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?

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  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.

Less Than 15mg of DHEA Exert Identical Beneficial Effects on Insulin Sensitivity as 1h of Cardio 5x Per Week. Both Effects Mediated Via Increases in Intra-Muscular DHT

Image 1: It has long been established that diabetics have particularly low DHEA levels (Loviselli. 1994), but what's the chicken and what's the egg here?

It is quite funny, sometimes you don't hear about certain supplements, (pro-)hormones, exercise-modalities etc. in years and then, all of a sudden, there are two studies on the respective topic in one week; and moreover, two pretty interesting ones! Last Friday, exactly 7 days ago, you've read here at the SuppVersity about the muscle-protective effects of low-dose dehydroepiandrosterone (DHEA) supplementation during a 5-day intense multiple-type exercise protocol (cf. "DHEA Blunts Muscle Damage During 5 Days of Combined Endurance, Strength and HIIT Training in Young Men"). Today, I have another interesting set of data for you - data which could not just shed some light onto the underlying mechanisms of the said protective effects against skeletal muscle damage, but also on DHEA's beneficial effects on insulin sensitivity.

Not younger, but leaner with a minimalist dose of DHEA?

In a 6 week trial, and thus over a more than eight times longer timespan than in the previously mentioned human study on skelatal muscle damage, Koji Sato and his (or her?) colleagues from the Ritsumeikan University, the Senshu University and the University of Tsukuba (all in Japan, as you probably already suspected) investigated the effects a low dose of DHEA (human equivalent: 0.16mg/kg per day => 10-15mg/day) supplementation on the insulin, QUICKI (=quantitative insulin-sensitivity check index) and intramuscular DHEA and DHT (dihydrotestosterone) levels in sedentary or exercised dietary obese male rodents.

Figure 1: Relative insulin levels, QUICKI, intramuscular DHEA and DHT content in obese male rodents after 6 weeks of DHEA or combined DHEA + exercise (1h, 5days/week) treatment (data adapted from Sato. 2013)

As you can see in figure 1 the effects of both 5x/week running on a treadmill (ETA: 1h) and orally administered DHEA were profound. If you compare the "exercise only" group (red) to the two DHEA groups (green and violet), you will yet notice interesting parallels. Not only were the decreases in serum insulin and the increases (=improvements of insulin sensitivity) in the QUICKI test very similar, the exercise regimen alone yielded a +56% increase skeletal muscle DHEA content and a +71% increase in DHT.

Exercise increases intramuscular DHEA & DHT...
 

Figure 2: Hormonal cascade from DHEA to DHT; all enzymatic conversions can take place on a systemic and intra-cellular level!)

At least the latter, i.e. the increase in DHT should not be news to you if you have been following the in-depth articles at SuppVersity over the past couple of months. From the Intermittent Thoughts on DHT you know that exercise in general and HIT endurance exercise in particular has been found to boost intramuscular dihydrotestosterone levels, as well. The bros, or friends of bros among you, will probably also have heard the horrific stories about creatine monohydrate leading to increased levels of DHT (van der Merve. 2009), of which every reasonable person must actually assume that they are nothing but a downstream effect of increased training loads and/or improved adaptation... I mean, think about it "paleo style": Why would the mammalian body (rodent and human appear to react alike here) increase the DHEA and, via 5-alpha reductase (cf. figure 2), the dihydrotestosterone levels in response to high volume exercise, if not as a means of adaptation?

