Optimizing the "Fat Burning Zone" : Chronic Endurance Training Boosts Fatty Oxidation - Does More Help More?

You as a SuppVersity reader should know that there is no "instant gratification" with  "doing cardio" and that doing it "in the zone" is totally 90s... 1990s, even ;-)

For decades, the "Fat Burning Zone" has been one of the holy grails of exercise sciences. Then somebody realized that maximizing the ratio of fat : glucose that's are being used as fuel during a workout doesn't really have an effect on weight loss and all of a sudden papers with titles like "Changes in peak fat oxidation in response to different doses of endurance training" (Rosenkilde. 2013) have become a rarity... although, if you look closely, you will realize that this is actually not another investigation into the realms of the "Fat Burning Zone", but an afford to quantify the effect of regular "cardio training" on your bodies ability to oxidize fat, instead of glucose.

Don't worry it's not really about the "fat burning zone"

Luckily Rosenkilde's most recent paper, which happens to be the third spinoff of the high (600kcal/day) vs. medium (300kcal/day energy expenditure from "cardio") training volume that already taught us (you can read more about the exact exercise protocol in the previous SuppVersity articles, below) ...

• 

  Learn more about the "Fallacy of Working Out To Burn Calories" 

  how futile it is to work out like a maniac if fat loss is your goal ("Some HIIT For Life & Less LISS For More! How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat!" | read more) and 
• how messed up the die hard belief that "exercise" just makes you hungry actually is and what the effects of endurance exercise on appetite and energy intake are ("Exercise: Does It Really Make You Hungry? The More You Train, The Less Hungry You Are." | read more)

In this second serving of the data, we can now learn whether regular endurance training increases peak fat oxidation in a dose-dependent fashion.

Figure 1: Pre & post respiratory exchange ratio (lower value = higher ratio of fatty acid : glucose oxidation) in sedentary control and 300kcal/day group, left; changes in the expression of mitochondrial enzymes (Rosenkilde. 2013)

As you can see in Figure 1 the outcomes of the experiment were not exactly surprising: While there was a persistent increase in fatty acid oxidation and the expression of the facilitative mitochondrial complexes, i.e. enzymes in the mitochondrial respiratory chain, the daily endurance training volume (MOD: 300kcal/day vs. HIGH: 600kcal/day energy expenditure during endurance training) had no effect on the effect size.

So, if it's not the volume, what determines the increase in fatty acid oxidation?

Rosenkilde have probably asked themselves something similar to the above, when they realized that there were no meaningful differences between the subjects in the medium vs. high dose cardio groups. The statistical analyses the researcher conducted did yet reveal, that

• VO2peak, generally regarded as a marker of cardio-respiratory fitness,
• fat free mass, the weight of everything (incl. bones, organs, etc.) that's not fat, 
• cycling efficiency, the power output at a given VO2 peak, and the
• mitochondrial complexes II–V, enzymes that facilitate the oxidation of fatty acids,

were all associated with higher increases in fatty acid oxidation, while the observed changes in fasting plasma insulin, glucose, FFA, or glycerol had no prognostic value with respect to the increase in fatty acid oxidation.

Don't forget that HIIT is an even more effective "long-term investment" in VO2 peak an mitochondrial power - just don't do it everyday | learn more

Bottom line: I guess you will start yawning, when I tell you that doing regular cardio training is not useful for its acute effects on energy expenditure (you know that, right?).

If you look around the gym, you will yet notice that "burning energy" is still what 90% of the cardio warriors have on their mind. What they fail to realize is that performing a sane amount of low-medium intensity cardio will be rewarded in the long run only and is (some of you may remember that from the SuppVersity Facebook News) associated with increased muscle strength throughout the life span (Crane. 2013), delays the age of decline in leg strength and muscle morphology (Tarpenning. 2004), improves muscle function in the elderly (Harber. 2009) and can have have minimal hypertrophy effects even in the elderly (Ozaki. 2013).

References: 

• Crane, J. D., MacNeil, L. G., & Tarnopolsky, M. A. (2013). Long-term Aerobic Exercise Is Associated With Greater Muscle Strength Throughout the Life Span. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 68(6), 631-638.
• Harber, M. P., Konopka, A. R., Douglass, M. D., Minchev, K., Kaminsky, L. A., Trappe, T. A., & Trappe, S. (2009). Aerobic exercise training improves whole muscle and single myofiber size and function in older women. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 297(5), R1452-R1459.
• Ozaki, H., Loenneke, J. P., Thiebaud, R. S., Stager, J. M., & Abe, T. (2013). Possibility of leg muscle hypertrophy by ambulation in older adults: a brief review. Clinical interventions in aging, 8, 369.
• Rosenkilde, M., Reichkendler, M. H., Auerbach, P., Bonne, T. C., Sjödin, A., Ploug, T., & Stallknecht, B. M. (2014). Changes in peak fat oxidation in response to different doses of endurance training. Scandinavian Journal of Medicine & Science in Sports.

To Spit or to Swallow - That is the Question! Carbohydrate Mouthrinse May Be Better Than Water, Yet Still Not an Option for Performance Oriented Athletes

Image 1: "You need carbs to fuel your workouts!" You know the whole litany... what may be news to you is that scientists are speculating that "intra workout carbs" do not necessarily have to be ingested to do their ergogenic magic.

Those of you, who already "friended" me on Facebook and are following what is going on on the SuppVersity Facebook page (just want to remind you that Facebook has now an option that allows you to be informed, whenever something new is posted), will probably remember the discussion revolving around "carbohydrate mouthrinsing" and whether or not it may be even more beneficial to spit and not to drink your Gatorade... now, all the health benefits of low-carbohydrate (when I am talking "low" I am not talking of Atkins type <80g) diets aside, it does seem pretty counter-intuitive that just swishing one of those carbohydrate-laden electrolyte drinks in between your teeth for a few seconds, to then spit it out again could actually have any merit. Yet, science, or I should say a handful of studies, do suggest otherwise.

As part of their recently published study into the effects of carbohydrate mouthrinsing on exercise capacity in the pre- and postprandial state (Fares. 2011), Elie-J. M. Fares and Bengt Kayser have compiled a list of the 8 hitherto published peer-reviewed papers on that subject. And if you just went by the column "increased perfomance", "yes or no", it appears like it was an established fact that carbohydrate mouthrinsing was highly ergogenic. After all, six out of the eight studies are marked with the tag "increased performance".

Figure 1: Performance increases and standard deviations of the respective measures from studies on the advantage of carbohydrate vs. artificially sweetened or plain water mouthrinse (data calculated based on summary in table 2 of (Fares. 2011)

If we do yet have a look at the quantity of those performance increases and the individual standard deviations (I compiled the respective data for you in figure 1), things begin to look less conclusive. I mean, there is obviously a standard deviation for both arms of each study and there also is a mean improvement (or decrease in performance), but if the "performance increment" is smaller than the standard deviation, for all but one study, this does make me feel uncomfortable with the statement that I would see "scientific evidence", let alone "conclusive scientific evidence" in support of carbohydrate mouth-rinses.

Mouthrinse vs. placebo = minimal (if any advantage), but what about vs. ingestion?

Regardless of what you think about the real world significance of an average performance increase of 1% (calculated based on the data from figure 1), for the small fraction of athletes for whom these minimal performance increases would actually count, i.e. high intensity endurance athletes, like time-trial Tour de France cyclists, the "control", or I should say the "benchmark" should not be plain or sweetened water, but rather one of these crab-, ah... pardon me, carb-loaden sugary electrolyte drinks these athletes are habitually consuming. I was thusly happy to see that Catherine Moss, a student of Sports and Exercise Sciences at the Massey University in Auckland, New Zealand has recently conducted an experiment for her thesis that has much more practical relevance for the high achieving athletes (Moss. 2011).

