well.

SuppTensity Workout Perform 3 cycles of these 5 drills, each drill lasts 1 min, 45s active recovery  between drills, 2 min between cycles

• Squats*
• Push ups
• Lunges**
• Clean & press*
• Rope skipping

use adequately loaded *barbell or **dumbbell

While the former was to be expected, it may appear somewhat odd at first, though, is the higher and longer-lasting post-exercise energy expenditure in the Insanity group (p < 0.05), which could yet be explained by an overall slightly more demanding (figure 1, left > exhaustion) workout, which - and this is just based on what I saw in the videos - appears to have more "complete" drills - or did you see things like push-ups in the Turbo Fire workout? Against the background that the minimal differences in intra- and post-workout energy expenditure and substrate utilization won't have any noticeable effect on the desired outcome variable, i.e. a leaner, still muscular physique, and in view of the fact that"EPOC comprises only 6-15% of the net total oxygen cost of the exercise" (LaForgia. 2006), anyway, I would fully subscribe to Sarah McGlinchy's recommendation to simply pick the workout you like - based on McGlinchy's interpration of her subjects' feedback that would be the ...

• Turbo Fire® for people who are "looking for more variety of movements with fun music"
• Insanity® for people for whom "music isn’t a priority", but who look for "intense motivation"

Before I conclude this pretty longish and therefore single "on short notice" item with the implications and go ahead to the promised truckload of "on very short notice" items, I would yet like to add one thing to this recommendation: You don't actually need to buy a DVD to do HIIT. It's actually pretty straight forward to compile your own personal HIIT 1min on, 30s off (alternatively 1min active rest) workout by handcrafting your drills from from simple sprints on the grass or beach, intense rope skipping, push-ups, pull-ups, squats, kettlebell swings, stair climbers and everything else you can think of - if you are at a loss now, check out my botchy sample workout on the upper right - took me ~1min to put that together and I know that each one of you can do better!

Image 2: I am not saying everyone needs one of those workout DVDs, but for those of you (or friends of yours) who are not already fed up with "motivational pics + statements" like the one above, which are handed around on facebook like the WWF cards 20y ago on my schoolyard, it my be worth looking into either of these.

Implications: I don't care whether you like it or not (I don't like those workouts either), but I am 2x more inclined to believe the numerous success stories the producers of these workout DVDs use to plaster the Internet than any of the reports on how great supplement X is working for Mr. Y on bodybuilding.com and the like.

Do I suggest you buy a DVD or hop around like a jackass in the gym, let alone in front of your TV, when you prefer going to the next best park or beach doing sprints and combine those with your regular strength training program in the gym? Certainly not! Would I rather see you, your friends or family perform any of these workouts than doing exclusively strength training (let alone ultra low volume 1-rep max style) or hours of steady state aerobics if your goal is to get jacked? Abs(!)olutely ;-)

On very short notice

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  Image 3: Not everything that's golden is good - the "golden" raisins for example have been treated with sulfur dioxide, to prevent them from darkening. At least in susceptible persons SO2 can lead to serious allergic reactions, 4-8% of asthmatics are (also) allergic to dietary sulfites and its general safety is still a matter of constant debate - commonly associated health effects are Urticaria, angioedema, and IgE-mediated anaphylaxis (Rangan. 2009).

  Commercial carbohydrate chews not better than plain raisins - I guess this one falls into the "Olympia tribute" category, aside from Albanian weightlifters, wo obviously prefer Stanozolol, most of the athletes probably use carbohydrate supplements in one form or another. Whether anybody relies on resins as is intra-competition carbohydrate supplement is yet questionable and that despite the fact that the dried grapes can easily compete with the far more expensive Cliff blocks carbohydrate chews. Aside from nonsignificantly faster time-trial performances, the fourteen healthy competitive runners from the University of California who consumed raisins instead of chews, also felt slightly less sore after and had lower insulin levels and greater fatty acid oxidation rates during the run.
  Reason enough for Brandon W Too and his colleagues to conclude "that consuming a natural CHO source (raisins) [..] is well tolerated and maintains blood glucose levels and running performance similar to a commercial CHO product (sport chews)" (Too. 2013). Did you hear that Michael Phelps?
• Epi-sesamine from Lindera obtusiloba could be novel source for potent anti-obesity drug - This is at least what a recently published study that was conducted by scientists from the German Charité Universitätsklinikum in Berlin would suggest (Freise. 2013). In their in-vitro tests the active ingredient of the Japanese spice bush, which has traditionally been used for treatment of inflammation and the prevention of liver damage in Oriental Medicine, did not just prevent the accumulation of lipid droplets, it also activated the pro-apoptotic enzymes caspases-3/-7, which initiated programmed cell-death in the treated fat cells. In view of my recent blogpost on the nasty persistence of lower body fat, the latter could turn out to be of extreme importance - especially for those of you who have already lost a significant amount of body fat and are now suffering from "relative leptin deficiency" (see "Nasty Insights into the Yo-Yo-Effect" for more on how this relates to the YoYo-Effect and weight loss plateaus).

