Eight HIIT Sessions on the Rowing Ergometer Cut Body Fat, Increase Adiponectin, VO2Max & Performance in National Level Rowers - Workmatched Classic "Cardio" Does Nothing

If you have hitherto ignored my previous advice (e.g. "Choosing Your Workout Style") to give the rowing machines a try, maybe the study at hand will rise your interest. Give it a try. It's an awesome whole body workout and highly effective, even if you just do 20min of steady state after lifting weights.

Yesterday you've learned that even the most idio... ah, I mean unconventional - not to say "experimental" in the literal sense - one-legged leg training routine is more likely to get you those six-pack abs, of which everyone appears to believe that it was a natural sign of outstanding health and a thing everybody must have (just like the new iPhone, you know ;-), than a bazillion of sit-ups. Today, you will see that a somewhat less "experimental" training regimen will not have you reach your goal faster and more efficiently, it will also have the welcome "side effect" of making you healthier and improving your conditioning. And you know what's the best about all that? It does not only work for sedentary baby-boomer, but also for highly trained athletes. 5 male and 2 female19(± 1.2)-year-old junior state and national level rowers from the Tasmanian Rowing Team (height: 1.77 ± 0.10 m, body mass: 74.0 ± 10.7 kg, body fat: 17.1%, VO2max 62.1 ± 7.0 mL·kg/min), to be precise (Shing. 2013).

Healthier, leaner, fitter - that's a HITTer ;-)

To evaluate the influence of two different training regimen, namely the traditional steady training (SST/LISS) on a rowing ergometer (a piece of equipment of which the regulars among you already know that I highly suggest you incorporate it into whatever cardio routine you may be doing), or a high intensity interval training (HIIT) variety of the latter the researchers from the School of Human Life Sciences at the University of Tasmania in Launceston, Australia put their participants, the aforementioned young national rowers, on two different workout protocols with matched cumulative energy expenditures (my emphases in Shing. 2013):

• SST: "The traditional training program involved rowers completing two ergometer sessions per week; one with a duration of 35 minutes and the other 40 minutes. [...] The intensity of each session
  was relatively low and more aerobic in nature when compared to the interval training protocol. The intensity of the traditional ergometer sessions was set to power outputs that corresponded to blood lactate concentrations of 2 and 3 mmol/l determined from the incremental exercise test."
• HIIT: "The interval training sessions consisted of eight 2.5 minute intervals at 90% of mean four-minute maximal power achieved during the incremental exercise test. Recovery between each interval was at an intensity of 40% of mean four-minute maximal power and the recovery duration was until heart rate returned to 70% of maximum heart rate, up to a maximum of five minutes."

The 2x four week experimental period (remember: we are dealing with a cross-over design, where all subjects participate in both protocols in random order) involved the incorporation of two ergometer sessions per week. Since all participants were part of the same squad the rest of their training regimen was identical, so that confounding factors - at least as far as the training is concerned - can be ruled out.

Body composition and adiponectin took a HIIT - a highly beneficial one that is ;-)

Performance tests were done and body fat mass (DXA), as well as a general blood profile and adiponectin values were taken at baseline and the end of both 4-week periods. Moreover, all participants had to keep a detailed training and diet log, so that the scientists could make absolutely sure that non of the effects they observed were due to unexpected changes in either activity levels or dietary habits.

Any potential influence of the randomized order, i.e. whether the rowers performed the classic training first and the HIIT sessions 2nd or vice versa was ruled out by statistical means before the scientists eventually analyzed their data sets and got the following results:

Figure 1: adiponectin levels before (pre) and after the respective workout at the beginning and end of the respective 4-week training period and body fat levels before and after 4 weeks of steady state (SST) or high intensity interval training (HIIT) in national level rowers (Shing. 2013)

I must admit, the changes are not earth-shattering, but there are changes - beneficial ones that is  - and they are statistically significant despite the small number of participants, and the fact that the subjects were already highly trained individuals and - I figure this may be the most convincing argument not to discard this effects - participated in no more than a total of only 8 HIIT sessions.

Bottom line: I guess, you could certainly argue that the novelty of the training stimulus was part of the reason, the HIIT regimen had so beneficial effects on the fitness, body composition and even the adiponectin levels of these already highly trained rowers (Adiponectin? That's the "new leptin", which promotes insulin sensitivity and exerts profound anti-inflammatory effects); but does this take away from the efficacy of this 4x2.5 min @90% max. + 5min active rest high intensity interval training regimen? I don't think so.

Click here to learn more about the "Iranian HIIT Solution" a minimalist program with maximal results

There is nonetheless one thing I want to add before I close the SuppVersity doors for today. The 4x2.5 minute protocol is certainly appropriate for trained athletes; in fact, previous studies even suggest that it requires those long(er) intervals in order to elicit gains in VO2max in highly trained (endurance) athletes (e.g. Franch. 1998; Laursen. 2002). The initially mentioned sedentary baby-boomer - obese or not - may however be better off, if they follows a different regimen, such as the one I outlined in the "Iranian HIIT Solution" (see image on the right) and incorporate that in a three-day split (e.g. A, B, hypertrophy, C strength) or a two-day full body circuit training.

The main message here is that starting out "low" (in terms of both volume and intensity) is not just possible, it's even advisable, so that there is still enough room to do more, and/or preferably up the intensity. I know I have been telling you that before, but I feel it's worth stating again: Real cardio training, i.e. the type of training that strengthens the cardiovascular system is progressive. If you do the same thing day in and day out the best you can hope for is to keep the status quo. Remember that before you start out way too high (esp. on the volume side of things) and either bunk directly, or end up without any room to make progress.

References:

• Franch J, Madsen K, Djurhuus MS, et al. Improved running economy following intensified training correlates with re-duced ventilatory demands. Med Sci Sports Exerc 1998; 30: 1250-6.
• Laursen PB, Jenkins DG. The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes. Sports Med. 2002;32(1):53-73.
• Shing CM, Webb JJ, Driller MW, Williams AD, Fell JW. Circulating Adiponectin Concentration AND BODY composition ARE Altered in Response to High-Intensity Interval Training. J Strength Cond Res. 2013 Dec 4.

Bigger, Stronger, Faster: CoQ10 for Brain & Muscle in Young & Old. The Optimal HIIT Regimen for Fun & Fat Loss - 8s at 100% 60s Idling! Protein Power From Oats? Plus: Rest Times, Clusters, Form & Hypertrophy Training

I decided against calling this the "Get Big, Green and Look Like the Hulk Quickie" (img. Paramount Pictures)

In view of the fact that most of you apparently enjoyed the "Get Lean and Stay Lean Quickies" I posted in the last weeks, I thought you may also be inclined to read a "Get Big, Green and Look Like the Hulk Quickie", but then decided that the name was too long for the headline and "big, green" and maybe even "hulk" in conjunction with "quickie" may have had the SuppVersity turn up on google and other search engines in too close vicinity to websites I do not exactly want this blog to be associated with (just kiddin' ;-)

Be that as it may, enjoy the ride and let me know whether you do prefer this thematically structured approach over the classic news-potpouris ala On Short Notice.

I mean you can obviously argue in favor of both and since this is a place I want you to look forward to visit everyday, I would be inclined to hear whether "innovations" like this make it better or worse.

• CoQ10 supplementations could offer beneficial effects on brain and muscle in elderly individuals and could - at higher doses - work for youngsters, as well (Shetty. 2013) -- In a rodent trial the provision of a relatively high dose of CoQ10 as part of the diet effectively blunted age-induced 'cognitive decline' (whatever that may be in a mouse ;-) and protein breakdown in heart, liver and muscle tissue of the 17.5 months-old mice.
  
  

  

  Figure 1: Carbonyl levels in liver and muscle of young and old mice.