Oral DHEA + exercise = double-whammy against obesity

The combined treatment, or I should say the exogenous support of the exercise induced changes had - and this is not visible from the data in figure 1, astonishingly profound effects on the diet induced weight gain of the lab animals. While all other rodents became fatter, those in the exercise + DHEA group remained at a steady body weight level; an observation the researchers comment as follows:

Although DHEA administration and exercise training each produced beneficial effects, 6-weeks of combination treatment were more effective for obesity. The precise mechanisms that reduced abdominal fat weight in the combination group remain unclear, yet we can propose several plausible hypotheses. 2 weeks of DHEA administration has been shown to activate fatty acid metabolism-related enzymes, such as long-chain fatty acyl-coenzyme A synthase, and to increase free CoA levels in liver (Mohan. 1998; Mohan. 1990). In addition, exercise training is  known to reduce adipogenesis via upregulation of fatty acid metabolism and increased energy expenditure (Hou. 2003). Therefore, 6-weeks of combination treatment may have promoted additive reductions in abdominal fat volume.

In other words, while DHEA increases the efficacy of fatty acid oxidation, exercise takes care of the increase in energy expenditure which is - all convictions wrt to "calories don't count" and the "calories in vs. calories out"-hypothesis aside - still a fundamental prerequisite that the fatty acids do actually get burned and are not released into circulation to be restored or replaced a couple of hours later.

"Ok, I am just ordering some DHEA, how much should I take?"

Before you head over to the online vendor of your choice to make sure you get your share of DHEA before the FDA hears that it could hamper the sales of diabetes drugs and removes it from the OTC market, I would like to remind you that despite the fact that Sato et al. rightly claim that a "combination treatment [with DHEA and DHT] may be more beneficial than either therapy alone", a cursory glance on the data in figure 1 should suffice to tell you that those additional benefits as statistically significant as they may be are just that "additional" and that exercise alone yielded about equal results, is free of negative and full of beneficial side effects (update: as long as you don't overtrain; thanks Stapedius for this important note) and does not have the same host of studies refuting its efficacy as DHEA has (Clore. 1995).

It is nevertheless intriguing that a hormone the medical orthodoxy has, more or less all of a sudden, dropped like a hot potato and declared "questionable" and "ineffective" is now, roughly 15-20 years being rediscovered... and I am pretty sure that this was not the last DHEA study you will see and read about here at the SuppVersity ;-)

References:

1. Clore JN. Dehydroepiandrosterone and body fat. Obes Res. 1995 Nov;3 Suppl 4:613S-616S. Review.
2. Hou CW, Chou SW, Ho HY, Lee WC, Lin CH, Kuo CH. Interactive effect of exercise training and growth hormone administration on glucose tolerance and muscle GLUT4 protein expression in rats. J Biomed Sci. 2003 Nov-Dec;10(6 Pt 2):689-96.
3. Loviselli A, Pisanu P, Cossu E, Caradonna A, Massa GM, Cirillo R, Balestrieri A. [Low levels of dehydroepiandrosterone sulfate in adult males with insulin-dependent diabetes mellitus]. Minerva Endocrinol. 1994 Sep;19(3):113-9.
4. van der Merwe J, Brooks NE, Myburgh KH. Three weeks of creatine monohydrate  supplementation affects dihydrotestosterone to testosterone ratio in college-aged rugby players. Clin J Sport Med. 2009 Sep;19(5):399-404.
5. Mohan PF, Cleary MP. Effect of short-term DHEA administration on liver metabolism of lean and obese rats. Am J Physiol. 1988 Jul;255(1 Pt 1):E1-8.
6. Mohan PF, Ihnen JS, Levin BE, Cleary MP. Effects of dehydroepiandrosterone treatment in rats with diet-induced obesity. J Nutr. 1990 Sep;120(9):1103-14.
7. Sato K, Iemitsu M, Aizawa K, Ajisaka R. Testosterone and DHEA activate the glucose metabolism-related signaling pathway in skeletal muscle. Am J Physiol Endocrinol Metab. 2008 May;294(5):E961-8. Epub 2008 Mar 18.
8. Sato K, Iemitsu M, Aizawa K, Mesaki N, Ajisaka R, Fujita S. DHEA administration and exercise training improves insulin resistance in obese rats. Nutr Metab (Lond). 2013 May 30;9(1):47. [Epub ahead of print]

Exercise Research Quickie: HIIT vs. Steady State, More on the Hormonal Response. Light Training, High TUTs & Peak Contractions - Not Just for The Elderly. Train Your Left, Grow Your Right Leg - Contralateral Training Effects

The role of the innervations between our muscles as well as to our brain is often overlooked, when we are talking about size gains. The image shows stained nerve fascicles from the Song study, which brings this wiring back onto the radar.