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  Figure 3: Mild exercise (5x 30 min / week, treadmill) boosts brain 5a- reductase and neurogenesis (Okamoto. 2013)

  Mild exercise and the brain: Is DHT what builds new neurons? If there was one hormone that really has gotten a bad rep over the past 50 years, it certainly is DHT: All of you who've read the respective installment of the Intermittent Thoughts (cf. "DHT - The All Things Male Hormone") or the latest news on the DHEA <> DHT muscle generation connection will be aware that the myth of the dangerous, carcinogenic bigger brother of testosterone is at least overtly simplistic if not totally devoid any scientific bases.
  Recently published data from the Laboratory of Exercise Biochemistry and Neuroendocrinology at the University of Tsukuba, in Japan does now add another piece to the "DHT is not bad" puzzle - one even women could come to appreciate (Okamoto. 2013): According to Masahiro Okamoto and colleagues, the exercise induced increase in 5-alpha reductase activity (5-ar converts testosterone to dihydrotestosterone) and the subsequent rise in neuronal DHT appears to be the driving force of neurogenesis (the generation of new neuronal networks / brain tissue and wiring).

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  Image 4: Those of you who have made the transition to physical culture too late or have friends or relatives who missed the boat completely may be interested to hear that researchers from the RIKEN Center for Developmental Biology successfully used stem cells to replete Purkinje neurons two years ago, already (Maguruma. 2010)

  Chronic exercise renders Purkinje neurons bullet proof - In a way unquestionably related to the previous "On Very Short Notice" item are the findings from Huang et al. have just published in Journal of Applied Physiology. In their paper the researchers describe the 8-weeks of moderate treadmill running had on the toxin resistance of 6-week old rodents. Specifically, Huang et al. observed that the "exercised rats not only performed better in the rotarod task [skilled behavior test, see video] but also showed finer Purkinje cell structure (higher dendritic volume and spine density)" (Huang. 2013). And while this is unquestionably reminiscent of the aforementioned neuron-building effects of DHT (which is, as you should know increased with aerobic / volume training; cf. "Intermittent Thoughts on DHT"), the big news is that the neurons of the exercised rodents were also protected against the immunotoxin OX7-saporin.
  If these results translate (I personally believe that this is not a question of yes or no, but only one of the extend to which these results translate) to any of the bazillion other toxins we are exposed to on a daily basis, this would imply that regular exercise may not just protect us from the "classic" neurodegenerative diseases such as Alzheimer's or Parkinson, but also from autoimmune diseases which have a neuronal component and often involve damage to the very Purkinje neurons the researchers found to be "bullet proof" in the study at hand.
• Children of diabetic parents benefit most from hitting the weights - "The offspring" of type II diabetics that's the somewhat surprising result of a 9-week training + 9-week detraining experiment Katherine Schofield and her colleagues from New Zealand and Denmark conducted respond particularly favorable to resistance training programs (Schofield. 2013). At the end of the initial 9 week training period, the insulin response of the children with diabetic parents was still worse than thatof their peers in the control group, but with improvements of roughly 30% they were already approaching what you may call the "normal zone", when the detraining phase begun. Contrary to the kids in the control group, whose insulin sensitivity did not change over the 9 weeks of laziness, the children of type II diabetics lost all their previously achieved improvements. Now, you could certainly argue how those poor kids are at such a disadvantage, but unless you want to feed them metformin for the rest of their lives, I suggest we should rather think of ways to teach them how to resist the bad eating habits of their parents and stick to a workout routine that will make the diabetes medication obsolete - don't you agree?

