0.3g/kg Bicarbonate Will Make Trained Cyclists Last 4.5 Min Longer (+9%) During Std. High Intensity Cycling Tests

Don't forget that cyclists are not the only group of athletes who can benefit from bicarbonate supplementation. Strength trainees who spend hours in the gym and train at high intensities will also benefit!

I know that most of you are into resistance not endurance training. So, before I even get into the discussion of the experimental procedures and the results of the latest study from the Institute of Sports and Preventive Medicine at the Saarland University in Saarbrücken, Germany, I would like to point you to an older SuppVersity article which indicates that bicarbonate supplementation is able to Up Your Squat (+27%) & Bench Press (+6%) Within 60 Min" (read more).

Now that you've hopefully put away your prejudices against "that endurance supplement", let's get to the previously mentioned study by Florian Egger, Tim Meyer, Ulf Such, and Anne Hecksteden (thanks to Conrad P. Earnest for bringing this to my attention).

You can learn more about bicarbonate and pH-buffers at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

HIIT + Bicarb = Perfect Match

Bicarb Buffers Creatine

Beta Alanine Fails to HIIT Back

To investigate the effects of BICA supplementation on performance during prolonged, high-intensity cycling to exhaustion in well-trained athletes, the scientists from the Saarland University recruited 6 male and 5 female "well-trained" cyclists (mean ± SD: age 24±8 y, BMI 21.3±1.7, VO2peak 67.3±9.8 ml/kg/min - the VO2peak value tells you that they were fit ;-).

In a double-blind, randomized cross-over design, the subjects underwent two stepwise incremental exercise tests and two constant load tests (with two phases) on an electrically braked cycle ergometer (Excalibur Sport, Lode, Groningen, The Netherlands).

Figure 1: Schematic representation of the general design.Time interval between tests is specified in days (d). Data are presented as means ± standard deviation respectively, with minimum (min) and maximum (max) values (Egger. 2014).

As the overview of the study design in Figure 1 tells you, each test type was completed twice. Once after the ingestion of 0.3 g/kg sodium bicarbonate (yes, that's roughly 24g for someone who weighs 80g and should not be consumed too fast, because otherwise it may trigger diarrhea) or a placebo supplement in form of 4 g sodium chloride that was chosen to make sure that any benefits that were observed were due to the natrium, not the bicarbonate content of sodium bicarbonate.

There is relatively little sodium in NaHCO3: Sodium bicarbonate, baking soda or NaHCO3, as a chemist would say is a molecule that contains natrium (or sodium as the Americans say) and bicarbonate. It has a total molar mass of 84.007 g/mol. This means that ~73% of the sodium bicarbonate powder you ingest are actually bicarbonate and only ~27% are sodium. The whopping dose of 20-30g of bicarbonate that is usually used in studies will thus deliver "only" 5.4g-8.1g of sodium. That's still plenty, but as you know for a trained athlete who's sweating like a pig during his workouts and may be losing up to 30g of sodium in his sweat, it's not a problem and can in fact be a performance enhancing blessing (see previous article on the dangers of low sodium diets in athletes).

Both the plain salt and the sodium bicarbonate were solved in 0.7 l water. The outcome measures were simple: Only if the subjects were able to pedal significantly longer until they were exhausted in the standardized constant load test, sodium bicarbonate could be considered to have practically relevant performance enhancing effects (maximum performance in the stepwise incremental exercise test, i.e. maximal workload and VO2peak were used as secondary outcomes).

Figure 2: Blood lactate (BLa) concentrations after ingestion (post drink) and during constant load tests (mean ± SD) for the BICA and placebo trials (Egger. 2014)

The other parameters the scientists measured, i.e. the blood lactate [BLa], pH, and bicarbonate concentration, were merely used determine the mechanisms for the potential improvements in exercise performance.

Speaking of auxiliary measures, if you take a look at Figure 2 you will see that the blood pH dropped significantly right after the ingestion of the bicarbonate supplement and remained "low" throughout the trial and afterwards. An observation that does not come unexpected. Previous trials have after all shown that it's the ability of bicarbonate to blunt the high-intensity exercise related perturbations in both blood and muscle acid-base that keeps the maximal work rate up and leads to performance increases compared to placebo supplements.