  This result is also interesting, because the mitochondrial protein breakdown in the brain was the one which was least beneficially affected. What's of greater importance, for this news quickie at least, is that the 2.81mg CoQ10 per gram of chow the high dose group received (the human equivalent would be roughly 33mg/kg or 2-3g per day!) elicited beneficial effects on the skeletal muscle carbonyl content, a marker of protein oxidation, in the young animals, as well (see figure 1).
  
  The notion that coQ10 in appropriate doses could be beneficial not just for statin users, but also for perfectly healthy people, even athletes, is also supported by the beneficial effects the administration of coQ10 had in a recent trial where it blunted the oxidative damage due to a high frequency endurance training program in rodents (Okudan. 2013). It does however stand in contrasts with a recent study by Bloomer et al., n which the supplementation of only 300mg (ca. 15% of the HED used in the study at hand) did not yield the desired effects on the exercise performance of 15 perviously individuals (10 men and 5 women; 30-65 years; Bloomer. 2013). Whether this really is just a matter of the correct dosing, or maybe a fundamental difference between mice and men will still have to be elucidated and I would not spent the bucks for anything that's only "maybe" going to work.
• Rats don't do well with hypertrophy training (Scheffer. 2013) -- According to a recently published paper by Scheffer et al., rodents who are afraid of increases in markers of oxidation should refrain from hypertrophy oriented muscle training and stick to lower volume resistance training.
  
  For their study, the Brazilian researchers had analyzed the effects of three different resistance training protocols, namely  muscular resistance training (RT), hypertrophy training (HT), and strength training (ST), which had to be performed twice a week for 12 weeks on muscle lactate and glycogen content, superoxide production, antioxidant enzyme content, and activities, as well as markers of lipid and protein oxidation.
  

  

  While you certainly don't want a fire inferno, doing too little is not going to yield the results you are looking for either (suggested read "The emerging role of an auto-/endocrine-immune axes")

  "Results showed increased superoxide production (UT = 5.348; RT = 5.117; HT = 8.412 ; ST = 6.354), SOD (UT = 0.078 ; RT = 0.101 ± 0.013; HT = 0.533 ± 0.109; ST = 0.388), GPx (UT = 0.290; RT = 0.348; HT = 0.529; ST = 0.384) activities, and content of GPx (HT = 3.8 times; ST = 3.0 times) compared with the UT group. CAT activity was lower (UT = 3.966; RT = 3.47; HT = 2.276 ; ST = 2.028) in HT and ST groups. Oxidative damage was observed in the HT group (TBARS = 0.082; carbonyl = 0.73; thiol = 12.78) compared with the UT group.

  The way in which the authors' conclusion that these "findings indicate that HT causes an imbalance in oxidative parameters in favor of pro-oxidants, causing oxidative stress in skeletal muscle" does implicitly suggest that this is a bad thing that has to be avoided at all cost, which is obviously totally beside the point - if you don't challenge your body he has nothing to adapt to and neither your conditioning, nor your strength or muscle mass are going to improve. The absence of statistically significant increases in oxidative damage in the low volume strength training routines, on the other hand supports the notion that you can use phases of very low volume training with heavy weights in between intense phases of overreaching to monetize on the muscular gains (which will probably keep coming in these 2-4 weeks) by taking all your lifts to another level and thus lying the foundation for future growth.
• Optimized HIIT regimen for overweight kids: 4s max sprinting + 60s active recovery do the trick - could work four you, as well! (Crisp. 2013) -- Either from the SuppVersity news or from listening to Super Human Radio you may remember that a recent study by Deighton et al. has found that sprinting will increase your appetite more and burn less calories than workload matched steady state cardio training. A novel study from Australia does now suggest that this may well be the case, but probably only as a result of doing it wrong - the sprinting, I mean.
  
  
  In their study Nicole A. Crisp and her colleagues from the School of Sport Science at the The University of Western Australia, describe how the combination of 8s all-out sprints on a cycle-ergometer with 60s of active rest easily outperforms its 30min steady state counterpart (30min moderate pace) and its "little brother" and "big" bother the 8s sprint, 120s active rest and the 8s sprint, 30s active rest protocol, respectively.
  
  

  

  This is not the first study to show the superiority of HIIT training in obese boys. In February 2013, I have already covered a very similar study where a brief HIIT session that burns "only" 360kcal was a major motor to teenage weight loos.

  In that, it's important to note that despite a linear increase in energy expenditure from the 60s to the 30s rest group, the latter failed to reach statistical significance (p = 0.076), ...
  

  "[...] likely as a result of decreased sprint quality as indicated by a significant decline in peak power output from SI₆₀ to SI₃₀ (p = 0.034)" (Crisp. 2013)

  In conjunction with the absence of the overcompensation effect at the following breakfast buffet (which was present in the 8/30s and to a lesser degree even the 30min steady state trial), this makes the 8/60s protocol the superior choice for everyone doing HIIT mainly to get or stay lean.
  
  And aside from its practical value, the 8/60s regimen was also the one the boys enjoyed the most.
  
  "And what about me?" I don't see why doing this very short sprints with large bouts of active recovery in between would not be right for you, as well. At least if the activation of your metabolism and / or fat loss during a diet is your primary goal and not an improvement in VO2 max., you would thus probably get many of the benefits at a smaller risk of overtraining. Just make sure you are actually sprinting all-out for the whole 8s and don't stop, when you are just about to get up to speed ;-)
• Long rest times necessary for high jumpers - with 8-12 min pause your performance on the next jump will increase not decrease (Gouvêa . 2013) -- In a recent meta-analysis that's soon going to be published in the Journal of Sports Sciences André Luiz Gouvêa and his co-workers report that the manipulation of rest intervals seems to affect post-activation potentiation magnitude and jump height.
  
  After analyzing fourteen studies, which met the criteria of having a crossover design, being randomised, or non-randomised and counterbalanced and observed the voluntary muscle action-induced post-activation potentiation on jumping performance, the scientists state that the...
  

  "[...]results demonstrated medium effect sizes for rest intervals 0–3 and 8–12 min (-0.25 for 0–3 min; 0.24 for 8–12 min) and a small effect for other ranges (0.15, CI: -0.08 to 0.38 for 4–7 min; for ≥16 min)." (Gouvêa . 2013)

  Since there was little to no evidence for heterogeneity among the sub-groups and no indication of publication bias, these results clearly suggest that rest intervals of 0–3 min have detrimental, rest intervals between 4-8 min neutral and rest intervals of 8-12 min beneficial impact on jump height. In that, the improvements are likely to be mediated by post-activation potentiation.
• The science of cluster training - Conventional wisdom prevails, 10 deep breaths would yield optimal rest time between reps (Hardee. 2013) -- At lest with respect to proper form, which may also have consequences for optimal muscle recruitment and hypertrophy, the optimal rest time between two reps in a cluster appears to be 20s, which is actually what the good old "10 deep breaths rule" would state, as well.
  
  
  What is a cluster? When you are "clustering" your sets you are doing one (sometimes also 2-3) rep(s), rack the weight, rest, do another rep etc. This is a very good technique to increase your strength and break through plateaus that's useful for powerlifters and bodybuilders alike.
  In order to examine the effects of three different cluster set configurations on power clean technique, the scientists recruited 10 male, recreational weightlifters who had to perform clustered or non-clustered power-cleasn: 3 sets of 6 repetitions at 80% of their individual repetition max with 0 (P0), 20 (P20) or 40 seconds (P40) inter-repetition rest.
  
  In the P0 (no cluster) condition, the scientists observed how the form suffered and got worse and worse from the first to the last rep (the catch and first pull were in a more forward position during repetition 6 as compared to repetition 1). With the long rest times in the P40 condition, on the other hand,  "differences in horizontal displacement were found between repetitions 1 and 6 for the second pull and the loop" (Hardee. 2013).
  