Table 1: Composition of the placebo and CHO supplement in the Moss study (adopted from Moss. 2011)

In a randomized, counter-balanced, double-blind study, Moss had eight recreationally trained cyclists perform a time trial (with a predetermined amount of work) in the course of which the cyclists ingested or rinsed (swirling 0.33ml/kg body weight of the solution for 8s) with either a placebo solution or a carbohydrate drink, whenever another 12.5% of the total work was done. In that it is worth mentioning that the composition of the CHO solutions differed for the one that was meant to be ingested and the one that was intended to be swished. With the former containing 7.5% and the latter 15% carbs, Moss mimicked solutions that had been used "successfully" previous studies. I do yet no idea, why the placebo did not contain electrolytes, as this could obviously have made a difference at least in the ingestion trials... I guess this is what distinguishes a thesis like this from a study that is worth being published in a peer-reviewed journal ;-)

Figure 2: Mean power output (in Watts) at different time points during time trial (data adapted from Moss. 2011).

As the performance data in figure 2 goes to show, only the ingestion of the carbohydrate led to significant improvements in mean power output, specifically at the later stages of the time trial. This "breakdown" may be explained by the "glycogen reduction exercise protocol" all participants had conducted the day before the time trial. So that after a "low carbohydrate" dinner, the participants were supposed to be glycogen depleted when they performed the time-trial on the subsequent morning.

Figure 3: Total time (in s) during time trial (data adapted from Moss. 2011).

In a way this is an unfair advantage, for the carb ingestion, which accordingly elicited way better time trial times. It does yet not lessen the significance of data on carbohydrate vs. water mouth rinse, which shows pretty conclusively that in a glycogen depleted state both forms of mouthrinsing (plain water or a 15% carbohydrate solution) are equally ineffective, when it comes to actual performance increases.

Figure 4: Pleasure / displeasure feeling during time trial (data adapted from Moss. 2011).

If you do however look at the pleasure/displeasure feeling scale data in figure 4, I would speculate that in a non-glycogen depleted state the carbohydrate-rinsers would have performed significantly better... I mean, without gas in the tank a car won't work even if it "wanted". In view of the fact that the carbohydrate ingestion group did yet pedal at a higher intensity, this would warrant further investigation.

Figure 5: Respiratory exchange ratio (higher values = higher carbohydrate oxidation) during time trial (data adapted from Moss. 2011).

That being said, there was what I consider an interesting effect of carbohydrate rinsing on the respiratory exchange ratio (remember higher values = higher carb oxidation), which would suggest that the theory Fares and Kayser propose (Fares. 2011), according to which the activation of sweetness taste receptors cells (T1R2 and T1R3) in the mouth would explain the previously cited performance "increases" in other studies, may have its merits. What else than the sensation of incoming carbs could explain that the cyclists burned more carbs in the carb mouthrinse compared to the placebo mouthrinse trial (cf. figure 5) - and that in the absence of significant differences in blood glucose or insulin levels?

Spit it or suck it? What's right for you?

While we do not know whether it would make sense to mouthrinse in a glycogen repleted state (yeah, I know +1% ;-), for any athlete interested in maximal performance, simply ingesting his carb + electrolyte drink would certainly be the best option. The (intermittendly) fasting dieter, who wants to maximize his fatty acid oxidation in the course of say his "morning cardio", on the other hand, would be best off with a non-carby electrolyte drink that helps him avoid dehydration and does not compromise (even if the effect is minimal) fatty acid oxidation... what? You want to know who would  benefit from spitting his carbs out? Well, at least based on the current data, mostly the cleaning contractors of your local gym - after all, they would have to work overtime (and be paid overtime) to clean up the mess ;-)

The IGF-1 Promoting, Myostatin Reducing, Muscle Building Effects of PGC-1 α-4: What It Does and Why Doing Cardio Before Weights Appears to Promote It's Expression

Warning: Reading this article won't make you look like Phil Heath over night.

As announced yesterday, I am about to get back to the study on PGC-1 alpha-4, the protein Carl Lanore and I talked about in the last installment of the SuppVersity Science Round-Up on Thursday. Since I am not going to simply repeat everything I already said during the show here, I suggest you download the podcast and listen to it before you read this article. Thus you would have a basic understanding of what the Ruas' study is all about and can class the additional information this article is going to provide with the stuff you've heard on Super Human Radio. If you don't have the time or are just sitting in the office, where listening to a radio show is not really an option, I would guess that those of you who have been around on the SuppVersity for some time now, should be able to connect the dots on their own.

PGC-1 alpha-4 the missing link between myostatin, IGF-1, hypertrophy and strength gains

With the combination of in-vitro and in-vivo data from rodents and humans the study Roas et al. published in the latest issue of Cell is a seam of information - literally. Actually, this is part of the reason, why I decided to restrict the following discussion to a summary of those findings that are either of general interest or can serve as a rational foundation for practically relevant conclusions, instead of simply reiterating the whole protocol.

• 

  Figure 1: Fluorescencemicroscopy analysis of myotubes expressing GFP alone or together with PGC-1 a1 or PGC-1 a4 (left) and effects on the expression of selected RNAs (Roa. 2012)

  PGC-1 alpha and its splice variants - The four known splice variants (alpha 1-4) the scientists tested for are expressed in most of the major organs of our body. Of particular interest for our discussion here are alpha-1 and alpha-4, with the former influencing 2002 and the latter controlling 519 gene function. The overlap between the two (98 genes) is actually pretty small, so that their downstream metabolic effects can be expected to be about as distinct as their underlying triggering mechanisms.
  
  While the energy sensing system appears to be responsible for the expression of PGC-1 alpha-1 (learn more about AMPK and how your body controls glucose uptake mitochondrial activity of the cells etc. depending on the local availability of energy), PGC-1 alpha 4 expression in skeletal muscle and thus the downstream effects on myostatin (inhibition) and IGF-1 (promotion) appear to be controlled by (contractile, but also metabolic) stress. Whether this is actually the case and in how far certain overlaps do exist will yet still have to be evaluated in future studies.
  
  

  

  Figure 2: Training or overtraining - good or bad inflammation; it's often difficult to hit the sweet spot (background adapted from Kramer. 2007)

  The same goes for the exact involvement of MAPK and other stress-sensors in our bodies and the dose-response relationship between the ROS and exercise induced expression of inflammatory factors such as IL-6 => NF-KappaB and their short term beneficial effects on the training induced adaptation processes (see figure 2). What can be said for sure, though, is that over-training and the downward spiral on the right side of  figure 2 is way more likely to be the underlying cause of suboptimal results, than an absence of adequate training stimuli on the left. Adequate recovery (primarily via rest + food and not by popping supplements or suppressing your well-deserved drowsiness with stims) is therefore about as, if not more important than the one additional rep you may or may not be able crank out at the end of an intense workout.

•  What exactly can PGC-1 alpha 4 do? The trends in RNA expression in figure 1 do actually give you an idea of what the ensuing effects should be, but I guess some actual data will make it even more obvious what all these gene essays mean.

  

  Figure 3: Effect of injected PGC-1 a  and DNA manipulation on muscle fiber composition and overall muscularity and phenotype of the rodents (Ruas. 2012)

  As the data in figure 3 goes to show, the effects of PGC-1 alpha 4 injections are almost identical to what you would see to a standardized hypertrophy training. And as you may remember from my dissertation on the podcast, the >17x increase in PGC-1 alpha 4 expression in response to reloading of a previously suspended hindlimb in the scientists' rodent model would confirm just that: PGC-1 alpha 4 is expressed in response to muscular overload (as it does obviously occur, when you have not moved your leg an inch for 10 days) and initiates adaptation processes that are meant to strengthen and "build" the muscle to ensure that it is up to future challenges like this.
  