Bicarbonate Serial Loading! Don't forget that you can reduce the side effects by repeatedly using smaller quantities of sodium bicarbonate aka "serial loading" (read more). Personally, I would expect that this procotol turns the acute performance enhancer into a permanent ergogenic you can use on both on and off days. Unfortunately, a corresponding study that would prove my hypothesis has not yet been conducted.

These performance decrements are caused by the accumulation of hydrogen ions (H+) in the myoplasm and their detrimental effects on myofilament interaction, glycolytic flux and sarcoplasmatic reticulum function. As Egger et al. point out

"[t]he ability of the body to prevent or delay these force limiting processes is determined by the capacity of its intrinsic buffering systems, which counteract the accumulation of H+ both inside and outside the cell," (Egger. 2014)

which explains why the benefits of both beta alanine (which increases the intra-cellular buffering capacity) and bicarbonate are most pronounced in athletes competing in high intensity sports.

Figure 3: Time to exhaustion and maximal workload (total) and maximal workload at the individual anaerobic threshold (IAT) during the bicarbonate and placebo trials (Egger. 2014).

Apropos ergogenic effects: I already gave it away in the headline. The consumption of the bicarbonate supplement lead to immediate increases in the time to exhaustion with 49.5 ±11.5 min being the maximum in the bicarbonate and 45.0±9.5 min being the maximum in the placebo condition.

The maximal workload in the stepwise incremental tests (BICA: 341±66 W; placebo: 339±67 W) and workload at IAT (BICA: 234±5.5 W; placebo 233±5.7 W), on the other hand, did not differ significantly.

Bottom line: In the end, the study at hand confirms what we already knew. Sodium bicarbonate is one of the few supplements with instant ergogenic effects. In that, these benefits are particularly pronounced, when it comes to high volume + high intensity exercises (in this case high volume means cycling for a comparatively long time).

Don't forget that serial loading, i.e. taking smaller amounts of NaHCO3 spread repeatedly, can reduce the side effects without compromising the benefits of sodium bicarbonate supplementation | learn more

Both of these qualities distinguish sodium bicarbonate from beta alanine which acts as an intra-cellular buffer, only, has to be taken for at least two, better four weeks and provides significant performance benefits of 2.85% on average only on exercises that last for 60-240s (Hobson. 2012).

Thus, in spite of the fact that you can obviously use both (see "Beta Alanine and Baking Soda (NaHCO3), a Synergistic Duo for 4-min All-Out Sprints Even in Highly Trained Athletes?" | read more), I personally think that sodium bicarbonate is the more powerful acid buffer for athletes... but as you know, I am willing to accept if you have a different opinion - as long as it is substantiated | Make yourselves heard on Facebook!

References:

• Egger F, Meyer T, Such U, Hecksteden A. "Effects of Sodium Bicarbonate on High-Intensity Endurance Performance in Cyclists: A Double-Blind, Randomized Cross-Over Trial". PLoS ONE 9.12 (2014): e114729.
• Hobson, Ruth M., et al. "Effects of β-alanine supplementation on exercise performance: a meta-analysis." Amino acids 43.1 (2012): 25-37.

Reduced Exertion High Intensity Training - A Minimalist 2x20s HIIT Protocol For The Male Convenience Generation.

Image 1: Looks like humans are not the only lazy creatures, in these days of unhealthy convenience.

Laziness, it seems, is utterly human. If you look around, these days, it appears as if we were genetically programmed to be bone idle. And, from an evolutionary perspective, we may actually be. After all, moving around, hunting and gathering was an obligatory part of our lives in 99% of the human history. It was thus only consistent that our genes would tell us to sit down at the fireplace and relax, once we had found enough to eat on a given day... (un-)fortunately things have changed since those early days. Not only have we moved out of our caves, we have also found ways to radically reverse the ratio of activity to inactivity in our lives.

"Convenience" is the buzzword of the modern western civilization and the obesity epidemic is its unwanted consequence.

A consequence, which is yet by no means inevitable. After all, we all know that getting our behinds off our couches and into the gym, and setting the dietary recommendations of the (fast-)food industry, ahh... pardon, the government at naught would solve the problem, if ... yeah, if there was not this aforementioned genetically programmed laziness that makes the couch so much more appealing to us than the hard benches in the gym...