  In the P20 condition the researchers did not observe any differences in horizontal displacement between repetitions 1 and 6 during P20. Reason enough for the scientists to conclude that their results would demonstrate that cluster sets with greater tha 20s of inter-repetition rest would be useful to maintain appropriate form without significantly dropping the density of your workout - whether this did actually facilitate strength or size gains was yet not evaluated in the study.
  
  The evidence for the efficacy of this training regimen (aside from simply providing a novel stimulus, which is obviously always a good thing) does come from a 2011 study by  Hansen et al who compared the response of highly trained rugby players to on traditional vs. clustered leg training program and found the latter to be slightly superior with respect to the increase in peak velocity and strength , while the classic continouus set training had an edge as far as total power increases in the lower limbs were concerned (Hansen. 2011).
• Oats healthy car source with performance protein? (Xu. 2013) Who would have thought that, oats are not just an excellent source of slow digesting carbs and potentially fat-burning beta glucan (listen to the SuppVersity Science Round-Up from two weeks ago), they also contain a non-negligible amount of protein of which researchers from the College of Food Science and Engineering at the Northwest A&F University in Yangling, China, have now shown that it ameliorates the increase in lipid oxidation (MDA) and decrease in antioxidant activity (SOD) during an exaustive bout of swimming in 30 male mice.
  
  After the oat protein had been purified from oat meal thirty male Kun-ming mice were divided kept on either a normal control diet, a diet that was enriched with oatmeal and a diet that contained only the protein fraction of the oats. After 20 days, the rodents were subjected to swim to exhaustion. Their swimming endurance and the major metabolic substrates were measured from serum, liver and muscle.
  

  

  Figure 2: Antioxidant enzymes up, lipid oxidation down. That's the result of a comparison of the detrimental effects of an exhaustive swimming test in mice fed regular, oat enriched or oat protein pimped diets for 30 days (Xu. 2013). What the study cannot answer is however whether identical effects would have been seen w/ any other high quality protein as.

  "The results showed that no significant differences were observed in swimming endurance test between the normal control group and the oat protein group (P > 0.05). Mice in the oat meal group had significantly longer swimming endurance compared to the normal control group (P < 0.05). Furthermore, dietary oat protein increased the levels of liver glycogen, enhanced the activities of lactic dehydrogenase and superoxide dismutase, and decreased the levels of blood urea nitrogen and malondialdehyde in serum." (Xu. 2013)

  Now the good news certainly is that id did work. The "bad" or at least not so good news, on the other hand is that there is no adequate control group, since the addition of both the oats and the oat protein will have increased the amount of essential amino acids in the rodent chow significantly.

That's it! At least as far as news on getting bigger, stronger and faster is concerned. In case yo are also interested in something else, for example...

• how scientists have successfully transformed former breast cancer cells back to benign mammary epithelial cells by placing them in a non-carcinogenic environment like a healthy non-inflamed mouse
• that continously taking 25,000IU of supplemental vitamin A is at least not particularly healthy for young lean and obese women
• why Munuka honey, when Greek or Cypriot Honeys are the more potent antimicrobials?

and whatever else I will still be posting before tomorrow's SuppVersity news, you are alway welcome to visit the SuppVersity Facebook Wall.

References:

• Bloomer RJ, Canale RE, McCarthy CG, Farney TM. Impact of oral ubiquinol on blood oxidative stress and exercise performance. Oxid Med Cell Longev. 2013;2013:465020. doi: 10.1155/2013/465020. Epub 2013 Aug 23. 
• Crisp NA, Fournier PA, Licari MK, Braham R, Guelfi KJ. Optimising sprint interval exercise to maximise energy expenditure and enjoyment in overweight boys. Applied Physiology, Nutrition, and Metabolism, 10.1139/h2013-111. 
• Gouvêa AL, Fernandes IA, César EP, Silva WA, Gomes PS. The effects of rest intervals on jumping performance: A meta-analysis on post-activation potentiation studies. J Sports Sci. 2013 Nov 9.
• Hansen KT, Cronin JB, Pickering SL, Newton MJ. Does cluster loading enhance lower body power development in preseason preparation of elite rugby union players? J Strength Cond Res. 2011 Aug;25(8):2118-26.
• Hardee JP, Lawrence MM, Zwetsloot KA, Triplett NT, Utter AC, McBride JM. Effect of cluster set configurations on power clean technique. J Sports Sci. 2013 Nov 5.
• Okudan N, Revan S, Balci SS, Belviranli M, Pepe H, Gökbel H. Effects of CoQ10 supplementation and swimming training on exhaustive exercise-induced oxidative stress in rat heart. Bratisl Lek Listy. 2013;113(7):393-9. 
• Scheffer DL, Silva LA, Tromm CB, da Rosa GL, Silveira PCL, de Souza CT, Latini A, Pinho RA. Impact of different resistance training protocols on muscular oxidative stress parameters. Applied Physiology, Nutrition, and Metabolism, 10.1139/h2013-115
• Shetty RA, Forster MJ, Sumien N. Coenzyme Q(10) supplementation reverses age-related impairments in spatial learning and lowers protein oxidation. Age (Dordr). 2013 Nov 10. 
• Xu C, Lv J, You S, Zhao Q, Chen X, Hu X. Supplementation with oat protein ameliorates exercise-induced fatigue in mice. Food Funct. 2013 Nov 12.

Science Round-Up Seconds: Vitamin E Succinate, How It's Extracted from Barley Leaves, Kills Cancer, Ramps up Growth Hormone & Spikes Prolactin. Plus: Testostosterone & Thyroid Hormone Decline Due To Plyometrics & HIIT

Regardless of all the hypocritical hoopla around his persona, Lance Armstrong has always been able to push himself like no one else. No wonder that intense plyometrics were part of his regimen.

If the SuppVersity Science Round Up was a meal, I guess you could say that Carl Lanore and I were sort of gluttonous, yesterday (click here to download the podcast, if you have not already done so). We almost raced from one topic to another and therefore all the good stuff from the list is gone already and I am a bit pressed on time to get some "private life" in, so that I am not psyched about the idea of writing about auxiliary stuff.

Against that background and in view of the fact that I felt that the pace of yesterday's show did not really leave enough room for some important details, I will stick to rehashing and expanding on the stories about Vitamin E succcinate and the detrimental effects of beating the crap out of yourself doing plyometrics or crazy HIIT workouts (too regularly), in today's installment of the SuppVersity Science Round-Up Seconds.

Let's see. Why don't we start at the end of yesterday's show?

• Vitamin E succinate the most potent anti-cancer tocopherol known to man. As you have heard on the show, vitamin E succinate attaches directly to a protein that's preferentially expressed in carcinogenic or pre-carcinogenic cells. It goes by the name α-Tocopherol-associated protein (TAP) and was found to be one of the major α-tocopherol binding proteins in serum, liver, brain and prostate. What has as of yet not been so clear, though, is that the expression of this protein increases with the malignancy of (breast) cancer (Tam. 2013). 
  