  

  

  Figure 4: Immunohistochemical analysis of gastrocnemius muscle from wild-type (WT) and Myo-PGC-1 a4 animals

  Due to the fact that the effects Roas et al. observed were muscle fiber specific and quasi non-existent in muscles that are predominantly slow twitch fibers (e.g. soleus or planatris), the concomittant boost in MHCIIa and MHCIIx myosin heavy chain types you see in figure 4 may easily be misinterpreted as a "transformation" of muscle fibers. If you look closely at the immunohistochemical analysis of the gastrocnemius muscle from wild-type (WT) and Myo-PGC-1 a4 animals in figure 4 the pictures do yet speak a very different language. If anything, the amount of the very fast twitch glycolytic (only) type IIb fibers may have dimished ever so slightly. The amount of slow twitch oxidative muscle fibers, on the other hand, remained constant, while the number of both MHCIIa and MHCIIx positive myofibers increased (the same happens, as you should remember from the Intermittent Thoughts in bodybuilders and recreational trainees, as well).
   
• PGC-1 alpha 4 boosting agents include clenbuterol 5x (see Friday's "SuppVersity Science Round-Up Seconds"), forskolin 25x (both in vitro) and cold exposure (4°C) in rodent (!) brown adipose tissue.

Aside from the anti-cancer cachexia effect which is not directly related to the topic of this post, the previous paragraphs and the podcast should actually give you the most important information about this recently discovered splice variant of PGC-1 alpha, so that we can now segue into the "real-world" part of the study and take a closer look at the interactions with strength and cardio training I have been talking about on Thursday, as well.

Exercise and PGC-1 alpha 4 in real human beings

You cannot tell me that you have never heard of the notion that doing cardio not after but either before or or in-between your lifts an have its merit. If you can't remember it anyway, go back and reread "Before, After or In-Between? Study Puts Another '?' Behind the Widely Accepted 'Cardio After Weights' Paradigm."

Previous research associated PGC-1 alpha increases primarily with endurance training and, albeit to a lesser degree, glycogen depleting high intensity interval training (HIIT), or high volume resistance training. Over the years all of these training forms have been shown to contribute to mitochondrial biogenesis, a repartitioning of fiber types towards a more versatile oxidative myosin heavy chain pattern (similar to what you see in figure 4), the AMPK mediated stimulation of fatty acid oxidation and glucose uptake, angiogenesis and the prevention of muscle atrophy (Arany. 2008). The discovery of this new splice variant of the PGC-1 alpha protein does not diminish the significance of any of these results, but it does make one thing pretty obvious: Building muscle, endurance and oxidative capacity (mytochondria) are not mutually exclusive processes and it is very likely that there is a strong overlap between the metabolic and mechanic triggering processes.

It does in fact look as if the PGC-1 alpha "family" stands, if you will, at the crossroads of the aforementioned pathways with the "classic" alpha 1 variety being triggered by AMPK (and maybe other nutrient sensors) and the alpha 4 variety responding to the exercise-specific increase in stress signals. The results of the 8-week human study, Roas et al. conducted does yet show that things are - once again - not as easy as it may seem. If you look at the three training groups the subjects (the researchers don't provide details about age or training status, but probably young untrained men) were randomly assigned to...

• 

  Figure 5: Mo & Thu and Tue & Fri workouts (top) and results of the analysis of the biopsies that have been taken 48h after the last training session (Roas. 2012)

  Endurance Training (ET): During week 1, participants completed 30 min of stationary cycling at 65% VO2 peak 3 days per week. During week 2, participants completed 45 min of stationary cycling at 65% VO2 peak 3 days per week. During week 3, participants completed 45 min of stationary cycling at 65% VO2 peak 5 days per week. During weeks 4-8, participants completed 60 min of stationary cycling at 65%VO2 peak 5 days per week. 
• Resistance Training (RT): During week 1, participants were familiarized with resistance training program and practiced the movements with light weight during each of the four training sessions. During week 2, participants completed 2 sets of 8-10 repetitions to failure 4 days per week. During week 3, participants completed 3 sets of 8-10 repetitions to failure 4 days per week. During weeks 4-8, participants completed 4 sets of 8-10 repetitions to failure 4 days per week. Table S1 presents the full exercise program. 
• Combined Training (CT): The progression of the ET was the same as that described for the ET group, except that the durations were half as long as the ET group (i.e., 30min versus 60min). The progression of the RT was the same as that described for the RT group, except that the number of lifts was less the RT group. 

... as well as the exact protocol they have been following (figure 5, top), you would probably not have expected that the combined training protocol would have an edge over the higher volume resistance training in terms of both PGF-1 alpha 4 expression, as well as the decreases in myostatingthe increases in IGF-1, and the effective mean strength gains on the leg press (+30% for both with a minimal, statistically non-significant edge for the combined regimen; not shown in figure 5).

Implications: Why doing "cardio" before a workout could be beneficial

Figure 6: Free fatty acid levels before depletion (S1) and before (S2) and after (S3) exercise trial, as well as PGC1-alpha and p-AMPK expression (Psilander. 2012)

In the absence of detailed information about the increases in muscle CSA and protein content, it may be a bit too early to formulate any implications, but since the question of "doing cardio before a workout" was at the heart of an interesting discussion some of you started in the comment area to Friday's installment of the Seconds, I want to pick up on that and present a couple of garbled thoughts and references that may explain why the combined training did produce greater increases in PGC-1 alpha-4, as well as more pronounced downstream effects on myostatin and IGF-1 than the "growth specific" strength training program.

Now, one of the beauties of having your own blog with 1020 individual posts is that you can often simply refer people to previous posts such as the one from which I just copied figure 6 into this article. In fact, the title "8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Intensity Exercise in Glycogen Depleted Elite(!) Cyclists" actually gives away most of the 'secret' that's probably behind the purported benefits of a combined training regimen: Glycogen depletion!

Can I do HIIT instead? Personally I don't see any reason why you could not replace the 30min of steady state exercise with 10-15 minutes of HIIT (including active rest), but you should be aware of the fact that this will be more taxing on your central nervous system and probably more likely to result in a decrease in exercise performance on the subsequent workout, than sitting on an ergometer cycling at 60% of your VO2max. If you feel that it works for you - fine, but don't complain if in a year from now you still don't look like Mr. Olympia ;-)

Now the Psilander study does show that glycogen depletion, which is essentially what will happen (at least to a certain degree) if you perform 30 min of cardio training at a non-exhausting, but still energy consuming pace of 60% of your VO2 max before a workout does work. Without differentiating the various iso-forms of PGC-1 alpha Psilander's 5x increase in PGC-1 does yet not tell us whether we are dealing with the "right form" of PGC here. After all, the Psilander protocol involved two endurance sessions, with the first being a depletion session that was conducted on the day before the actual test and the second being a HIIT-esque exercise test (go back to the original post for more details).  Fortunately, there are 2019 other articles on the SuppVersity so that I don't even have to refer you to a study I have not already written about to add another piece to the puzzle.

A blast from the past and a glimpse into the future

On Wednesday, October 31, 2012, I wrote about the results of a study by Lundberg et al.. Again a slightly different protocol, this time with "cardio" in the morning and strength training later in the day, yet the exact same benefits in terms of PGC-1 alpha (total) expression:

Figure 7: Selected markers of mitochondrial biogenesis and protein synthesis before during and 15, respectively 180min after the resistance training bout in the AE + RE and the RE only leg (a.u.; data adapted from Lundberg. 2012)

With the more pronounced drop in myostatin in the combined training group in the Lundberg study, the only thing we would still need to further support the practical value of the more recent results from the Roas study would be a concomitant increase in IGF-1, as we would expect it, if working out in a (partly) glycogen depleted state would actually be the reason for the increase in PGC-1 alpha 4 Roas observed in the subjects of his study. Now I could copy and paste another graph, but I guess it will be enough, when I refer you back to the detailed elaborations on the connection between IGF-1 and it's muscle-specific splice variants and exercise induced beneficial, since acute and hormetic inflammation in the "IGF, MGF & Inflammation" part of the Intermittent Thoughts on Building Muscle (click here for an overview).