Sacrifice 30min per week of your TV-time and live to see your grandchildren graduate

A recent study from scientists from the United Kingdom does yet show that you could still spend more than enough time in front of your beloved television set, if you just performed what what Richard S. Metcalfe and his colleagues from the United Kingdom call the "minimal amount of exercise for improving metabolic health" (Metcalfe. 2011) - a 3x per week 10min exercise regimen with no more than two (yes, only 2x!) all-out sprints.

Figure 1: Outline of the training protocol, the black bars indicate all-out sprints at a breaking force equivalent to 7.5% of the individuals body weight (directly adapted from Metcalfe. 2011. Fig. 1)

As you can see in the outline of the experimental protocol, the 29 healthy and normal-weight, but sedentary young (~23y) men (n=13) and women (n=16) did not even have to start with 2x20s sprints. They rather built up to it, by starting out with a single 10s all-out cycle-ergometer sprint at a braking force equivalent to 7.5% of their body weight in the first week of the 6-week study period and built their exercise capacity from there.

Image 2: "Cardio" does not have to be steady state.

Note: If you have not read my previous blogposts on HIIT, you may have missed the information that interval training (not necessarily at the maximal intensity, though) is suitable for everyone - even heart disease patients (cf. Interval, not Steady State Aerobics is the Way to Go - Even for Patients with Myocardial Infarctions!). This has been confirmed only recently by Neil A. Smart et al. who found that "[i]ntermittent exercise may improve functional capacity [of congestive heart failure patients] to a greater extent than continuous exercise" (Smart. 2011) - and that despite the fact that both continuous (30min), as well as interval training (60min, 1 min cycling, 1 min rest) were performed at the same low intensity.

The rest of the 10-min exercise sessions, the subjects were pedaling along at 60W, which is about as much as it takes so that you do not fall off the bike, because of the lack of resistance that is required to stabilize yourself on the bike. The latter would have been tragic, at least if you are a man, because that would have counteracted the surprisingly (not for who has read about the magic of HIIT here at the SuppVersity before) profound effects this regimen, for which the scientists coined the name "reduced exertion high intensity training" (REHIT), had on the glucose homeostasis of the male subjects.

Figure 2: Changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test in men and women after 6 week of "reduced exertion high intensity training" (data calculated based on Metcalfe. 2011)

As the data in figure 2 shows, the statistically more than significant decreases in the area under the glucose (-12%) and insulin (-39%) curve (AUC) measured during an oral glucose tolerance test was exclusive to the 13 male participants - and that despite the fact that both, male as well as female study participants exhibited similar improvements in their individual VO2Max (+15% in men; +12% in women).

(RE)HIIT only for men?

As far as the underlying reasons for these gender differences are concerned, the scientists are pretty much at a loss, stating that this could be due to "the low statistical power of our study, with only eight female subjects performing the REHIT", " differences in metabolic perturbations during the brief high-intensity cycle sprints",  and the 3-day delay after the last HIIT session before the glucose tolerance test was done (as a SuppVersity reader you will be familiar with the notion that the "anabolic barn door" is wide open for 24-48h), so that "insulin sensitivity was improved in female subjects at an earlier time-point". Now, I do not want to sound like a himbo, but I would say that another observation the scientists made, provides a much better explanation:

[...] we observed that some of the female volunteers struggled with the transition from 60 W to the all-out sprints, and were unable to substantially increase their pedal frequency, and thus their power output during the sprints. This may have increased the aerobic contribution to energy supply and reduced glycogen depletion.

In other words, what was supposed to be a sprint turned out to be a sluggish ordeal. The slightly, but statistically significantly higher rates of perceived exertion (+10%) in the female study participants corroborates the assumption that the women simply did not burn enough glycogen. If we do now also consider the results of a 2008 study by Hagobia et al. who report that

[...] in women, exercise altered energy-regulating hormones in a direction expected to stimulate energy intake, regardless of energy status. In men, the response to exercise was abolished when energy balance was maintained.

It appears obvious that an increase in pedaling frequency by adapting the resistance to the individual fitness levels and dietary controls may be necessary to render this minimalist "REHIT" protocol productive for the fairer sex.