  

  

  Figure 1: Effects of alpha tocoperyl succinate alone (TOS), doxorubicin alone (DOX) or both (DOX + TOS) on cell viability in human MB231 breast cancer cells (my edits, original from Tam. 2013) - note: The effect was less pronounced in other cancer cells, so that it is reasonable to assume that the efficacy of the therapy will depend on the exact genotype of the cancer (for those tested in the study it was MB231 > SKBR3 > MCF 10A)

  When alpha tocopherol succinate binds to the protein on the cancer cells, this will either alone, or in combination with chemotherapy trigger apoptosis and cell death. It is as of yet not fully elucidated why vitamin E succinate is highly cancer-specific and leaves the healthy cells intact, but this could be related to the high metabolic rate and exuberant ROS production of cancer cells. There is however some research that would suggest that the cancer cells literally suffocate in their own radical oxygen specimen (ROS), which can no longer be cleared from the cell, due to the alpha-tocopheryl succinate induced displacement of ubiquinone from CII and the subsequent blockade of succinate dehydrogenase (SDH) activity (Dong. 2013).  If this hypothesis holds true it would therefore appear that long-term chronic supplementation with vitamin E succinate cannot be recommended until future studies on its general safety have been undertaken. As an adjuvant to chemotherapy, on the other hand, it could drastically reduce the dosage requirements during chemotherapy in specific types of cancer (see figure 1) and thus minimize side effects.
  
  You see, there is more to it than you can say in two minutes on the radio and this is why I will make sure we don't rush through the items that fast, in the next show. Ah,... of course the dietary source. I had almost forgotten about that one. As mentioned on the show, alpha tocopheryl succinate was originally extracted from Barley leaves. An while this may not be the first paper dealing with this "natural vitamin E analog", the one by Badamchian et al. is probably the one you will be most interested in.
  
  Published in the Journal of Nutritional Biochemistry the paper does not only describe the isolation of vitamin E succinate from green barley leaf extract (BLE)...
  

  "BLE [barley leaf extract] powder (50 mg/mL) was suspended in water and stirred for 1 hr at room temperature. The mixture was then centrifuged at 3000g for 30 minutes using a bench-top centrifuge. The pellet was discarded and the supernatant was pre-filtered through a Millipore DEPTH filter. The filtrate was then filtered through 0.45 I.tM mem- brane and stored at -20 ° C for HPLC or biological assays." (Badamchian. 1999)

  ... it does also shine another spotlight on its potential biological effects, as far as it's ability to increase growth hormone, but (unfortunately?) also prolactin in isolated anterior pituitary cells from female rodents:
  

  

  Figure 2: Prolactin and growth hormone release in anterior pituitary cells of female rodents after incubation with different amounts of green barley extract in which vitamin E succinate had been deterimed as the main ingredient before (based on Badamchian. 1999)

  It's really hard to estimate whether or not one of these effects would translate from a rodent cell in the petri dish to you or me popping a cap with vitamin E succinate everyday. That's particularly true in view of the fact that the underlying mechanism of the increase in GH and the imho more concerning increase in prolactin is neither mediated by increases in intracellular C-AMP, as it would be the case for GRF (old acronym for growth hormone releasing hormone), nor is it induced by the hydrolysis of polyhoshpoinositide, which is the underlying mechanism of the stimulative effect of TRH (thyrotropin releasing hormone). So basically we neither know how it works, nor do we know, whether the oral ingestion of vitamin E-succinate would be sufficient to produce serum concentrations in the pituitary that would be high enough concentrations to make any difference at all (note: the scientists excluded the influence of other components of the extract by testing alpha tocopherol succinate on its own in a separate trial)
  
  Bottom line: Based on roughly one dozen of in-vitro studies there is simply still to little evidence to decide who, outside of people with a history of cancer or someone who is just undergoing chemotherapy would benefit. Therefore, I suggest you wait before you add vitamin E succinate to your list of 'must have' supplements. Is it promising? Sure! Is it exciting, yeah! Is it save for a healthy being to be taken chronically??? I can't tell.
• The detrimental hormonal effects of pushing yourself beyond the tolerable threshold - Hardcore plyometrics and heavy HIIT and their impact on testosterone, cortisol, thyroid hormone and co: I guess you did already get the main message when you listened to the show, but just to give you an idea about the actual quantities, I thought it would be nice to provide you with two graphs as a reference.
  

  

  Figure 3: Comparison of the hormonal responses measured in the plyometrics (left) and the HIIT vs. LISS (right) study (based on Ozen. 2013 and Hackney. 2013)

  If you focus mainly on the differential cortisol responses in the two studies, it would appear likely that we are dealing with two very different forms of 'overtraining' here. While the HIIT protocol (90s at 100-110%, 90s active recovery at 40% matched for workload with steady state jogging at 60-65% of the VO2 max) probably wouldn't be a problem, if the athletes would get adequate rest and nutrition in the days after the session, the 6-weeks of plyometrics (15 session, increasing density, 90-195 reps per session) were enough to send the participants right into the vicious circle of the Athlete's Triad (if you have not done so already, I suggest you read up on that in the eponymous SuppVersity series).
  
  And you know what? Despite, or I should probably rather say due to their compromised hormone levels the guys in the plyometrics study did not lose a single gram of body weight. Good for their muscle, bad for the fat which was likewise preserved by the hormonal shut down, which affected both cortisol and testosterone in a similar way. So is that good or bad news? Well, let me say it this way:. Usually I see people training for a purpose and while the outcome often is stagnation and chronic fatigue, I would suspect that only few of you will have that on their mind, when they are hitting the gym, right?

Apropos viscous circle, and overtraining in order to avoid "overblogging" I will call it a day for today. Come back tomorrow for a couple of wholly new studies from the realms of exercise and nutrition sciences and in case you are planning to drink this evening, I highly suggest you check out the SuppVersity Facebook newspost on the effects of green tea extract on the uptake of alcohol. It may well be that those old fatburner caps of yours can be put to a way better use ;-)

References:

• Badamchian M, Spangelo BL, Bao Y et al. Isolation of a vitamin E analog from green barley leaf extract that stimulates the release of prolactin and growth hormone from rat anterior pituitary cells in vitro. Journal of Nutritional Biochemestry. 1994; 5: 145-150.
• Dong LF, Low P, Dyason JC, Wang XF, Prochazka L, Witting PK, Freeman R, Swettenham E, Valis K, Liu J, Zobalova R, Turanek J, Spitz DR, Domann FE, Scheffler IE, Ralph SJ, Neuzil J. Alpha-tocopheryl succinate induces apoptosis by targeting ubiquinone-binding sites in mitochondrial respiratory complex II. Oncogene. 2008 Jul 17;27(31):4324-35. Epub 2008 Mar 31.
• Hackney AC, Kallman A, Hosick KP, Rubin DA, Battaglini CL. Thyroid hormonal responses to intensive interval versus steady-state endurance exercise sessions. Hormones (Athens). 2013 Jan-Mar;11(1):54-60.
• Ozen, SV. Reproductive hormones and cortisol responses to plyometric training in males. Biol Sport.2013; 29 (3).
• Tam KW, Ho CT, Lee WJ, Tu SH, Huang CS, Chen CS, Lee CH, Wu CH, Ho YS. Alteration of α-tocopherol-associated protein (TAP) expression in human breast epithelial cells during breast cancer development. Food Chemistry. 2013 [ahead of print]

Health & Exercise Quickie: Vitamin D Deficiency, Taurine & Glycine. Multiple Sclerosis & Epstein-Barr. Paracetamol & Muscle Gains. Gender & Fatigue from Workouts. HIIT, LISS & Appetite. Plus: Scientists Debate: Light vs. Heavy Weights

While there is a positive trend in the percentage of US adults who meet the 2008 federal physical activity guidelines according to which they have to "devote at least 150 minutes/week to moderate, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination", the number of people who have gotten the message that a combination of both strength and aerobic training (red line) is much more efficient than doing just aerobics (blue line) remains the same (CDC. 2013)

48%! That's the SuppVersity figure of the week and the percentage of US adults aged 18 and over who met the 2008 federal physical activity guidelines for aerobic activity in 2013 - that's 5% more than in 1997. It would be better to see it up in the 75%+ region, but it's nice to see that more and more people are devoting at least 150min/week to moderate intensity exercise, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination.