• 

  Suggested reads for everyone interested in some background info on nitrates: (1) Ask Dr. Andro: Is Creatine Nitrate Worth it? (2) Nitrates Work! First NO2 Victim in ER

  Nitrate supplements don't work for athletes and could mess with blood pressure regulation - At least if you are a trained athlete who wants to improve his/her performance, the use of sodium nitrate is a waste of time and money - this is at least what the soon to be published results of a randomized, double-blind cross-over study by Spanish scientists would suggest. For their experiment, Bescós et al. recruited 13 trained athletes and had them perform a 40-min ergometer distance-trial test after a 3-day supplementation regimen with either sodium nitrate (10mg/kg body weight) or placebo (Bescós. 2013).
  Contrary to earlier trials in non-trained subjects, the athletes' performance did not benefit from the supplemental nitrate - despite statistically significant increases in plasma nitrate (+17%) and nitrite (+56%), by the way. Moreover, the concommitant increase in endothelin-1, a protein that constricts blood vessels, raises blood pressure and thus counters the vasodilating effects of the nitrates raises concerns regarding potential side effects that could occur once you drop the supplement.

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  Image 5: Mineral supplements are usually not necessary, as long as you pick the right foods and drinks! What's much more likely in the Western hemisphere than deficiencies, though, are imbalances - and weekend warriors and gymbros are even more likely than your average obese pre-diabetic to run into oftentimes self-inflicted problems... there is going to be a Super Human University seminar Carl Lanore and I are currently working on - and let me tell you this, this is a topic that is literally very dear to Carl's heart.

  Decrease your risk of heart disease by 5% with each mg/L of Magnesium in your drinking water! - I am certainly not among the magnesium enthusiast who propose supplementation with whichever form of oral mg supplement (let alone the scientifically hitherto not verified use of oils) as the latest panacea, but as you may have heard on Super Human Radio on Wednesday, July 25, 2013 (click here for the podcast), I do believe in the overlooked importance of getting your ratios straight; and that, i.e. having the right ratio of Ca:Mg begins at the most fundamental level - with the mineral ratios in your drinking water! Finish scientists who recorded the mineral intake of 14,495 male subjects (aged 35-74), for example, found that with a constant and roughly two times too high mean Ca / Mg ratio of 5.39 / 1 in the drinking water of the area, every additional milligram of magnesium per liter drinking water (e.g. from 2.61mg/L to 3.61mg/L), would help to reduce the risk of acute myocardial infarction by 4.9% (Kousa. 2006)!
  This is an impressive figure and yet, the real beauty of this study is that it emphasizes the need to re-evaluate your nutritional mineral intake, instead / before considering using dietary (let alone oily ;-) supplements!

References:

• Bescós R, Ferrer-Roca V, Galilea PA, Roig A, Drobnic F, Sureda A, Martorell M, Cordova A, Tur JA, Pons A. Sodium Nitrate Supplementation Does Not Enhance Performance of Endurance Athletes. Med Sci Sports Exerc. 2013 Jul 17.
• Freise C, Trowitzsch-Kienast W, Erben U, Seehofer D, Kim KY, Zeitz M, Ruehl M, Somasundaram R. (+)-Episesamin inhibits adipogenesis and exerts anti-inflammatory effects in 3T3-L1 (pre)adipocytes by sustained Wnt signaling, down-regulation of PPARγ and induction of iNOS. J Nutr Biochem. 2013 Jul 18.
• Huang TY, Lin LS, Cho KC, Chen SJ, Kuo YM, Yu L, Wu FS, Chuang JI, Chen HI, Jen CJ. Chronic treadmill exercise in rats delicately alters the Purkinje cell structure to improve motor performance and toxin-resistance in the cerebellum. J Appl Physiol. 2013 Jul 26.
• Kousa A, Havulinna AS, Moltchanova E, Taskinen O, Nikkarinen M, Eriksson J, Karvonen M. Calcium:magnesium ratio in local groundwater and incidence of acute myocardial infarction among males in rural Finland. Environ Health Perspect. 2006 May;114(5):730-4.
• LaForgia J, Withers RT, Gore CJ. Effects of exercise intensity and duration on the excess post-exercise oxygen consumption. J Sports Sci. 2006 Dec;24(12):1247-64.
• Muguruma K, Nishiyama A, Ono Y, Miyawaki H, Mizuhara E, Hori S, Kakizuka A, Obata K, Yanagawa Y, Hirano T, Sasai Y. Ontogeny-recapitulating generation and tissue integration of ES cell-derived Purkinje cells. Nat Neurosci. 2010 Oct;13(10):1171-80.
• McGlinchy SA. The Effect of Two High Intensity Interval Training Protocols on Heart Rate, Caloric Expenditure, and Substrate Utilization During Exercise and Recovery. University of Toledo - Submitted to the Graduate Faculty as partial fulfillment of the requirements for The Master of Science Degree in Exercise Science. 2013.
• Okamoto M, Hojo Y, Inoue K, Matsui T, Kawato S, McEwen BS, Soya H. Mild exercise increases dihydrotestosterone in hippocampus providing evidence for androgenic mediation of neurogenesis. Proc Natl Acad Sci U S A. 2013 Jul 17.
• Schofield KL, Rehrer NJ, Perry TL, Ross A, Andersen JL, Osborne H. Insulin and Fiber Type in Offspring of T2DM with Resistance Training and Detraining. Med Sci Sports Exerc. 2013 Jul 17.
• Rangan C, Barceloux DG. Food additives and sensitivities. Dis Mon. 2009 May;55(5):292-311.
• Too BW, Cicai S, Hockett KR, Applegate E, Davis BA, Casazza GA. Natural versus Commercial Carbohydrate Supplementation and Endurance Running Performance. J Int Soc Sports Nutr. 2013 Jun 15;9(1):27.

Cold Thermogenesis - A Safe Ephedra Alternative? 70kcal Increase in 24h Energy Expenditure is Negligible, 50% Lower Than Ephedrine, Not Likely to Occur Obese or Older People

Image 1 (odditycentral): Jin Songhao, one of China’s most seasoned icemen and not exactly as lean as you may expect based on what you currently read around the blogosphere, managed to beat the previous world record for the longest ice bath - 120min! Congrats, Jin!

Ephedrine for years the go-to OTC fat burner for physique athletes and average Joe's and Jane's alike is no longer (officially) available: No matter how bold the label claims about X mg of "ephedra extract" may be - NONE(!) of the currently available "ephedra based" over-the-counter (OTC) fat-burners contains significant amounts of the active alkaloids, which made the old Mua huang based herbal ephedra products so effective. Against that background, dieters are constantly on the look-out for novel "gimmicks" to help them finally get rid of those annoying love-handles. One of those gimmicks, which has caught quite some attention as of late, is called "cold thermogenesis" and revolves around the idea that our bodies should consume more energy to keep a normal body temperature in a cold, compared to a normal temperature environment.

How is that different from a "thermogenic fat burner"

The most obvious difference between cold thermogenesis and "thermogenic fat burners" is actually so straight forward that I hardly dare stating that the former is induced by exposing yourself to low(er than normal) temperatures, while the promise of the latter is that the various ingredients of currently or formerly available OTC "fat burners" will induce a thermogenic response, irrespective of the current ambient temperature.

Figure 1: Antropomorphic data of the study participants (Cypess. 2013)

The results of a recently published study from the the Boston Harvard Medical School does yet provide somewhat more sophisticated insights into the differences between cold exposure and a sympathomimetic (i.e. an activator of the sympathetic nervous system), such as ephedrine. On three separate, independent study visits that took place in random order the ten healthy volunteers (age 27.1 years) who participated in the study (see figure 1 for DEXA based anthropometric data) and had been fasting since 12am the day before were exposed to one of the following "stimuli":

• ephedrine - a single intramuscular dose of 1mg/kg ephedrine
• saline control - an equal volume of saline
• cold exposure - in a surgeon’s cooling vest (Polar Products) w/ water temperature 14 °C

60min after the injection of ephedrine, saline, or the initiation of cold exposure, the change in metabolic rate was measured and blood was drawn to determine several metabolic and endocrine markers. Another 60min later, PET-CT scanner images (cf. figure 2, right) to quantify BAT mass and activity were taken. Since the participants obviously had to get rid of their cooling vests for this procedure, the total cold exposure time was limited to 120min, so that it is questionable how valid the 24h energy expenditure calculation (cf. figure 3) actually is. After all, it is not very likely that the norepinephrine levels would constantly stay at 200% over baseline (cf. figure 2).