Figure 2: Comparison of changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test subsequent to 6 weeks of REHIT, or 10 months of "classic cardio" exercise, or dietary intervention (data calculated based on Metcalfe. 2011 and Dengel. 1996)

The comparison of this 6 week exercise program with the results of a 10 months intervention program in likewise healthy sedentary, but older men (45y) who exercised 3x a week for 40min (steady state) at 75-85% of their maximal heart rate, goes to show that it would well be worth making the REHIT protocol work for women, as well (Dengel. 1996). After all, the steady state endurance protocol in the Dengel study was not only four times more time-consuming (plus, the intervention period was 6.6x longer) than the modified HIIT protocol in the Metcalfe study, it also failed to improve the glucose response to the oral glucose tolerance test and produced less pronounced improvements in insulin sensitivity (cf. insulin AUC in figure 3). The mild caloric reduction (-300-500kcal/day) that was imposed on another group of the study participants, on the other hand, yielded similar reductions in glucose and insulin AUCs as the REHIT protocol in the Metcalfe study that was accompanied by a body weight reduction of ~10%, a reduction in body-fat of -5.8% and essentially no loss in fat free mass!

Note: Unfortunately, Metcalfe et al. did not measure the body composition of the study participants. In view of the results of the Whyte study (Whyte. 2010), I cited in the Intermittent Thoughts on Healthy Weight Loss, where the participants lost -2.4cm of their allegedly obese bellies within no more than 2 weeks of doing HIIT, as well as the well-established correlation between insulin resistance and the size of your beer-belly, it is very well possible that the male participants in the Metcalfe study will have lost some body fat doing no more than 8.67 minutes of all out cycling spread across 18 training sessions in 6 weeks... and if they didn't their diet probably was still too convenient ;-)

The (in-)convenient truth about your future

Taken together the results of these studies suggest that a) steady state aerobic exercise is pretty pointless, b) even a minimalist HIIT regimen goes a long way, as long as c) you really hit it hard and d) adhere to your regular (hopefully non-convenient) diet, or even better e) introduce a slight calorie deficit. In other words, without at least some "inconveniences" as far as nutrition and exercise are concerned, chances are that YOU will either remain or become one of the 34,004,946 obese human beings that are now populating a planet where the US alone spend 1,550,566$ per day on the detrimental health consequences of the"convenience" of its citizens (data from Obesity Statistics).

Leucine Only Tops Ergogenic Effects of BCAAs: Increased Alanine Cycle Activity Spares Muscle Glycogen, Boosts Endurance Performance - BCAAs Have Opposite Effect

Alanine is the liver's favorite gluconeogenic amino acid and leucine appears to increase its usage.

Being among the first to learn about the "Glucose-Repartitioning Effect of Iso-Leucine" in February 2013 (read up on it), you, as SuppVersity reader, belong to the selected few who know that valine and isoleucine may be more than unnecessary props in the leucine-powered BCAA show. With the recent publication of a rodent study from the University of Sao Paulo in Brazil (Campos-Ferraz. 2013), however, it looks as if you had to revise your perspective on the purportedly auxiliary BCAAs - at least, with respect to their ability to reduce fatigue, and muscle and liver-glycogen degradation, in trained rats and possibly (!) humans.

So what did the Brazilian researchers do?

Basically, the idea Campos-Ferraz et al. had in mind, when they came up with their 8 week exercise + 2 week supplementation protocol (see Table 1) was to ...

Table 1: Exercise progression; suppl. was initiated in w7 after lactate test

"evaluate effects of the use of supplementation with leucine or a mixture of BCAAs in trained rats submitted to an exercise-induced protocol of glycogen depletion.

Furthermore, we attempted to investigate muscle and liver biochemical parameters that were not performed in the previous study in order to elucidate the role of BCAAs in glycogen depletion. " (Campos-Ferraz. 2013)

In other words: The researchers wanted to find out whether or not leucine would exert identical, less or more pronounced effects on muscle glycogen use and endurance performance in rodents that the full spectrum of branch-chained amino acids, i.e. leucine, valine and isoleucine.

Contrary to what bro-science and the shiny ads of the supplement industry are suggesting, the scientists' fundamental hypothesis was that the BCAAs supplementation would impair the rodents endurance capacity, because the branched-chain amino acids would be used in muscle to yield acetyl-CoA. This, in turn could reduce the activity of the glucose-alanine cycle, by which the muscles are supplied with alanine-derived glucose from the liver and (once the BCAAs got burne) result in an earlier onset of fatigue.