What's not so nice is that people are still way too focused on aerobics and the number of US citizens that's combining resistance and aerobic training to reach their exercise goals is stagnating below 20%. Moreover, best-agers and baby boomers, who would probably benefit even more from some weight lifting than the 36% of the young men (age 18-24) who make up the lion's share of the 'real' physical culturists who know about the importance of both, 'weights' and 'cardio', are - if they work out at all - still sticking to the tried and disproven LISS only regimen.

On Short Notice, today: A Health & Exercise Quickie

Apropos "LISS" as the headline of today's On Short Notice news quickie already gave away, light intensity steady state aerobic training aka LISS is one of the exercise related topics today. We will however start out with the health related news... and don't wonder that the first post is about polar bear health. I promise you will be intrigued, when you've read it ;-)

• 'Westernized' polar bears' bones look as if they would need vitamin D supplements, in reality all they are probably missing is sufficient taurine in their diet. I don't know but maybe you've asked yourself before: "How on earth can a white bear survive in the Arctic, when his nose is the only part of his skin that's exposed to the sun and would thus be able to produce vitamin?" (Please mind that this is not a serious question ;-) He eats his vitamin D!
  
  

  

  Scientists speculate: Their cousins in captivity suffer from rickets and fractures due to secondary vitamin D deficiency in consequence of insufficient taurine intake.

  Ok, first question first answer, but what about question #2: "How come that the clubs of his brethren and cousins in captivity get rickets and fractures as if they were vitamin D deficient, although they get the exact same amount of vitamin D from mother's milk and their later diet (sometimes the latter is even supplemented) as their wild counterparts?" Answer? No idea? Well, if you ask the researchers from the The University of Tennessee Health Science Center the answer is (Cheesney. 2009): A lack of taurine in the diet.
  
  Taurine plays a fundamentally important role in the conjugation of ursodeoxycholic acid to TUDCA and facilitates the uptake of fatty acids and fat soluble vitamins. With insufficient taurine in the diet polar beers (and human beings) can probably drink as much vitamin D in olive oil or whatever other fat base they deem more appropriate then dry tabs without any effects on their 25-OHD => calcitonin levels and consequently bone health (suggested read "Fat D-Ficiency! Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat").
  
  Moreover, a recent guinea pig study from Department of Internal Medicine at the Medical College of the National Cheng Kung University suggests that glycine could be another 'pro vitamin D amino acid' due to its beneficial effect on the liver and subsequent protection of disturbances in vitamin D metabolism and low 25-OHD levels (Chen. 2008) - now, what if any of these, i.e. taurine or glycine, or simply insufficient bile acid, which incidentally depends on the consumption of the "bad, bad" cholesterol (cf. Kern. 1994), is the actual reason of the rampant vitamin D deficiency in our meat-, fat- and cholesterol-o-phobic societies?
• "Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years." (Décard. 2013) Usually I don't simply copy the study titles, but this one says it all. Even before the first symptoms of multiple sclerosis occur, i.e. in the so-called pre-CIS (=clinically isolated syndrome) interval, patients with quiescent multiple sclerosis have 50% lower 25OHD levels than their healthy peers and - what could actually be the causal factor, here - three times higher Epstein-Barr specific IgG levels (EBNA1). Can these observations a group of scientists from the Department of Neurology at the St. Josef-Hospital of the Ruhr-University Bochum in Bochum, German, really be mere coincidence?
  
  

  

  Figure 1: While it would be best never to be infected with Epstein-Barr your risk of EP-related MS is more than twice as high if you are exposed late (Ascherio. 2010)

  At least as far as the Epstein-Barr relation goes the answer of a 2010 review of the literature would be 'no, probably no coincidence' (Ascherio. 2010). It appears to be established that Epstein-Barr (EB) plays a pivotal role in the etiology of MS. Based on the observation that people without EB are virtually MS free, and the fact that their own previous research has clearly shown that late infections with EP increase your risk to develop MS by more than 2x (compared to people who have been exposed in childhood; see figure 1), Ascherio et al. argue that it is very unlikely that EP is not at least the trigger, if not the ultimate cause of MS.
  
  The scientists also refer to the hygiene hypothesis which has been advanced by other authors before, unfortunately, however, getting rid of the 'cleanliness' and exposing your immune system to the training it needs by exposing yourself to the virus at an earlier age, is of little use, if not totally stupid. After all it would only reduce your risk to develop MS to a level that's still more than 1,000% higher than in people who have never been exposed to the virus in the first place (see figure 1).
  
  Due to the inconclusive data on the long and short term effects of Epstein-Barr infections on the B-cell and T lymphocyte response, the Ascherio et al. are not yet sure about the exact mechanism by which EP stimulates, triggers or drives the development of MS. All that can be said with relative certainty is that Epstein-Bar infections contribute to the increase in multiple sclerosis. Aside from the previously mentioned correlations the mere fact that those regions of the world where Epstein-Barr is quasi non-existent are virtually MS free is probably the best evidence of its involvement in autoimmune attacks on your brain. So if you want to protect yourself you better make sure you don't get infected!  Since EP is part of the herpes family and transmitted via saliva this is unfortunately not exactly easy...

• 

  Figure 2: Overall there is no statistical significant downside to chronic paracetamol supplementation, but there is a slight advantage for the NSAID free group in term of increases in lower body strength - the time course (not shown) of the strength gains was by the way identical for both groups, as well (Jankowski. 2013)

  Paracetamol does not interfere with muscle gains in elderly men. The issue whether or not NSAIDs will interfere with resistance training induced gains in skeletal muscle is certainly relevant for everyone. If there is one group of people for whom it could be of paramount importance, though, this would be the men and women in their best ages (>50 years) who have finally realized that muscle is not just metabolic currency, but a true life insurance.
  
  Against that background the most recent results from the College of Nursing at the University of Colorado Anschutz Medical Campus may be important news (Jankowski. 2013). I mean, if the use of N-acetyl-4-amniphenol (ACET) aka paracetamol would hamper or even forestall muscle gains, the training efforts of the men and women who take ACET would be to no avail.
  
  Now the good news is that the chronic use of paracetamol at a daily dose of 1,000mg did not reduce the lean mass gains in the 17 men (age >50y) who actually participated (instead of giving up) in all of the 3-5 days A/B resistance training sessions
  
  • workout A: R three sets of lateral pull down, bench ress, hip abduction and adduction, biceps curls, seated row, and ssisted chin ups
  • workout B: overhead press, leg press, triceps xtension, knee extension and flexion, heel raise, and shoulder external rotation
  • warm up / cool down: 10 min warm-up on the treadmill, a stair climing intermezzo after the first warm up sets and another 10 min cool down
  that were performed with at 80% of the 1-RM and with at least 1 day off in-between over a period of 16 weeks.
  
  
  The chronic ingestion of paracetamol is not advisable regardless of its negligible detrimental effects on skeletal muscle gain. Only recently, Kane et al. have shown that older people in are particularly prone to the hepatoxic effects of this (imho falsely OTC available) NSAID (Kane. 2013). If there is no way around it, because you cannot stand the pain, a safer (at least for the liver) and more effective medical approach could be the combination of tramadol (75 mg), a weak opioid analgesic, with low dose of paracetamol (325-650mg, max!; cf. Pergollizzi. 2013).
  In as much as the nonexistent negative effects are good news, they are likewise strange news, because according to the expression of proteins involved in the protein synthetic response to exercise, it should actually have hampered the gains:
  

  "[...] in the ACET group that the expressions of the anabolic gene p70S6K and the catabolic gene MAFbx were significantly reduced at week 16 of PRT. Given that the increases in FFM in response to PRT were not significantly different between the groups, it is possible that the suppression of catabolic signaling was sufficient to offset reductions in anabolic signaling in the ACET group." (Jankowski. 2013)

  As the authors point out future studies will have to elucidate the exact mechanism this at first sight contradictory results.
  