Figure 2: Metabolic and endocrine effects (expressed relative to saline) of ephedrine injection and cold exposure (main image); CT scans with green arrows in the combined scans indicating  the principal cervical, supraclavicular,
and thoracic depots of BAT (Cypess. 2013)

As far as the acute phase is concerned, it is yet quite obvious that both cold exposure and ephedrine elicited statistically significant effects on various metabolic and endocrine parameters. The exact nature and the purported mechanism that is responsible for these metabolic and endocrine effects are however very different for both treatments:

• while ephedrine lead to an increase in blood glucose (probably subsequent to increased glyconeogenesis), cold exposure did not 
• while ephedrine lead to significant increases in lactic acid levels (corresponding to increases in glucose + glucose oxidation), cold exposure did not
• while ephedrine lead to profound increases in β-hydroxybutyrate (increased ketone productions from fat), cold exposure did not
• while ephedrine increased serum non-esterified fatty acid (NEFA) concentrations (due to increased lipolysis), cold exposure did not
• while ephedrine elevated insulin production (probably due to stress induced insulin resistance), cold exposure did not (p = 0.29)
• while ephedrine lead to highly significant (p < 0.001) increases in C-reactive peptide, cold exposure elicited "only" significant elevations (p = 0.005)
• while ephedrine produced already highly significant increases in noripenephrine levels, those were even more pronounced upon cold exposure
• while ephedrine lead to statistical significant increases in thyroid hormone Total T3 (+14%, p = 0.026) and Free T4 (+19%, p = 0.014), cold exposure did not
• while ephedrine lead to a profound (-22%) and statistical significant (p = 0.007) drop in ghrelin ("hunger hormone" and metabolic regulator), cold exposure did not

In conjunction with the combined CT scans from figure 2 these differences clearly indicate that contrary to ephedrine, which is a mere sympathomimetic (put simply a potent "stim" ;-) without depot-specific (here brown adipose tissue) thermogenic effects, mild cold exposure (remember: those were no ice-baths!) has the ability to stimulate brown adipose tissue (BAT) energy expenditure without significant systemic effects on heart rate or thyroid hormone metabolism.

What does that mean? Is GNC soon going to carry cooling vests instead of fat burner pills?

If you read the scientists' rave conclusion that "[i]n contrast to ephedrine [...] mild cold exposure stimulates a specific response by the SNS [sympathetic nervous system] to activate BAT and increase energy expenditure with few other metabolic effects" and their subsequent reference to the "obesity and diabetes pandemics" and the demand for "safe and novel treatments" of the latter, it is quite understandable that people who are referred by their gurus to "scientific evidence" like this are willing to believe that "cold thermogenesis" would help them to finally get rid of their beer-, burger- and burrito-bellies.

Figure 3: Increase in 24h energy expenditure (kcal/day, left) and detectable BAT volume (right; Cypess. 2013)

If you do yet take a look at the actual metabolic effects (cf. figure 3) the 2x more pronounced effect of ephedrine on 24h energy expenditure (+140kcal/day vs. 70kcal) confirms what my previous overview of the metabolic and endocrine effects of ephedrine and cold exposure already suggested: Ephedrine does not simply have more "side effects" it is also more effective.

Figure 4: Activity of BAT activity in relation to body fat levels (van Marken Lichtenbelt. 2009)