BCAAs are "glycogen depleters"?!

If you take a look at the data Campos Ferraz et al. gathered in the testing sessions at the end of the supplementation period, in the course of which the rats received an oral gavage of 166mg/kg per day (in human terms this would be ca. 3-3.5g per day) of BCAAs or leucine, it is quite obvious that the  the leucine group had a significantly lower muscle and liver glycogen degradation ratios than the BCAA group.

Figure 1: Liver & mucle glycogen degradation and time to exhaustion (expressed relative to placebo); muscle TCA intermediate content and enzyme activity / concentration (Campos-Ferraz. 2013)

Compared to the placebo group, only the ratios were different.  While the placebo group had the lowest liver glycogen use and a high muscle glycogen use, the supplemental leucine induced a shifted from muscle to liver glycogen and did thus exert muscle specific glycogen sparing effects.

As the researchers point out, these observations stand in line with their original hypothesis: Leucine can spare a significant amount of muscle and liver glycogen and thus produce a highly significant increase in resistance to exhaustion compared to the mixture of BCAAs (P<0.001).

This is not the first study to cast a bad light on BCAA supplementation. As a SuppVersity veteran, you will remember my November 2012 article "Chronic High Dose BCAA Supplementation Reduces Endurance Performance by 43%" | read more, as well as the more recent investigation into the  "Neurotransmitter Depleting Effects of Branched Chain Amino Acids (BCAAs) and Their Potential Ergolytic, Anxiogenic & Depressive Downstream Effects" | read more.

If we compare the endurance performance of the leucine rodents to that of the placebo group, this does yet cast a slight shadow on the overall image of the glorious ergogenic, and, even more so, the purported performance enhancing effects of BCAAs. Despite measurable differences in the time to exhaustion, the actual endurance increase in response to the leucine supplement is relatively small.
 
If you take another look at the data in Figure 1 you will probably notice the significant increase in TCA cycle intermediates (citrate and malate) in the BCAA group. These changes provide further evidence that the provision of all three branch-chain amino acid emphasized the use of glucose as a main substrate to sustain the endurance activity.

"Mouse vs. man": Can we ignore the differences in BCAA metabolism?


At this point, it may however be about time to point out that the activity of the BCAA catabolizing enzyme branched-chain keto acids dehydrogenase complex (BCKD) in humans is quite different from that in rats.

"In the latter [the rat], liver BCKD is almost completely unphosphorylated (activated) in basal state, making it possible to metabolize more rapidly BCKA from the portal blood; in humans, BCKD in liver is normally phosphorylated (inactivated) in order to spare BCAAs for protein synthesis." (Campos-Ferraz. 2013)

In other words: While rodents use BCAAs mostly as an energy source, the human body spares them as a potential protein anabolic.

In view of the fact that the BCAAs are not used to the same degree as an alternative substrate in the human vs. the rodent liver, it is actually not very surprising that the results of the study at hand appear to conflict with data from a previous study by the same laboratory (Gualano. 2011). In the corresponding experiment, Gualano et al observed measurable increases in exercise capacity and lipid oxidation in human subjects during endurance exercise after muscle glycogen depletion in response to the provision of 300mg/kg BCAAs per day.

So, the study is totally irrelevant, right? Not really, no. The fact that we are not able to use BCAAs as a readily available energy source like rodents does after all not mean that they must necessarily have the opposite effects on us. In fact, you all know that the vast majority of studies investigating the beneficial effects of BCAAs on endurance performance in humans yielded a null-result (!) - despite the fact fact that generations of researchers have been convinced that the inhibition of tryptophan uptake must blunt the exercise induced onset of fatigue (learn more in the articles cited in the red box).

Don't forget the endurance reducing increase in glucose usage that appears to be caused by isoleucine (and maybe valine) can also be beneficial: "The Glucose Repartioning Effects of Isoleucine" | read more.