  In the mean time Jankowski et al. do yet speculate that the loss of prostaglandin signalling and supsequent increases in p70S6K, the protein that's responsible for muscle protein synthesis may be countered by the normalizing effects paracetamol exerts on the expression of Akt, the ameliorative effect on the overexpression of nitric oxide synthase (iNOS) and the reduction of the age-relatedly increased myocyte apoptosis.
  

• 

  Compared to Hope Solo or Serena Williams Olympian Brian Lochte, is probably a weakling - of course only as far as the fatigabilty of his skeletal muscle is concerned - as far as the risk do develop the Athlete's Triad is concerned, this may yet be advantage.

  Men and women tire differently - men (once more ;-) the weaker sex Let's face it guys,  we are weaklings. At least this is what Beth W. Glace and her colleagues from the Nicholas Institute of Sports Medicine and Athletic Trauma at the Lenox Hill Hospital in New York report in their latest paper. Other than the quadriceps muscles of our significant others, our muscles fatigue after 2h of cycling with intermittent one minute sprints every 20 minutes.
  
  In women, in this particular case just like their male counterparts trained cyclists or triathletes with a training load of at least 100km per week, on the other hand, it's solely the central nervous system fatigue that will keep them from cycling 'forever'. Unfair, right? Us men have to battle both, central as well as local muscular (=peripheral) fatigue.
  
  Now what seems nothing but advantageous can however turn against you. In a way the low fatigability of female muscle is also part of the reason why are way more susceptible to the athlete's triad (click here to learn more) than men: They are simply able to work their CNS into the ground, because their peripheral musculature is less prone to exhaustion.
• Recent study puts question mark behind assumed appetite reducing benefit of HIIT sprints vs. classic aerobics - but does that mean that aerobics is the way to go? Not yet in press, but already intriguing are the results of a recent study by  Kevin Deighton et al. from the School of Sport at the Loughborough University who say that they found that ...
  

  "[a]n acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise" (Deighton. 2013)

  

  Figure 3: Intentionally or not, based on the conclusion of the abstract you would probably not have expected to see these results (data adapted from Deighton. 2013)

  Now this sentence from the abstract certainly suggests that sprinting would have nothing but negative effects. The actual data you see in figure 3 does yet tell you something different. The sprinters may have had increased ghrelin and lower PYY levels with the expected downstream effects on perceived hunger, but this did not translate into significant differences in food intake. In other words, even longish sprint exercises like the ones in the study at hand won't put you at danger of overeating - despite transient increases in ghrelin levels.
  
  In fact, the increased ghrelin amplitude can actually be an advantage (see August 04, 2013) and the calories in vs. out calculation the scientists do is so irrelevant to the real world health and body composition effects of exercise that I refuse to repeat it here ("No, you cannot eat that extra piece of layer cake because you ran on the treadmill earlier today" ;-)
  
  In the end, comparisons like this always suggest you had to choose between doing one or another mode of "cardio", when a combination of both, i.e. cycling HIIT and LISS, yet not both in one session, would be the most productive way to go. And no, Mr. Taubes, none of them is "just going to make you hungry" (see "Every Dog Has His Day: Dr. Oz Was Right, Exercise Does Not "Just Make You Hungry", But Reduces Energy Intake!")
  
• Researchers debate the "low vs. high weight" conundrum. In the editorial to the next issue of the Journal of Applied Physiology Mark D. Schuenke, Jennifer Herman, and Robert S. Staron reject the criticism they received from Nicolas Burd et al. for the pro heavy weights arguments they put forward in their recently published study on the effects of high vs. low weight training (Schuenke. 2013a; covered on the SuppVersity on October 01, 2013). Now while this back and forth between the two groups does not deliver any new data, I believe that it is still interesting and highly educative to see how science is actually a matter of negotiated not set truths. So, let's see how Schuenke et al. respond to Burd's assertion that ...
  

  

  Figure 4: Changes in body composition (left) and changes in muscle fiber cross-sectional area in response do different training regimen (Schuenke. 2013a; this study was discussed here on the SuppVersity on October 01, 2013)

  "[t]he authors’ views continue to contribute to a resistance training doctrine that is incorrect, most notably the belief that heavier weights are better concept. This conclusion is likely due to the relative dearth of quality studies assessing the hypertrophy potential of lower load resistance training paradigms, in contrast to the large number of studies employing ‘traditional’ resistance training intensities (*70 % of maximal strength).

  Clearly, evidence exists to support the concept that light(er) loads can support training-induced muscle hypertrophy both independently and by comparison to heavy loads. We would propose that so long as the stimulus is an overload, performed with high effort (fatigue), and progressive then even the most seasoned lifters would see progression,  at the very least no regression, in strength or muscle mass." (Burd. 2013)

  I will briefly summarize the most important points the researchers from the University of New England College of Osteopathic bring forward to defend their "go heavy or go home" argumentation:
  
  • The list of previous studies which confirm the the efficacy of training with high(er) weight for "optimal" gains in hypertrophy and strength is extensive.
  • Low load training is not as Burd et al. suggest "simply a milder form of low-load blood flow restrictive exercise", of which the researchers state that it is "interesting".
  • Schuenke et al. specifically refer to a Y2k study by Takadara et al. which shows that without the cuffs light loads don't build anything (Takadara. 2000).
  • The researchers point out that the claim by Burd et al. that "maximal muscle fiber activation can be achieved in any circumstance as long as the effort is to failure is unwarranted and unsubstantiated".
  • The study by Mitchel et al. Bird et al. cite to prove their hypothesis may not report significant differences between knee extensions performed at 30 % of 1RM for 3 sets, 80 % of 1RM for 1 set, or 80 % of 1RM for 3 sets as far as the isometric strength and hypertrophy between the three types of training are concerned, but
    

    "[t]his result is not surprising considering the following: (1) no control group was used, (2) each subject trained each limb using a different protocol (cross-over effect), (3) only one single-joint exercise was used (low volume versus a much higher volume of training used, for example, in Schuenke et al.: 3 sets each of leg press, squat, and knee extension), and (4) only fiber types I and II were delineated (severely limiting interpretation of the results).

    In that the last parentheses is obviously another direct criticism of what Schuenke would probably call "cherry picking" studies and specific results to support an unwarranted hypothesis.
  Based on this line of argumentation, Schuenke et al. conclude their deliberations on the note:
  

  

  One should not forget that it's not only about light vs. heavy, but in as much about appropriate and inappropriate weights. If you go by the quantity of the evidence there is however no debating that those weights are too light - probably even for a Lady in her best years.

  "Low-load training appears to have some merit. How-ever, our data support the use of high-load, high-intensity resistance training to maximize fiber hypertrophy and strength. In addition, heavy loading of the muscle has an impact on bone and other connective tissues which are minimized/lacking using low-load training. Finally, Burd et al. appear to oversimplify the field of exercise physiol-ogy. To claim that any training load (light or heavy) con-fers the same physiological adaptations as long as the end point is volitional failure is shortsighted and similar to claiming that running for any distance or time will elicit the same effects as long as fatigue is reached." (Schuenke. 2013)

  If you asked me, both are right. While I personally tend to agree with Schuenke, the main reason that I do is that the heavy weights approach is tried and proven, while - just as Burd says - the sceintific evidence pertaining to low weights is scarce and ambiguous and the anecdotal evidence from 'big guys' is non-existent. I am still curious about the next move(s) on both sides of this divide. And by the way, conflicts like these have always been among the driving forces of scientific progress, so I am pretty sure that we as trainees can only benefit from this debate as well as potential follow-up studies, both groups will feel inclined to conduct in order to 'prove' their point.