Please keep in mind: Regardless of the fact that previous studies did not test for the PGC-1 alpha subtypes, we cannot ignore the existing evidence that PGC-1 is not mandatory for the beneficial effects of endurance exercise on mitochondrial biogenesis (e.g. Rowe. 2012) and should therefore not overestimate the importance of PGC1 alpha 4 as the "one and only" muscle builder. I have said that before, but I guess it's important to repeat it - this is another missing link it's just like mTOR, testosterone and whatever other magic bullets people will tell you about not exclusively responsible for increases in muscle mass, mitochondrial capacity and whatever else you may just be dreaming of.

If we now add a couple of additional findings to this intellectual brew, like ...

• the 100% increase in the expression of the heat shock protein HSP72 in a glycogen depleted vs. normal leg during a workout (Febbraio. Feb 2002)
• the 150% increase of intramuscular HSP72 in response to an infusion with low doses of interleukin-6 (Febbraio. Sep 2002)
• the non-existant negative side effects of IL-6 on muscle glucose uptake in healthy individuals (Steensberg. 2003)
• IL-6's importance as a regulator of glucose metabolism during exercise (Helge. 2003; Febbraio. 2004) and it's satellite cell proliferation promoting effects (McKay. 2009) 
• the Dr. Jakyll and Mr. Hyde nature of inflammation, in general and IL-6 in particular on glucose uptake and fatty acid oxidation, when it comes to its local and temporary (=beneficial effects) vs. systemic and chronic (=detrimental effects) presence in our body (Fisman. 2010)

...we do actually arrive back at where we came from, namely the difference between training and overtraining in figure 2.

Bottom line - cardio pre-workout as an intensity technique: On the basis of these considerations you can think of doing cardio before a workout as an intensity technique that will increase the beneficial stress and thus the demand for greater adaptive responses. That the latter will go hand in hand with an increased propensity of overtraining, particularly if you are not willing to (A) supply your body with the nutrients it needs after the workout and (B) to rest for an adequate amount of time before you hit the gym again, is something of which I would appreciate if it wasn't something I had to repeat in each and every SuppVersity article, but since this is and will probably remain the #1 reason why people don't make progress physique- or performance-wise, it's still the most important take home message at least for those of you who are new to the site. I hope this did not ruin this allegedly pretty lengthy post for you and believe I am not promising too much, when I say that you are soon going to read more about this protein here - after all, it's almost certain that we are going to see follow-up studies in the months to come.

References:

• Arany, Z. PGC-1 coactivators and skeletal muscle adaptations in health and disease. Curr. Opin. Genet Dev; 2008: 426–434. 
• Febbraio MA, Steensberg A, Walsh R, Koukoulas I, van Hall G, Saltin B, Pedersen BK. Reduced glycogen availability is associated with an elevation in HSP72 in contracting human skeletal muscle. J Physiol. 2002 Feb 1;538(Pt 3):911-7.
• Febbraio MA, Steensberg A, Fischer CP, Keller C, Hiscock N, Pedersen BK. IL-6 activates HSP72 gene expression in human skeletal muscle. Biochem Biophys Res Commun. 2002 Sep 6;296(5):1264-6.
• Febbraio MA, Hiscock N, Sacchetti M, Fischer CP, Pedersen BK. Interleukin-6 is a novel factor mediating glucose homeostasis during skeletal muscle contraction. Diabetes. 2004 Jul;53(7):1643-8.
• Fisman EZ, Tenenbaum A. The ubiquitous interleukin-6: a time for reappraisal.
  Cardiovasc Diabetol. 2010 Oct 11;9:62.
• Helge JW, Stallknecht B, Pedersen BK, Galbo H, Kiens B, Richter EA. The effect of graded exercise on IL-6 release and glucose uptake in human skeletal muscle. J Physiol. 2003 Jan 1;546(Pt 1):299-305.
• Kramer HF, Goodyear LJ. Exercise, MAPK, and NF-kappaB signaling in skeletal muscle. J Appl Physiol. 2007 Jul;103(1):388-95.
• McKay BR, De Lisio M, Johnston AP, O'Reilly CE, Phillips SM, Tarnopolsky MA, Parise G. Association of interleukin-6 signalling with the muscle stem cell response following muscle-lengthening contractions in humans. PLoS One. 2009 Jun 24;4(6):e6027.
• Psilander N, Frank P,  Flockhart M, Sahlin K. Exercise with low glycogen increases PGC-1agene expression in human skeletal muscle. Eur J Appl Physiol. 02 Oct 2012 [ahead of print]
• Rowe GC, El-Khoury R, Patten IS, Rustin P, Arany Z. PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle. PLoS One. 2012;7(7):e41817. Epub 2012 Jul 24.
• Ruas et al. APGC-1aI soform Induced by Resistance Training Regulates Skeletal Muscle Hypertrophy. Cell, December 7, 2012; 151:1319–1331.
• Steensberg A, Fischer CP, Sacchetti M, Keller C, Osada T, Schjerling P, van Hall G, Febbraio MA, Pedersen BK. Acute interleukin-6 administration does not impair muscle glucose uptake or whole-body glucose disposal in healthy humans. J Physiol. 2003 Apr 15;548(Pt 2):631-8. Epub 2003 Mar 14.

SVSR: Supplement-Drug Interactions, Exercise & Your Pysche, Running vs. O-Lifting vs. Heart Health, N3-to-N6 Ratios, CYP Enzymes, Cannabinoids & Telomeres

The SuppVersity Science Round-Up every Thursday live on Carl Lanore's Super Human Radio -- tune in live at 1PM (EST=  6PM GMT)!

I hope that most of you have already had a chance to listen to yesterday's installment of the SuppVersity Science Round Up on Super Human Radio. In case you didn't, or have been waiting for me to post the link to the podcast (just a reminder: you can always download the latest show, from the navigation bar on the right, where it says: "Physical Culture for your Ears"), I'd suggest you go and download the podcast either now, or after going through today's SuppVersity Science Round Up Seconds.

The "Seconds" are as the name implies no "leftovers", but actually yet another selection from the selection of god knows how many interesting newsbits I usually pile up for the short 1h show, Carl and I are doing every Thursday. I would therefore encourage everyone to do both, listen to the podcast and read the "Seconds" one day later. After all, the things Carl and I discuss on the air won't reappear here, they are "SHR exclusives", so to say ;-)

Apropos, in yesterday's show, the topics we did cover were

• premature ejaculation, and how only two hormones seem to make a difference,  
• peptides as prostate cancer vaccine, and how Harvard scientists build them from scratch,
• supps vs. medications, and how fatal commonly overlooked interactions can be, and
• copper, and why it may well matter than raw milk has 2-3x more than pasteurized milk

and before we go on with the actual "seconds", I must acquit myself of a promise -- the promise to provide you with more information on #3 on the above list.

Supplemental data: Supplement vs. drug interactions

Figure 1: Important supplement drug interactions based on Tsai (2012)

Those of you who have already listened to the podcast will probably be waiting eagerly for the supplemental material with more information about the potential pitfalls with supplement-drug interactions, Carl and I have been talking about on yesterday's show. With some digging, typing, searching, excerpting and formatting on my part, I have actually come up with a quite comprehensive and for people who are not familiar with all the funky drug names, probably even more understandable version (see figure 1) of the tabular overview H.H. Tsai and colleagues from the China Medical University Hospital and the College of Pharmacy at the University of Illinois at Chicago have included in their latest review of the literature (Tsai. 2012).