The actual new information this study brings to the table is thus not that BCAAs are not ergogenic. It's rather the previously overlooked leucine induced acceleration of the glucose alanine cycle in liver. It is the activation of this (catabolic!) powerhouse by the means of which leucine "might have an interesting use in physical performance in prolonged or submaximal exercise, where muscle glycogen stores are more likely to be depleted" (Campos-Ferraz. 2013). It should be noted, though, that these effects are probably only observed after the glycogen levels are fully depleted - after an intense workout, towards the end of a race or after an fasted training - in those situations, the performance benefits may even be more more significant than in the study at hand.

Reference:

• Campos-Ferraz PL, Bozza T, Nicastro H, Lancha AH Jr. Distinct effects of leucine or a mixture of the branched-chain amino acids (leucine, isoleucine, and valine) supplementation on resistance to fatigue, and muscle and liver-glycogen degradation, in trained rats. Nutrition. 2013 Nov-Dec;29(11-12):1388-94.
• Gualano AB, Bozza T, Lopes De Campos P, Roschel H, Dos Santos Costa A, Luiz Marquezi M, et al. Branched-chain amino acids supplementation enhances exercise capacity and lipid oxidation during endurance exercise after muscle glycogen depletion. J Sports Med Phys Fitness 2011;51:82–8

Building a Bigger Engine: Resistance After Endurance Training Increases Mitochondrial Biogenesis & Protein Synthesis and Ramps Up Fat Metabolism

Image 1: There is nothing wrong with some "classic cardio" training, especially if you spike it up to build your mitochondrial engine

In a recent review of the literature, J.M. Wilson from the University of Tampa analyzed the results of 27 studies to determine whether and to which extend concomitant endurance training does / could have detrimental effects on the outcomes of resistance training (Wilson. 2011). And I suspect that it will not surprise you that Wilson found negative correlations "between frequency (-.26 to -.35) and duration (-.29 to -.75) of endurance training [and] hypertrophy, strength, and power." What is yet also noteworthy is a similarly significant (p<0.05) correlation with lower body fat levels and maximal heart rates on part on those strength athletes who did some sort of endurance exercises. Now, a more recent study which is soon going to be published in Journal of Applied Physiology sheds some more light on the complex interplay of endurance and resistance training and the potential benefits of combining both to build a "bigger mitochondrial engine" (Sahlin. 2011).

Interestingly, the Swedish scientists started out with a diametrically opposed hypothesis. Sahlin et al. expected that the signaling of mitochondrial biogenesis, of which it is common knowledge that it is promoted by "classic" low(er) intensity endurance exercise, would be impaired by resistance exercise. To validate their hypothesis, the scientists had a group of ten healthy subjects (7 males and 3 females; age, 26 ± 1.2 (mean ± SE) yr; height, 177 ± 2.9 cm; weight, 72 ± 3.5 kg) perform either 60min of endurance exercise (65% of VO2Max on a cycle ergometer) alone (E), or in combination (R+E) with a subsequent bout of 6 sets of leg presses at workloads corresponding to 70, 75, 80, 80, 75 and 70 % of the individual 1RM with 3 min rest between each set (cf. figure 1)

Figure 1: Graphical overview of the study outline (based on Sahlin. 2011).

Muscle biopsies were taken before and after the exercise protocol, to which the subjects had been randomly assigned and which was repeated 2 weeks (4 weeks in the female participants to avoid any influence of the menstrual cycle) later with subjects from the E group performing E + R and vice versa. The results, I'll say so much, were by no means what the researchers had expected.

Figure 2: Changes in lactate and muscle glycogen content in response to endurance (E) and combined endurance and resistance (E+R) training (calculated based on Sahlin. 2011).

While there were the expected differences in lactate levels, and glycogen content of the biopsied legs (cf. figure 2), the increase in the phosphorylation of mTOR and its upstream regulator Akt (you should know these promoters of protein synthesis from the posts in the Intermittent Thoughts series and my dissertations on other studies, by now ;-) was not only exclusive to the endurance + resistance training group (E+R), it was probably also much more pronounced than one might expect with 6 sets of leg presses and lead to an almost dramatic increase in p56Sk1 phosphorylation (do I have to mention that this happened "although" the subjects trained >12h fasted and remained fasted for the whole study period?) - a relatively reliable marker for protein synthesis (cf. figure 3).

Figure 3: Changes of key enzymes envolved in the phosphorylation of key enzymes in the protein synthetic cascade in response to endurance (E) and combined endurance and resistance (E+R) training (calculated based on Sahlin. 2011).