That's all for today! I hope you enjoyed the stay, all have electricity and an intact water supply ... I mean it's nice if you have a fully charged iPhone to get your daily dose of SuppVersity news, but even I have to concede that some other things in live are way more elementary.

References

• Ascherio A, Munger KL. Epstein-barr virus infection and multiple sclerosis: a review. J Neuroimmune Pharmacol. 2010 Sep;5(3):271-7.
• Burd NA, Moore DR, Mitchell CJ, Phillips SM. Big claims for big weights but with little evidence. Eur J Appl Physiol. 2013 Oct 20. 
• CDC. Early Release of Selected Estimates Based on Data From the January–March 2013 National Health Interview Survey. September 2013
• Chen CY, Wang BT, Wu ZC, Yu WT, Lin PJ, Tsai WL, Shiesh SC. Glycine ameliorates liver injury and vitamin D deficiency induced by bile duct ligation. Clin Chim Acta. 2013 Oct 23-
• Chesney RW, Hedberg GE, Rogers QR, Dierenfeld ES, Hollis BE, Derocher A, Andersen M. Does taurine deficiency cause metabolic bone disease and rickets in polar bear cubs raised in captivity? Adv Exp Med Biol. 2009;643:325-31.
• Deighton K, Barry R, Connon CE, Stensel DJ. Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise. Eur J Appl Physiol. 2013 Oct 31.
• Décard BF, von Ahsen N, Grunwald T, Streit F, Stroet A, Niggemeier P, Schottstedt V, Riggert J, Gold R, Chan A. Low vitamin D and elevated immunoreactivity against Epstein-Barr virus before first clinical manifestation of multiple sclerosis. J Neurol Neurosurg Psychiatry. 2013 Aug 11.
• Kane A, Mitchell SJ, Carroll PR, Matthews S, Hilmer SN. Characteristics of older and younger patients with suspected paracetamol toxicity. Australas J Ageing. 2013 Sep;31(3):190-3.
• Kern F Jr. Effects of dietary cholesterol on cholesterol and bile acid homeostasis in patients with cholesterol gallstones. J Clin Invest. 1994 Mar;93(3):1186-94.
• Kappenstein O, Vieth B, Luch A, Pfaff K. Toxicologically relevant phthalates in food. EXS. 2013;101:87-106.
• Pergolizzi JV Jr, van de Laar M, Langford R, Mellinghoff HU, Merchante IM, Nalamachu S, O'Brien J, Perrot S, Raffa RB. Tramadol/paracetamol fixed-dose combination in the treatment of moderate to severe pain. J Pain Res. 2013;5:327-46.
• Schuenke MD, Herman JR, Gliders RM, Hagerman FC, Hikida RS, Rana SR, Ragg KE, Staron RS. Early-phase muscular adaptations in response to slow-speed versus traditional resistance-training regimens. Eur J Appl Physiol. 2013a Oct;112(10):3585-95.
• Schuenke MD, Herman J, Staron RS. Preponderance of evidence proves "big" weights optimize hypertrophic and strength adaptations. Eur J Appl Physiol. 2013b Oct 25.
• Sioen I, Fierens T, Van Holderbeke M, Geerts L, Bellemans M, De Maeyer M, Servaes K, Vanermen G, Boon PE, De Henauw S. Phthalates dietary exposure and food sources for Belgian preschool children and adults. Environ Int. 2013 Nov 1;48:102-8.
• Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000; 88:2097–2106.

Eccentric Exercise IGF1 & Athlete's Heart; Long or Short Intervals, Both Improve Arterial Stiffness. Plus: Exercise Heals Wounds & Makes You Rust Proof Within One Year!

Controlled exhaustion = positive adaptation; continuous exhaustion = wear and tear = one out of 57,002 who suffer from cardiac arrest during a marathon (data based on Webner. 2013)

As announced on Saturday, already this is a "special edition" of the On Short Notice series, focusing exclusively on exercise related studies. With

• two studies on heart health, 
• one on wound healing and the last one on the 
• bullet proof endogenous anti-oxidant system of trained athletes, 

this installment of the "Exercise News Roundup" and two studies on different HIIT, it does however have both a health, as well as a HIIT focus.

I know that does not sound as sexy as being big and buffed, but what's the use of that if you don't fit the coffin, you're about to need, when your looks are more important to you than your health?

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IGF-Response to exercise implicated in "athletes heart" A group of polish researchers describes in their latest paper that's been published ahead of print in the International Journal of Sports Medicine, how the differential IGF-1 response to eccentric (ECC) and concentric (CON) arm exercise in 10 trained strength athletes (1.5-2.0 h on 3-5 days weekly) and 10 age-matched healthy non-trained subjects could explain the differences in the degree of left ventricular hypertrophy, the scientists had measure via M-mode and 2D Doppler echocardiography beforehand (Zebrowska. 2013).

IGF1 and left ventricular hypertrophy (LVH): The correlation stands out of question, but what about the implications? Is this a causative relationship? And what's more: How dangerous are LVH  and having an athlete's heart, at all?

The athletes with LVH did not only have higher IGF-1 levels at baseline (52±5 nM vs. 46±7 nM for controls, p<0.05), they also showed a significantly more pronounced IGF-1 response during the eccentric (ECC) exercise test, with athletes with LVH exhibiting 30% higher and athletes without LVH 15% higher IGF-1 levels than untrained controls (54±6 nM). Moreover, both CON and ECC exercise resulted in higher serum IGFBP-3 levels in LVH athletes compared to controls (242±57 and 274±58, athletes, vs. 215±63 and 244±67, controls, nM, p<0.05), while no differences in other hormones were found between groups. Yet though the scientists' conclusion that these findings would "suggest a role of IGF-1, possibly released from contracting muscle, in stimulating LV hypertrophy in resistance training" is certainly right, we would be ill-advised to jump to any conclusions, hastily by simply (and faultily) equating correlation and causation, here.

Moreover, we should acknowledge that the previously accepted paradigm that LVH, per se, is a bad thing that has to be avoided at all costs is actually not supported by empirical evidence, or as Florescu et al. have it "'Supranormal' cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with 'supranormal' cardiac function, and there are no markers of myocardial fibrosis." (Florescu. 2010)... in short: in the absence of myocardial fibrosis, a big heart is nothing you will die from - how IGF-1 could actually prevent the latter, i.e. the occurrence of fibrotic structures due to uncompensated growth of the heart muscle, would yet be the topic for another quite lengthy blogpost ;-)

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This image shows a study participant of another study during a VO2 max test on the exact same bike Rakobowchuk et al. used (WSCU.edu). Wrt to the protocols the researchers remark "the protocols involved an identical total training volume and time commitment but differed regarding metabolic stress" With the HIIT trial inducing greater metabolic stress due to the longer periods at supra-amaximal workloads (cf. Turner. 2006).

Heavy or moderate interval training equally heart healthy - at least if you take their effect on arterial stiffness and heart rate dynamics as a measure. That's the message of an article that was published ahead of print in the European Journal of Applied Physiology at then end of last week. During a six-week experiment, Mark Rakobowchuk and his colleagues from the University of Essex and the University of Leeds investigated which of the following protocols (all performed three times per week, for a total of 18 session; 2min warm-up for each; cf. Rakobowchuk. 2013),

• MIIT - moderate intensity interval training consisting of 10s : 20s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression), or
• HIIT - high intensity interval training consisting of 30s : 60s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression),

would elicit more favorable changes in carotid artery stiffness, blood pressure, and heart rate variability in a group of 20 healthy, previously untrained young men and women (n = 7 men and 13 women; age 23.5y; BMI 23).