What I left out are the two pages (!) part on St. John's wort. With 147 drug (!) interaction ranging from "A" as in "amiodarone" to "W" as in "warfarin" and covering almost every drug type from anti-depressants, protease inhibotors, calcium channel blockers, PDE-5 inhibitors (viagra & co), SERMs, proton pump inhibitors, etc.. In view of the fact that these are only the known interactions, it would be easier to list those drugs with which St John's does not conflict, anyway. So, unless you have a study at hand which conclusively shows that St. John's is no problem, I would rather err on the side of caution, than end up in the ER.

Top 5 of the most frequent interactions observed with medication that act on (ranked by frequency, figure in brackets indicates percentage of all drugs in the study; based on Lin. 2012):

1. nervous system (19.6%)
2. cardiovascular system (17.7%)
3. antiinfectives for systemic use (14.7%)
4. alimentary tract and and immunomodulating agents (12.2%)
5. musko-skeletal system (6.4%)

As far as the supplement list in figure 1 goes, the most frequent potential side effect due to supplement-drug interactions affected drugs / supplements that play a role in blood coagulation. Danshen, evening primrose, gingko, glucosamine, white willow bark, garlic, vitamin E, fish oil to name only the most common ones, they all can increase the risk of bleeding not only, but specifically in patients who are taking warfarin (aspirin, ibuprofen, heparin and others were on the list, as well).

"What’s wrong with telling a patient, 'If you don’t hear from us with your lab results a few days, give us a call'? The answer is plenty, if that patient is receiving warfarin therapy. Because warfarin has a narrow therapeutic range and complex pharmacology, insufficient monitoring or errors in dosing can lead to severe and possibly life-threatening bleeding and clotting in patients receiving it." (Bush. 2002)

In view of the "top 5" above, this certainly sounds counter-intuitive, but we are dealing with a practical research bias here. As I mentioned on the air, there is simply an overabundance of research on potential interaction with warfarin, because finding the right dosage and adapting it appropriately is already hard even when there are no confounding variables, so that a sudden supplement-drug interaction and subsequent increase in the risk of bleeding can potentially be fatal (see the quote in the red box to the right)!

Regardless of what medication you may be on, rules that apply for a healthy individual that does not take any medication chronically (not even 'harmless' NSAIDs), don't apply to you! So please for one, follow the recommendation you find on each and every supplement to "talk to your medical practitioner" before you add another 'harmless' supplement on top of the 'harmless' over-the-counter or prescription drugs you are taking.

The Seconds: Interesting news that have been missing from yesterday's show

After this pretty lengthy addendum, let's get to three other items I had actually planned to have on the show, two of them are exercise, while the third one is a health and supplementation... and, when I come to think about it, obviously also diet related news-item:

• Exercise makes you happy and puts an end to the greed for money! That's not exactly the result of a recently conducted study from the Charité in Berlin (Bothe. 2012), but it is more or less what follows from the differential response Bothe et al. observed in their untrained and highly trained subjects to monetary stimuli after they had completed a standardized running exercise (30 min at 60-70 % VO2max, T) or placebo (P).
  

  

  Who would have thought that: Exercise reduces the anticipatory response to monitary incentive delay (MIT) test (Bothe. 2012)

  "Acute exercise was found to influence gain anticipation. In the P compared to the T group a more pronounced anticipation-related BOLD response was found in mesolimbic and mesocortical dopamine-innervated regions like the VS, hippocampus (Hipp) and subgenual anterior cingulate cortex (sgACC). [...] Additionally, several brain structures potentially associated with motor preparation (primary and supplementary motor areas) as well as structures belonging to the ventral (lingual gyrus) and dorsal (cuneus, precuneus) visual pathway showed stronger BOLD responses to gain anticipation in the P group compared with the T group." (Bothe. 2012)

  Moreover, according to the paper which is going to be published in one of the upcoming issues of Medicine and Science in Sports and Exercise, all 43 healthy men between the age of  20 - 32 years who participated in the study showed similar increases in mood (effect size F=11.70).
  
  With both, the beneficial outcome of the positive and negative affect schedule and the decrease in anticipatory signalling (= the greedy "I am about to win!") in the psychological testing session (the so-called monetary incentive delay) in an fMRI brain scanner, being identical it becomes evident that you don't have to be an athlete to monetize (all puns intended ;-) on the beneficial psychological effects of exercise.

• 

  Figure 1: Changes in total lean mass, aerobic fitness, strength (mind the scaling with x10!), right ventricular mass and end-diastolic volume in subjects in the endurance (runners) and strength training arm (O-lifting) of the 24-week study (based on Spence. 2012)

  Changes to the heart (right ventricular) due to exercise are mild, and if anything more pronounced in response to endurance than resistance training! " Left ventricular (LV) adaptation to exercise training has been the focus of 'athlete's heart' research to-date, information regarding right ventricular (RV) adaptation is sparse, due to its complex structure and imaging technique limitations." (Spence. 2012) So scarce, in fact, that this recent study that has been conducted by researchers form the The University of Western Australia, the University of Leeds, a and the Liverpool John Moore's University is the first to take a closer look at the impact endurance or resistance training have on the morphology of the RV.
  
  For their randomized trial, the researchers recruited twenty-three young untrained men.. The men were assigned to either
  
  • endurance training (E; n = 10)  - consisting of a progressively overloaded program of walking/jogging/running, divided into three training phases over the 24-week period, or
  • resistance training (R; n = 13) - with a focus on periodised R program was Olympic weightlifting with incorporated assistance exercises (e.g. deadlift, squat, bench press, overhead press) to develop overall strength and technique
  for a total timespan of 6 months, in the course of which body composition, aerobic fitness, muscular strength, RV morphology (MRI) and function (speckle tracking echocardiography) were continously monitored.
  
  The results Spence et al. are going to publish in one of the future issues of Medicine and Science in Sports and Exercise refute even two pieces of common "knowledge". Firstly, a still totally benign, right ventricular hypertrophy was exclusively observed in the endurance training group, yet not in the heavy lifters who were doing their squats, deadlifts and military presses (by 2.7g following E and by 1.4 g  following R training). Secondly, both strength and size gains were no prerogative of the lifting weight group. Contrary to the increase in total lean mass (+1.3 kg vs. +2.1 kg), the strength increase of +53.8 kg vs. +35.3 kg was yet much significantly more pronounced in the weight lifters.
  
  On the other hand only the endurance training group saw significant statistically improvements in their aerobic fitness level. This correspondence of endurance exercise, mild ventricular hypertrophy and increased fitness levels is unquestionably telling in terms of "how bad" a physiologically enlarged heart where the ratio of left-to-right ventricular  mass remains intact (which was the case in the study at hand), don't you think so?
• Omega-3s, omega-6s, telomere length, CYP enzymes, endogenous cannabinoid and the liver you need all of them to see the complete picture While the epidemiologists are still debating who will and who won't benefit from omega-3 supplementation, those who still care about how our bodies works and why their colleagues over at the epidemiology department are still debating, have made quite some progress as far as the underlying health benefits of rectifying the omega-3 to omega-6 balance are concerned.
  
  
  Why are endocannabinoids problematic? One of the answers is: "They will make you fat!" Basically we have known that forever, but a recent study which tracked the conversion of dietary linolic acid (n-6) to it's endocannabinoid metabolits, 2-AG and anandamide has recently confirmed not just that, but also that the provision of no more than 1% of the total energy of the diet in form of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) can already make a huge difference (Alvhem. 2012). With the addition of the long-chain omega-3s, the rodents in the study had a 8:1 ratio of linolic acid (LA) to long-chain omega-3 fatty acids in their diets. Still much higher than what you will hear is necessary, but sufficient to reverse the overabundance of arachidonic acid, in the phospholipids of liver and erythroctes, and the +200% increase in endocannabinoid levels that had been brought about, when the researchers had increased the linolic acid content of the diet from 1% to 8% of the total energy intake. In view of the fact that the same goes for the increased food intake, feed efficiency, and adiposity the mice had developed on the 60% fat (total) diet with a high linolic acid content, this study - despite being done on rodents - clearly shows that it does not necessarily have to be a 1:1 ratio to grasp major health benefits.
  