I know that we have had the short news on Saturday only and that there are of course tons of short news on Facebook everyday, but the studies I am going to present you in this exercise research quickie were so in-between (meaning not really worth a full post, but still way too good to be wasted on facebook) that I decided to devote a post of its own to the research on the hormonal effects of interval vs. steady state training by Hackney et al. (Hackney. 2013b), the impressive and certainly not totally irrelevant effects of slow movement, low-intensity resistance training in the elderly Watanabe et al. describe in their latest paper and the surprising muscle building (Watanabe. 2013) and growth priming carry over effects Song et al. observed in response to unilateral electrical muscle stimulation (Song. 2013).

Although, the latter post is pretty theoretical I hope that all of you will find something that enlightens, amuses or entertains them in this "threesome" ;-)

More T, more DHT, more cortisol - that's the HIIT vs. LISS formula

(Hackney. 2013b) -- In fact the results of two subsequently published papers by Hackney et al. would suggest that it's about as easy. Work out hard and fast and see greater increases in testosterone levels, but also testosterone turnover (into DHT via 5-alpha reductase), but don't forget that aside from these (questionable) anabolic benefits, your thyroid hormone levels are going to take a dive (as reported previously), as well.

Figure 1: Comparison of the hormonal responses measured in the plyometrics (left) and the HIIT vs. LISS (right) study (based on Ozen. 2013 and Hackney. 2013)

The figure above is actually from a post where I discussed this before, so if you cannot remember all the details, briefly go back before you take a look at the summary of results of the more recent study by Hackney.

"Dihydrotestosterone (DHT) - Bigger, Stronger, Faster or just Balder, Fatter and Unhealthier?" That's the question I asked in one of the installments of the Intermittent thoughts on building muscle. A post I would highly suggest you read, by the way ;-)

In this 2nd paper that was published right before Christmas in the Journal of Endocrinological Investigations the researchers were able to show that repeated periods of 90-sec treadmill running at 100-110% maximal oxygen uptake (VO2max) and 90-sec active recovery at 40% VO2max for 42-47 min (which is obviously pretty long!) caused  just a significantly more pronounced increase not just in free testosterone, but also in its conversion to testosterone's big brother DHT (as indicated by statistically higher levels of the 5α-reductase marker 3-α Diol G at 12POST HIIT vs. LISS). This is interesting, as dihydrotestosterone (DHT) which is often falsely associated only with hair loss, prostate cancer and even obesity, does also play an important role in strength development (click here to learn more) and appears to do it's magic via the MAPK receptor. Now, MAPK in turn can activate PGC-alpha and that the latter is way more than just the endurance / mitochondria builder it was long thought to be is something you should still remember from the post on the"The IGF-1 Promoting, Myostatin Reducing, Muscle Building Effects of PGC-1 α-4" (read more).

Bottom line: It is becoming more and more clear that HIIT is in fact somewhat of a chimera that shares beneficial and detrimental effects of both classic cardio and classic strength training with mammoth sessions like the one performed in the studies at hand triggering similar hormonal cascades that will - despite probably causing beneficial adaptations - simply require longer rest times than a classic LISS regimen.

A  note of caution: Both these studies point to the highly questionable "value" of taking a bunch of people letting them do whatever type of training once, measure some stuff of which you do only have a very rough idea of what it's actually doing and then have a bunch of morons like myself try to come up with "practical implications"

So if you do HIIT, stick to the principles "short and hard" (I would never suggest doing the >40min interval sessions for anyone whose primary goal is to be healthy and look good naked, by the way; add a walk on the treadmill if you want to train longer like on a combined HIIT + LISS cardio only day. But most importantly don't forget to enjoy your well-deserved, highly productive off-time and remember that it's during those hours, when all the hard work is paying off... ah I almost forgot, this is a tried and proven way that happens to be confirmed by studies like Hackney's and not vice versa.