Trainees who want to increase their VO2max should still do HIIT, because only the subjects in the HIIT training group achieved statistically significant increases with respect to this outcome measure (+14% in HIIT vs. +3% VO2 max in MIIT).

Just as the scientists had speculated, their hypothesis that irrespective of the metabolic stress, which would be higher in the HIIT vs. the MIIT trial, the total volume, which was identical would determine the overall adaptive response. For them it was therefore not surprising that all measured parameters of  heart health, i.e.blood pressure, heart rate dynamics and carotid arterial stiffness, improved without significant inter-group differences. Most notably, though, those with the highest arterial stiffness before the trial saw the greatest reductions!

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Figure 2: Additional exercise sped up the wound healing process only in the obese rodents, not the lean ones (Pence. 2013)

Exercise speeds healing of subcutaneous wounds in obesity. This was allegedly observed only in obese rodents, but since the underlying mechanism was neither mediated by gene or protein expression of proinflammatory cytokines interleukin-1A and tumor necrosis factor-alpha or the anti-inflammatory cytokine interleukin-10 in the wounds, I felt it was still worth mentioning, also because it is, as the scientists point out,

"the first report of an exercise effect on wound healing that is unrelated to alterations in wound site inflammation." (Pence. 2013) 

Future trials will have to elucidate whether clotting and homeostasis, which occur in the earliest stage of wound healing, approximately 30 min after the trauma may be involved in this phenomenon.

In this context, some of you will probably remember my recent post on the "Antithrombotic effects of caffeine blunt platelet activity in response to interval training" that exercise increases the tendency of your blood to clot - a tendency that does obviously come handy, when you are bleeding. That the increase in coagulation factors came into effect only in the obese, yet not in the normal weight control, in turn, could be related to the presence of existing hemostastic imbalances due to obesity which would have been corrected by the 30min of treadmill running the rodents in the exercise groups performed at a pace of 12 m/min on a 5% incline for the final 30 min of the light period (0930–1000 h), three days before until five days after the wounding.

A bunch of maggots on a diabetic wound.

Be that as it may, there are more than enough sedentary, "SAD dieting" (and the standard high fat diet rodents are fed in studies like this is nothing but a clone of the S-tandard A-merican D-diet) full-blown or pre-diabetic obese human beings who could likewise benefit from as little as 30min of daily aerobic activity. I mean think about it, if you could thus avoid having 50-100 maggots being placed on those nasty diabetic wounds (see picture on the right) that would never heal without those tiny critters secreting their salivary juices onto the wound to liquefy and subsequently ingest and further degrade the dead tissue in their gut, you can hardly argue that this is too much to ask for, can you?

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"Rust proof" athletes don't need vitamin pills with copious amounts of anti-oxidants and don't have to be afraid of fruit with their synergistic blend of small, but highly effective and synergistic amounts of vitamins and polyphenols, either.

Oxidation proof after 1 year+ of regular aerobic + anaerobic training. According to a paper that's soon going to be published in Medicine & Science in Sports & Exercise trained athletes between the ages of 21 and 35yrs who had been participating in a structured exercise training program (including both aerobic and anaerobic) for the past 12 months, with each session lasting no less than 45 min per session, as well as no less than three sessions per week, are virtually "rust proof".

That's at least my allegedly nonchalant interpretation of the non-existent increases in serum markers of oxidation the scientists from the University of Memphis observed in their 12 male subjects (BMI 25kg/m², body fat 12.8%; VO2Max 20 ml/kg/min) in response to four training sessions separated by 1 wk.

The Sessions were counterbalanced and included either a no-exercise condition (subjects simply rested for the entire period) or one of the these three:

• MISS - moderate intensity + duration steady state: 70% HR reserve for 60min; total time: 60min with 60min of actual work
• HIIT - high intensity + moderate duration interval sprints: 5x60s at 100% + 225s recovery yielding a 1:3.75 work-to-rest ratio ("Within each interval, subjects were instructed to pedal between 80 and 100 rpm for the first 45 s, and then for the final 15 s, subjects were instructed to pedal as fast as possible"); total time: 20 min with 300s of actual work
• MaxIIT - maximal intensity + short duration interval: 10x15s at a wattage of 200% of VO2max, followed by 116s of recovery (1:7.7 work-to-rest ratio); total time: 20 min with 150s of actual work

All exercise bouts were performed on the same cycle ergometer used for the GXT, and subjects reported to the laboratory in the morning (0600–0900 h) after a minimum 10-h overnight fast. The HR was continuously monitored via Polar (TM) HR monitors and blood was drawn at the end of the 20-min rest period  (corresponding to the immediate postexercise blood samples) and 30 and 60 min after the 20-min rest period (corresponding to the postexercise blood samples).

Figure 3: Total antioxidant capacity (TEAC), SOD, CAT and GPx values immediately (0min), 30min and 60min after the respective exercise bouts (data based on Farney. 2013)

The respective total work performed during the trials was 461.1kJ, 96.9kJ, 96.9kJ for the MISS, HIIT and MaxIIT trials, respectively, the perceived exertion was highest in the MaxIIT trial (16.7 vs. 15.6 for HIIT and 13.5 for MISS), while the maximal heart rate 171.7bpm was achieved in the HIIT trial. Still,

"No differences were noted in malondialdehyde, H2O2, advanced oxidation protein product, or NOx between conditions or across time (P > 0.05) [while the a]ntioxidant capacity was generally highest at 30 and 60 min after exercise and lowest at 0 min after exercise." (Farney. 2013; my emphases)

If you will, you could even go one step further and argue that the total antioxidant capacity increases in well-rested, well conditioned athletes in response to exhaustive exercise bouts. Though, this increase reaches statistical significance in the MaxIIT trial only (see figure 3).

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That's it for today, ... but only as far as SuppVersity posts go. In about 2h at 1PM (EST), to be precise you can - if you want - listen to me on Super Human Radio. I am going to pick up on the topic of the first hour which is "Moderate Alcohol Consumption how (Un-)Healthy is it really" and do my best to provide some insights into the discrepancy that exists between reliable scientific evidence, the media coverage on the topic and Mr Average Joe's interpretation of the latter. And if you ain't into booze, just work out ;-) [update: download the podcast]

References:

• Farney TM, McCarthy CG, Canale RE, Schilling BK, Whitehead PN, Bloomer RJ. Absence of blood oxidative stress in trained men after strenuous exercise. Med Sci Sports Exerc. 2013 Oct;44(10):1855-63.
• Pence BD, Dipietro LA, Woods JA. Exercise Speeds Cutaneous Wound Healing in High-Fat Diet-Induced Obese Mice. Med Sci Sports Exerc. 2013 Oct;44(10):1846-1854.
• Rakobowchuk M, Harris E, Taylor A, Cubbon RM, Birch KM. Moderate and heavy metabolic stress interval training improve arterial stiffness and heart rate dynamics in humans. Eur J Appl Physiol. 2013 Sep 16.
• Turner AP, Cathcart AJ, Parker ME, Butterworth C, Wilson J, Ward SA (2006) Oxygen uptake and muscle desaturation kinetics during intermittent cycling. Med Sci Sports Exerc 38:492–503.
• Webner D, Duprey KM, Drezner JA, Cronholm P, Roberts WO. Sudden cardiac arrest and death in United States marathons. Med Sci Sports Exerc. 2013 Oct;44(10):1843-5.
• Zebrowska A, Waśkiewicz Z, Zając A, Gąsior Z, Galbo H, Langfort J. IGF-1 Response to Arm Exercise with Eccentric and Concentric Muscle Contractions in Resistance-Trained Athletes with Left Ventricular Hypertrophy. Int J Sports Med. 2013 Sep 7.