Important:  One thing the scientists wink at in both the abstract as well as the conclusion are the profound inter-individual differences in terms of detectable BAT volume and activity. While the median volume of detectable brown adipose tissue in men and women was 22mL and 20mL, respectively, there was one female subject with a BAT mass of 190mL (85x over median!), one with 7ml and one woman without any detectable brown adipose tissue. Similarly, the BAT mass in the men ranged from 46mL to 12mL. Both the existence of individuals without any significant amounts of metabolically active body fat, as well as the observation of high inter-personal variability in the study at hand stand in line with previous results of Saito et al. who found a ratio of 15/32 (45%) non-responders in young (23-35y) and 22/24 (92%!) in older (38-65y) subjects (Saito. 2009). And as if that alone would not render the practical value of cold exposure as a means to battle the "obesity and diabetes pandemic" questionably enough, van Marken Lichtenbelt et al. report that exactly those people for whom ephedrine and other sympathomimetics such as sibutramine would actually pose a non-negligible health risk, i.e. obese and metabolically deranged people, don't just have 40% less brown adipose tissue, but also a -76% reduced BAT activity (van Marken Lichtenbelt. 2009; cf. figure 4). The implications of these findings should be obvious: It is a) by no means certain that sitting in a non-heated room, let alone an ice-bath, is not just going to give you a cold, but even if it works it is b) probably not going to make a difference for those people who need it most - I mean, let's do the math: "70kcal/day minus 76% of the former equals 16.8kcal per day"!

That being said, even the profoundly greater total increase in energy expenditure in the ephedrine group is of a "magnitude" (I would write "minitude" if such a word existed) that would be completely negligible if it were not for the bad and "dangerous" sympathostimulating side effects (Andraws. 2005), which will allow you to train longer, to diet harder (Astrup et al. ascribe 75% of the weight loss effect due to the ingestion of the infamous ECA stack to anorexia, i.e. loss of appetite; cf. Astrup. 1992) than any ice-filled bathtub in the world will ever do.

Skip on ice-baths, stop winning about the ephedra ban. Get your diet & workouts in check!

Image 2: I don't think Francine Sablan, IFBB Figure Pro and like Adelfo one of Myotropics' sponsored athletes, uses the air-conditioning, let alone a funky cooling vest or ice-baths to propel her fat loss. And why would she? She loves working out and she has her diet in check ;-)

I know this is not going to be a popular conclusion, but believe me, the additional +70kcal/day you could expend in the cold, if you are one of the lucky non-obese "responders" (see red box above), won't make you lose a single pound. Even the "good old" ECA stack (remember: the Cypess study used intravenously administered ephedrine; hence, the effect sizes are directly comparable with pertinent studies from the late 1980s and 1990s using orally administered herbals) worked its fat burning magic only, when it was combined with a comprehensive diet and exercise protocol - and in those scenarios it was mostly the influence of its sympathostimulating activity on your ability to adhere to your diet and to endure the hardships of strenuous workouts and not its often-touted and largely overestimated "thermogenic" effects (cf. Astrup. 1985; Astrup. 1992) that were mostly responsible for the larger-than-life results, people are still raving about.

References:

1. Andraws R, Chawla P, Brown DL. Cardiovascular effects of ephedra alkaloids: a comprehensive review. Prog Cardiovasc Dis. 2005 Jan-Feb;47(4):217-25. 
2. Astrup A, Bülow J, Madsen J, Christensen NJ. Contribution of BAT and skeletal muscle to thermogenesis induced by ephedrine in man. Am J Physiol. 1985 May;248(5 Pt 1):E507-15.
3. Astrup A, Toubro S, Christensen NJ, Quaade F. Pharmacology of thermogenic drugs. Am J Clin Nutr. 1992 Jan;55(1 Suppl):246S-248S.
4. Cypess AM, Chen YC, Sze C, Wang K, English J, Chan O, Holman AR, Tal I, Palmer MR, Kolodny GM, Kahn CR. Cold but not sympathomimetics activates human brown adipose tissue in vivo. Proc Natl Acad Sci U S A. 2013 Jun 4. 
5. van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, Drossaerts JM, Kemerink GJ, Bouvy ND, Schrauwen P, Teule GJ. Cold-activated brown adipose tissue in healthy men. N Engl J Med. 2009 Apr 9;360(15):1500-8. Erratum in: N Engl J Med. 2009 Apr 30;360(18):1917.
6. Saito M, Okamatsu-Ogura Y, Matsushita M, Watanabe K, Yoneshiro T, Nio-Kobayashi J, Iwanaga T, Miyagawa M, Kameya T, Nakada K, Kawai Y, Tsujisaki M. High incidence of metabolically active brown adipose tissue in healthy adult humans: effects of cold exposure and adiposity. Diabetes. 2009 Jul;58(7):1526-31. Epub 2009 Apr 28.