  If you get down from  30:1 to 8:1 you've come a tremendous way, already; and guess what: The easiest way to achieve that is to just cut out all seed and vegetable oils as well as processed foods that contain them.
  In a recent review on the differential effects of fatty acids on human metabolism in the Italian journal Medical and surgical pediatrics G. Caramia emphasizes the role of omega-6 derived endocannabinoids:
  

  "[E]ndocannabinoids like anandamide (N-arachidonoylethanolamine) and 2-arachidonoylglycerol [that arise from the enzymatic conversion of linolic acid by enzymes from the cytochrome P450 family at the liver are] capable of mimicking the pharmacological actions of the active principle of Cannabis sativa preparations such as hashish and marijuana (-)-Delta9-tetrahydrocannabinol. They act as true 'endogenous cannabinoids' by binding and functionally activating one or both [of the] cannabinoid receptor present on nervous and peripheral cell membranes." (Caramia. 2012; my emphases)

  Unfortunately, the same enzymes which are responsible for the generation of those endocannabinoids, are also responsible for the conversion of n-3 PUFAs into more potent metabolites of EPA and DHA, which will actually do most of the the vascular- and cardioprotective magic that is commonly ascribed to "fish oil".
  
  And how does all that relate to telomeres?
  
  These competitive effects in turn segue directly into the observations of a double-blind 4-month trial that involved 106 healthy sedentary overweight middle-aged and older adults. The participants supplemented their diets with capsules containing either (1) 2.5 g/day n-3 PUFAs, (2) 1.25 g/day n-3 PUFAs, or (3) a placebo that mirrored the proportions of fatty acids in the typical American diet.
  
  Now, it's not news that this led to decreases in inflammatory markers. I am not going to bore you with those, don't worry!
  
  What is news, and in my eyes very important, is that neither the provision nor the dosage of additional long-chain omega-3s had an effect on telomere length, the only variable that mattered was were the changes in the n-6:n-3 PUFA plasma ratios, which "helped clarify the intervention’s impact: telomere length increased with decreasing n-6:n-3 ratios (p= 0.02)" (Kiecolt-Glaser. 2012).

That's it as far as today's seconds go... you want more? Man, I could certainly give you more, but you know that gluttony was once considered a sin, right? Tomorrow is another day, and if you can't wait, just head over to the SuppVersity Facebook wall, which is always bursting from the seems with the latest tidbits from the realms of health, exercise and nutrition sciences.  

References:

• Alvheim AR, Malde MK, Osei-Hyiaman D, Hong Lin Y, Pawlosky RJ, Madsen L, Kristiansen K, Frøyland L, Hibbeln JR. Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity. Obesity (Silver Spring). 2012 Oct;20(10):1984-94.
• Bothe N, Zschucke E, Dimeo F, Heinz A, Wüstenberg T, Ströhle A. Acute Exercise Influences Reward Processing in Highly Trained and Untrained Men. Med Sci Sports Exerc. 2012 Oct 10.
• Bush J. Preventing errors in your practice. Reducing risks for patients receiving warfarin. Fam Pract Manag. 2002 Jul-Aug;9(7):35-38.
• Caramia G. [Essential fatty acids and lipid mediators. Endocannabinoids]. Pediatr Med Chir. 2012 Mar-Apr;34(2):65-72.
• Kiecolt-Glaser JK, Epel ES, Belury MA, Andridge R, Lin J, Glaser R, Malarkey WB, Hwang BS, Blackburn E. Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial. Brain Behav Immun. 2012 Sep 23. pii: S0889-1591(12)00431-X.
• Spence AL, Carter HH, Murray CP, Oxborough D, Naylor LH, George KP, Green DJ. MRI-derived Right Ventricular Adaptations to Endurance versus Resistance Training. Med Sci Sports Exerc. 2012 Oct 15.
• Tsai HH, Lin HW, Simon Pickard A, Tsai HY, Mahady GB. Evaluation of documented drug interactions and contraindications associated with herbs and dietary supplements: a systematic literature review. Int J Clin Pract. 2012 Nov;66(11):1056-1078.

Exercise News Round-Up: The Latest on Weight Lifting, Steady State, HIIT, Pyramid Training & Co, Their Effects on Body Composition, Leptin, Muscle Morphology & More

Running may be the "original exercise", but there is more to physical culture than that - irrespective of your gender, by the way; HIIT would be one thing, weight lifting the other that must not be missing from your regimen which can yet still benefit from one or another classic cardio session (img womanshealthmag.com).

I must admit that I am a bit lazy today and not really in the mood of writing a lengthy post on circadian rhythms. The weather is awesome and I think I'd better spend the time in the sun recharging the batteries of my circadian clock, than sitting in front of a computer screen.

Since I do know that the former, i.e. the good weather won't apply to all of you and that reading these posts does not take anywhere as long as writing them, I will yet put together the promised post on "exercise news" - and I can tell you there is half a dozen of them, such as

• liver health, aerobics and strength training
• no leg-based cardio on leg day
• aerobics alone won't cut it
• intramuscular arguments in favor of HIIT 
• reverse or classic pyramid about equally effective
• intense exercise has leptin plummeting

You see, more than enough for one day, so we better get right down and dirty... ah, I mean, sweaty - yeah, sweaty ;-)

• Putting weights into the equation squeezes the fat out of your liver and belly In a recently conducted study into the effects of long-term exercise on the weight and fat loss in post-pubertal overweight adolescent with non-alcoholic fatty liver disease, the combination of aerobic and resistance training was "more effective in significantly improving noninvasive biomarkers of NAFLD that are associated with the highest risk of disease progression in the pediatric population" (de Piano. 2012). The main facts about the program
  

  

  Figure 1: Only combined aerobic and resistance training offers the body recompositioning effect we are all looking for: more muscle, less fat - and that works optimally, only, if your liver is still fully functional (de Piano. 2012)

  • one-year intervention + dietary counseling
  • 60min of personalized aerobic training, or
  • 30min aerobic + 30min resistance training
  • performed three times a week

  In the abstract of their study the scientists unfortunately fail to point out that the additional resistance training, which consisted of a standardized, progressive full-body training with 3 sets of 6-20 reps (depending on exercise) had the extra bonus of building more muscle and cutting more body fat than the less versatile three times pe -week 60min aerobics program.
  Moreover, the fact that only the participants in non-NAFLD, "just obese" control group were able to increase their muscle mass, goes to to show you, how important an optimally functioning liver actually is, when it comes to building muscle, losing weight and staying healthy.

• 

  Image 2: If you train legs with a similar volume as Arnold & Franco did, back in the day, you don't want to and probably also don't have to do any additional cardio before or after your workouts.

  Doing 30min of cardio on the elliptical reduces the number of reps you will be able to perform on a subsequent leg workout, but the bench press performance won't suffer. That's the very unsurprising result of a hitherto unpublished dissertation by Jeremy Tan from the University of California in Fullerton (Tan. 2012).
  Tan had recruited twelve young men who had completed four trials in random order. In two of those trials the guys performed 30min on the elliptical machine at 70% of their age-predicted (not measured!) HRmax followed by either 3 sets of back squats or bench presses performed to failure at 75% of their predetermined 1RM - not exactly an "Arnold-esque training volume, anyway, right (see image 2)?
  Bottom line: Better don't do a lengthy cardio workout before your leg training - but also: Don't believe the bro-scientific myth that 30min of cardio were so exhausting (systemically) that you could not train a body part that was not heavily involved in the cardio session (in this case the upper body), afterwards.