 Light training, high TUTs and peak contractions - not just for the elderly?!

You cannot only implement"light" training into your established routine (see last paragraph), but should also think of the often forgotten benefits of periodization, detraining & co (learn more), as well as times, when you may be injured or otherwise disabled and cannot lift heavy.

(Watanabe. 2013) -- It may sound like a study for the elderly, but just as the best-agers among the SuppVersity readers can learn something from studies done in the the younger fellows, the younger weightlifters may well get some intriguing insights from studies with older participants - studies like the one by Watanabe et al., for example.

When the researchers from the Department of Life Sciences at the University of Tokyo compared the hypertrophy and strength gains of two exercise regimen using a low resistance of 50% of the personal 1-RM max of their 59-76yr old subjects, the scientists found that slow movements with tonic force generation were superior to the regular 1s concentric vs. 1s eccentric reps I guess most of you will be employing in their training routines.

The subjects who had been randomized to the LST group and performed their reps with a 3s concentric, a 3s eccentric and phase and most importantly a peak contraction in-between did gain a similar amounts of strength as those subjects who performed the standard protocol for 10 weeks (the 12-week study had a 2-week familiarization phase), but contrary to they did also record statistically significant increases in muscle size.

Alternative exercises on which peak contractions work well, are the fly (preferably on a machine or using cables), the lat pulldown, cable crunches, all sorts of triceps extensions, the scott curl (where you would do them midrange), every form of calf raises. Always remember, though: A peak contraction is never done in the full stretch position, but always either midrange or as the name implies at the peak of the contraction, before the eccentric phase begins.

So what does that mean? Certainly not that all of you should stop lifting heavy weights, because 50% 1-RM was enough if not superior to the regular 70-90% that are recommended in most serious training regimen. Rather, these results should remind young and old trainees alike of keeping an eye on your form and making sure that you stimulate the muscle and don't just move whatever weight from place A to place B.

That said, try to incorporate peak contractions with every rep on the auxilliary movements of your next workout. Start your leg workout with regular squats, for example, 5x5 TUT 101 (meaning 1s eccentric, 0s rest at the bottom, 1s concentric), but instead of the 4x10 leg extensions you would usually do for your quads, you lower the weight somewhat and do them with a slower rep-speed (somewhere in between 1-3s) and a peak contraction (meaning you really squeeze the muscle in a position, where your knees are almost locked out). Done right, this is going to give the word DOMS (=deep onset muscle soreness) a whole new meaning + you will have to reduce your weights, anyways.

Train your left leg and your right one will grow as well

(Song. 2013) -- Do our bodies know something about aesthetics? Well, if that were the case, the legs of some of the gymbros who "don't train legs, because [they] play soccer" shouldn't look the way they do... but I am digressing here. According to the study by Yafeng Song et al. have just published in the open access journal Plos ONE, there appears to be a certain carry-over effect - at least if the growth stimulus is chronic and profound.

To achieve the latter, i.e. a chronic and profound training stimulus, the researchers from the Umea University in Sweden exposed the soleus and gatrocnemius muscles of rabbits to a 6-week electrical muscle stimulation + exercise protocol and measured muscle changes and inflammation on weeks 1, 3 and 6 of the study. Now, the clue of the study was that the unilateral "exercise" was actually mechanically and electrically enforced, so to say:

"The movements are produced by a pneumatic piston, in which the range of motion can be controlled. The range of movement was set to 9.5 cm, given a range of motion in the ankle of 55–65u of which 20–25u was dorsiflexion and 35–40u was plantarflexion. The right leg was attached to the piston and the pelvis/hip region was strapped down to restrict the motion in the left non-exercised leg. The left leg was unattached. During the plantar flexion of the right leg, an active contraction was induced by electrical muscle stimulation via surface electrodes placed 2 cm apart over the right triceps surae muscle. The stimulation was synchronized with the plantar flexion movement of the piston by a microswitch, which trigged the stimulator unit".