• 

  Figure 2: Cardio alone won't change your body for the better and the changes in CRP and leptin are not statistically significant (data expr. rel. to baseline; based on Bijeh. 2012)

  Aerobics alone won't really cut it and this goes not just for advanced male athletes, but even for middle aged (42y) women (BMI 25-27) who have never trained before. At least this is what the results of Bijeh, Hosseini and Hejazi from the University of Mashhad (Iran) would suggest, because even after 6 months with 3x 60 minutes (55-65 HRmax) none of those body composition parameters women are usually trying to improve, when they are taking up an exercise regimen did come about (Bijeh. 2012): Other than a minimally, but statistically non-significant reduction of body fat a prominent but not significantly different (P=0.2 for the variation) increase in leptin levels in the exercise group were the only "beneficial" changes the "workouts" brought about.
  Plus, in how far the increase  in leptin actually is a good thing does still remain to be seen, also because the CRP levels (inflammatory marker) in the training group increased (likewise not statistically different) and the allegedly statistically significant difference in the waist to-hip ratio (-0.01 in the aerobics group vs. no change in the sedentary control) of the women is so small against the standard deviations of the respective value that I am not sure about how significant it really is - regardless of what ANOVA, a program that's often used to do the statistics on data like that, say.
  Bottom line: If for whatever reason you can only do light "classic cardio" there is no way it will make a difference if you don't combine it with a sound dietary regimen.
• HIIT and classic endurance training equally effective in increasing muscle microvascular density The latest study from the UK shows that HIIT is more and more being accepted by researchers as a viable alternative to the classic aerobic training programs. In a 6-week intervention, Cox et al. assigned 16 young previously sedentary men (age 21±0.7 yrs, BMI 23.8±0.7 kg/m²) randomly to either 40-60 min cycling at ~65% VO_2peak, 5 times per week (ET), or a much less time-consuming HIIT protocol that comprised 4-6 Wingate tests, 3 times per week (HIIT).

  

  Image 3: While the study used the classic wingate test protocol with a stationary bike you can also do 30s all-out sprints, use a spinning bike or whatever else allows for maximal efforts and temporary exhaustion without you hurting yourself or the equipment breaking down (or both ;-)

  Other than most of their colleagues the scientists were yet less interested in the beneficial effects this exercise would have on VO2Max, let alone simple weight loss, but analyzed muscle samples for their microvascular endothelial eNOS and NOX2 content (indicative of the vascularization) and the actual morphological capillarization of the muscle by quantitative immunofluorescence microscopy. Whole body insulin sensitivity, arterial stiffness, and blood pressure were also assessed.
  The results showed that both protocols were equally effective in inducing the adaptive changes in microvascular capillarization and NOX2 expression, while the short intense exercise bouts during the HIIT protocol yielded 12% greater increases in eNOS content (ET 14%; P<0.05, HIIT 36%; difference p < 0.05).
  Now, eNOS is actually better known for its preventive role in CVD (and hypertension), but its negative correlation with body fat levels (higher eNOS <> lower body fat - note: this is almost certainly not a causal relationship(!); cf. Hickner. 2006), its central role in the maintenance of exercise capacity (Lee-Young. 2009) and its putative role the maintenance of mitochondrial function and integrity into the old age (Chanséaume. 2009) it should be obvious that time-efficiency is not the only thing that speaks in favor of HIIT, here. 

• 

  Figure 3: Strength gains (no idea what the scientists mean by "compression", just think about it as the effect size) of 6 weeks, 18 lifting sessions, employing a classic or reverse pyramid loading scheme on chest (bench press), quads (leg extension) and biceps (curl) strength (adapted from Bostani. 2012)

  No statistical significant differences in strength gains between classic and reverse pyramid While Bostani and Shariati did in fact not find statistically significant differences between the strength gains of their physically active, but "non-athlete" (sic!) study participants (N=10 for the two active and the control arm) a closer look at the data in figure 3 to the right does still reveal that it could make a difference, whether increase the weight from set to set (regular pyramid) or decrease it from set to set (reverse pyramid) - at least for your extremities, with the quads responding more favorable to the reverse pyramid and the biceps to the classic pyramid training.
  If the study was not so hilariously poorly described and the translation so sloppy, I would love to use these insights for a recommendation on how to train.
  In the absence of set number, reps and everything else that would be necessary, I can yet just say that this appears to confirm my personal experience, which tells me that you have to hammer your legs to grow and get stronger, while the classic pyramid with it's generally lower overall volume matches the "hit it hard and short" approach that appears to work best for biceps, in the longer run.

• 

  Figure 4: Eight weeks of intense exercise in the presence of a negative energy balance (as evidenced by the weight loss) take their toll on leptin levels, it is yet not sure for whom that's a bad thing (data based on Ferdosi. 2012)

  Intense exercise will make make your leptin levels drop and that irrespective of whether you do endurance training, strength training or both! That's the long and short of a study that has been published in the latest issue of Procedia - Social and Behavioral Sciences (Ferdosi. 2012), which did not even find a quantitative difference between the effects 8 weeks of 3 session of either 40 minutes (increasing from 25 in the first two, to 35min in weeks 3-6 and 40min in weeks 7-8) cycling at 75-85% HRmax (aerobic), a standard full-body workout (resistance) or both strength and aerobic training concomitantly (concomitant).
  It is thus obvious that done at a high enough intensity and in the presence of a negative energy balance, the same endurance exercise that elicited an increase in leptin in the Bijeh study (remember, this was more of a leisurely walk and without a build-in progression) will decrease leptin levels significantly.
  Now, that's great if you got a lot of fat to lose and are leptin resistant anyway, if you are yet lean already (with a BMI of 29kg/m² the healthy but untrained 48 male study participants, here, were not exactly ripped, but far from being obese) this can become a problem that could not just forestall fat loss, but could precipitate endocrine imbalances - and that's nothing that can only happen to women, in whom it usually manifest as amenorrhea (Christo. 2008)

That's it for today, but since I know you will be asking, yes, there I will catch up with the circadian rhythm series and yes I understand that the last item of today's installment has left at least some of you very dissatisfied. So, yes, I will finally address the issue of amenorrhea (but also hypogonadism in men) in an individual post, although I still don't have the clearcut "do this, don't do that" solution to the problem, I wanted to find before, I write the respective post... ah, and in case neither of those things does interest you, don't worry there will of course be other posts in the next days, as well ;-)

References:

• Bostani M, Shariati M. The Comparison of Between the Effects of Two Training Methods on Dynamic Strength of Non-Athletes Males Procedia - Social and Behavioral Sciences. 2012; 46: 417–420
• Bijeh N, Hosseini A, Hejazi K. The Effect of Aerobic Exercise on Serum C - Reactive Protein and Leptin Levels in Untrained Middle-Aged Women. Iranian J Publ Health. Sep 2012; 41(9).
• Chanséaume E, Morio B. Potential mechanisms of muscle mitochondrial dysfunction in aging and obesity and cellular consequences. Int J Mol Sci. 2009 Jan;10(1):306-24. Epub 2009 Jan 13. 
• Christo K, Cord J, Mendes N, Miller KK, Goldstein MA, Klibanski A, Misra M. Acylated ghrelin and leptin in adolescent athletes with amenorrhea, eumenorrheic athletes and controls: a cross-sectional study. Clin Endocrinol (Oxf). 2008 Oct;69(4):628-33. Epub 2008 Mar 10.
• Cocks M, Shaw CS, Shepherd SO, Fisher J, Ranasinghe AM, Barker TA, Tipton KD, Wagenmakers AJ. High intensity interval and endurance training are equally effective in increasing muscle microvascular density and eNOS content in sedentary males. J Physiol. 2012 Sep 3.
• de Piano A, de Mello MT, Sanches PD, da Silva PL, Campos RM, Carnier J, Corgosinho F, Foschini D, Masquio DL, Tock L, Oyama LM, Oller do Nascimento CM, Tufik S, Dâmaso AR. Long-term effects of aerobic plus resistance training on the  adipokines and neuropeptides in nonalcoholic fatty liver disease obese adolescents. Eur J Gastroenterol Hepatol. 2012 Aug 27.
• Ferdosi MH, Asad MR. The Effect of Endurance, Resistance and Concurrent Trainings on Plasma Leptin Levels of Non-Athlete Males. Procedia - Social and Behavioral Sciences. 2012; 46: 311–315.
• Hickner RC, Kemeny G, Stallings HW, Manning SM, McIver KL. Relationship between body composition and skeletal muscle eNOS. Int J Obes (Lond). 2006 Feb;30(2):308-12.
• Lee-Young RS, Ayala JE, Hunley CF, James FD, Bracy DP, Kang L, Wasserman DH. Endothelial nitric oxide synthase is central to skeletal muscle metabolic regulation and enzymatic signaling during exercise in vivo. Am J Physiol Regul Integr Comp Physiol. 2010 May;298(5):R1399-408. Epub 2010 Mar 3.
• Tan J. Acute effects of lower body aerobic exercise on lower body and upper body resistance training workshops. California State University. 2012. Publicatin no. 1513816.

Gear for Your Ear! Fast & Slow Songs Can Both Speed You Up on the First 800m of a 5K. Plus: Calm Songs Increase Vagal Tone & CNS Activity, Fast Songs Spike You Up!

One of the runners in the study (original image from Bigliassi. 2014)

Music-related interventions have been widely used in sports and exercise; and despite the fact that you've read about respective studies here at the SuppVersity before I thought the publication of a recent study from the Center of  Physical  Education  and  Sports at the State  University of Londrina was a good reason to address the issue once more.

It goes without saying that there are numerous external factors which determine the optimal workout music, as well as how and when to use it. Against that background, it should be obvious that the following study outcomes are not entitled to be "universal".

HIIT workouts probably require different music than LISS workouts

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.

Just think about personal preferences, for example. A classic fan is probably not going to work out listening to music by Dr. Dre... well unless he's boxing, maybe! A thought that takes us to another important factor: Who knows if the same music that helps you to lift harder will also make you run longer and vice versa?

Why is this important? Well, in the study at hand, the exercise of choice was running. An exercise type the authors considered particularly fit for their study, because it's "a common physical exercise worldwide, due to its own features (low cost and availability for practice) and high aerobic benefits". Moreover, previous research has demonstrated that music can aid running by acting in parallel to exercise. It was thus logical to try to expand our still incomplete knowledge of the effects of music on exercise performance - albeit this time in a long term study with many degrees of freedom:

"Acoustic gear" - (Re-)Read my previous research summary from 2013 | go ahead

"This study was divided into 3 stages that were performed in the course of 30 weeks. In the first stage, all participants were interviewed separately before the experiment. At this time, they gave their anthropometric measures (weight and height), personal information (age, time of continuous training, number of running competitions and training volume), and answered the Eysenck personality questionnaire (EPQ), which gives possible stratifications according to personality, checking whether music could act differently in accordance with personal features."

The subjects had to select 30 motivational songs (10 – slow speed tracks, 10 medium speed tracks and 10 fast speed tracks) and the only provided information was to select songs capable of increasing their vigor and motivation to accomplish a severe aerobic physical exercise (when the number of tracks did not achieve the required number, they were asked to choose other songs to complete the playlist). The song stratification was performed initially via specific software solutions and thereafter by the examination of an expert musician.

How did the tests look like? The actual exercise tests consisted of 5 physical tests. Each of them involved a 5km run which was to be completed as fast as possible. The time between the tests ranged from 3-7 days. All tests were performed at the same time of the day.

In the second stage, all participants were called in to the laboratory, where they had to fill their questionnaires and to perform a neuroimaging test involving listening to a variety of songs. This technique was conducted to demonstrate how self-selected songs could act in emotional areas of the brain and how the subsequent activation of specific brain correlates with physiological assessments and the effectiveness of motivational music in inducing emotional consequences and downstream metabolic / ergogenic effects. All-in-all, the present study evaluated five experimental conditions:

• PM: Motivational songs, ranging from 110 – 150 bpm, applied before 5 km of running; 
• SM: Slow motivational songs, ranging from 80 – 100 bpm,applied during 5 km of running;
• FM: Fast motivational songs, ranging from 140 – 160bpm, applied during 5 km of running; 
• CS: Calm songs condition – calm songs applied after 5 km of running; 
• CO: Control condition, without intervention. 

The CO trial was considered the baseline, all other trial were compared to. The CO trial was performed in a silent environment to allow the subjects to focus exclusively on their body signals.

Figure 1: Parasympathetic tone during recovery (in min on x-axes) after control trial (no music)
vs. calm music (left) and motivational music (left | Bigliassi. 2014)..

As you can see the 15 amateur runners (24.87 ± 2.47 years;78.87 ± 10.57 kg; 178 ± 07 cm; 24.92 ± 2.79 kg/m²; 4.85 ± 1.85 years of training; 7 ± 3.49 weekly training hours; 5.67 ± 2.85 competitions) had a significantly reduced parasympathetic tone during recovery, when they trained with motivational music (low parasympathetic tone = "spiked up").

Slow or fast? Does it matter or is it just about music in general?

The calm music (Figure 1; left), on the other hand, led to an increase in parasympathetic tone, as you would expect to see it in someone who meditates or "chills" as the kids like to call it ;-) Now that sounds great for weed-heads, but from a performance perspective it was obviously as detrimental - interestingly, though, not much more detrimental than not listening to music at all.

Figure 2: Effects of control (CO), motivational (PM), slow (SM), fast (FM) and calm (CS) music / songs on fatigue, tension, vigor, and 5k times (in s) - the effects are visible, but not significant (Bigliassi. 2014).

The most important and yet unquestionably somewhat disappointing observation Bigliassi et al. made is however the statistical non-significance of the the visible time-differences in Figure 2. 

If we investigate, why the visible advantage was "no advantage" in the strict sense (i.e. it was statistically non-significant), we will obviously get back to what I said initially: Inter-individual differences and preferences loom too large to make any generalizable recommendations with respect to the optimal workout music.

Performance ain't everything: What could be of interest in future studies, are the recovery effects of an increase in vagal turnus (=pa- rasympathetic acti- vity) after 5 km of running with calm music (P < 0.05) - it's not ergogenic, but could be a great tool to calm down after an intense strength training workout; and thus probably even to speed up recovery and re- duce the likelihood of overtraining.

Bottom line: The scientists are right when they highlight that "the present study accomplished a very real training situation (5 km of running – open space and self-selected songs), making the present findings useful for further applications" (Bigliassi. 2014). Accordingly, the prefrontal cortex activity the researchers observed and the positive emotional consequences they detected via autonomous system analyses have a similar real-world relevance.

Whether this is also true for the significant performance increases on the first 800 meters in the slow and fast music trials is questionable. Personally, I suspect that some of you will benefit from the fast, while others from the slow songs. This conclusion would also be supported by the significant inter-individual differences in the study at hand.

So, if there is any general take home message from the study at hand, it would probably be the notion that there is a "high probability of improving running performance when music [is] applied (SM: 89%; FM: 85%; PM: 39%)," at all - which one is the "best", on the other hand, will depend on the individual, as well as the type of exercise | comment on Facebook!

References:

• Bigliassi, Marcelo; León-Domínguez, Umberto; Buzzachera, Cosme F.; Barreto-Silva, Vinícius; Altimari, Leandro R. "HOW DOES MUSIC AID 5 KM OF RUNNING?" Journal of Strength & Conditioning Research: Post Acceptance: July 15, 2014.