I will spare you the further details... just think of a modern rabbit torture machine that was designed to "work the rabbits right extremities out". As you would expect from any good torture machine this device brought about a significant amount of tissue damage and a corresponding increase in the number of necrotic fibers.

Figure 2: Variability in fiber size, fibers with internal nuclei, inflammation in soleus (left) and gastrocnemius muscle (right) in response to the exercise + electrostimulation program. Mind the similar responses in the exercised (E) and the non-exercised (NE) limb (Song. 2013)

Now what's surprising though is the fact that despite the local damage, the inflammation had a systemic component, which happened to be more pronounced in the untrained soleus vs. gastrocnemius muscle (slow vs. fast twitch, by the way).

Against that background it is still only a little less surprising that the variability in fiber size, the number of fibers with internal nuclei (=sign of restructuring process, cf. "The Skeletal Muscle Hypertrophy 101") and even the fiber splitting were virtually identical. After all, this would mean that systemic parameters do matter. But haven't we just discarded this notion yet another time in the first of the items in today's exercise research quickie? Yes we have, but in that case we were talking about the usual subjects, the "anabolic" and "catabolic" hormones, Song et al. on the other hand speculate that

"[t]he collateral muscle changes and inflammation after unilateral EMS/E observed in this study may be caused by [a] neuronal mechanism. Since there is some evidence for a commissural system in the spinal cord that mediates transmedian signaling with a fairly precise bilateral representation, nerve signals from the trained side may pass over to the contralateral muscles through commisural inter-neurons. If this is the case, unilateral injury caused by EMS/E may cause a cross-transfer up-regulation of neuropeptides that can be involved in the inflammatory response in the contralateral muscles." (Song. 2013)

The researchers indicate that their current, as well as previous results from their laboratory would support this hypothesis and that any systemic or circulatory effects must actually be excluded, because these would not have occurred only focally, but generally within all muscles. They also point towards previous studies in which the signalling between contralateral and ipsilateral limb was blocked and the observed cotralateral responses were abolished.

So what's the point? I will openly admit that the practical relevance of these results (esp. for you as a hopefully healthy trainee) is as of now still very questionable, but the fact alone that it brings the nervous system back on the "scientific" radar was certainly worth including it in this "threesome" - don't you think so? No, well... maybe you like the scientists own rational who argue that the findings are (a) important in the context of a wide range of musculoskeletal and neuromuscular disorders and (b) relevant for each and every unilateral exercise experiment, where the contraleteral limb is used as a control - and you know there are plenty of them!

References:

• Hackney AC, Kallman A, Hosick KP, Rubin DA, Battaglini CL. Thyroid hormonal responses to intensive interval versus steady-state endurance exercise sessions. Hormones (Athens). 2013a Jan-Mar;11(1):54-60.
• Hackney AC, Hosick KP, Myer A, Rubin DA, Battaglini CL. Testosterone responses to intensive interval versus steady-state endurance exercise. J Endocrinol Invest. 2013b Dec;35(11):947-50.
• Ozen, SV. Reproductive hormones and cortisol responses to plyometric training in males. Biol Sport.2013; 29 (3).
• Song Y, Forsgren S, Yu J, Lorentzon R, Stål PS. Effects on contralateral muscles after unilateral electrical muscle stimulation and exercise. PLoS One. 2013;7(12):e52230.
• Watanabe Y, Tanimoto M, Ohgane A, Sanada K, Miyachi M, Ishii N. Increased muscle size and strength from slow-movement, low-intensity resistance exercise and tonic force generation. J Aging Phys Act. 2013 Jan;21(1):71-84.