Morover, and totally contrary to what the scientists had expected, the expression of the key enzyme for mitochondrial biogenesis and increased fatty acid oxidation, PDK4 was significantly elevated, not suppressed, in response to the additional leg training (cf.  figure 4).

Figure 4: PDK4 phosphorylation (arbitrary units) in response to endurance (E) and combined endurance and resistance (E+R) training (calculated based on Sahlin. 2011).

The research hypothesis that a (relatively short, but intense) bout of resistance training subsequent to a mitogenic "classic" cardio regimen would blunt the beneficial effects of the latter on mitochondrial biogenesis is thusly more than falsified. As it turns out, the 6% increase in total work-load due to the addition of the 6 sets of leg presses makes a huge and desirable (!) difference (way beyond what an over-simplified workload = output equation would explain) in terms of "building a bigger engine" - an engine that will keep you lean on a bulk and help you lean out while your dieting.

If you are no powerlifter, it is thus probably no mistake to keep some "classic cardiovascular" exercise in your regimen, especially if you spice it up with a subsequent short bout resistance exercise - another option, and I am repeating myself here, would obviously be a high intensity cardio session (cf. HIIT). That being said, change has time and again proven to be the key to continuous improvements in exercise performance, muscular growth and strength, to incorporate both spiced up "classic cardio" and HIIT in your routine could not only improve your results (in view of the protein synthetic response, you could even "grow" on such an E+R day), it will also prevent you from getting bored with performing the same routine day in and day out and if you asked me, that is an even more fundamental key to success than a X% increase in the phosphorylation of whatever key enzyme ;-)

Endurance Training ↔ Overtraining & Muscle Loss? Run to Exhaustion & Sympathetic, Medium Intensity Steady State & Parasympathetic, HIIT-Like Training & No Overtraining

HIIT-like 400m sprinting is exhausting, but unlike running to exhaustion and medium intensity steady state cardio it's not going to mess up your nervous system.

Not one but two recent studies confirm what many of us have experienced first hand: Endurance training - specifically during a cut - is a double-edged sword. On the one hand, it's a neat way to augment the energy deficit, when you're dieting and maintain in a eucaloric state, when you're not. On the other hand, however, even moderate endurance training can alter the sympathetic and parasympathetic balance and thus create an imbalance that is characteristic of any form of overtraining.

Speaking of overtraining: As a SuppVersity reader you should actually be aware of the fact that scientists distinguish two different types of overtraining: Sympathetic and parasympathetic overtraining

You can learn more about HIIT, which appears to be less overtraining prone than MISS.

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.

Due to the fact that the symptoms (see Figure 1) closely resemble those Morbus Basedow (engl. Grave's Diseases) and Addison's Disease, respectively, sympathetic and parasympathetic overtraining are also called Basedowoid and Addisinoid overtraining.

Figure 1: Overview of the symptoms of the two major forms of overtraining.

You can see that the symptoms partly overlap. That's yet not the only problem you have if you want to diagnose the type of overtraining. In many resistance trainees, for example, you find either mixed forms or see a transition from classic sympathetic to parasympathetic overtraining over time (assuming the athlete doesn't do anything to normalize his / her sympathetic nervous system function).

There is no formula to calculate how much exercise you can sustain, but I'd suggest you take a look at my previous articles on heart rate variability and overtraining ("Are You Overtraining? Two Scientifically Proven Methods to Test Yourself - Method 1: Heart Rate Variability Analyses" | read more). They will help you to check, where you're at, if you have a baseline reading that was taken, when you've been completely rested  | learn more.

For the average study participant in a recent experiment that was conducted by scientists from the , The 42nd Hospital of PLA, the Xinqiao Hospital and the Chongqing Normal University in China, the duration and intensity of their cardio workouts (running) determined, whether the prescribed workout routines that consisted of ...

• 

  There is such a thing as overtraining, folks | read more

  4 times a week running at 100% of their maximal heart rate until they were exhausted (utmost intensity group)
   
• 30 minutes of running four times per week (moderate intensity group)


• 3 - 5x 1200 m runs per day with a  5-min break every 400 m four times per week (high intensity group)

made them overtrain or not, and whether their para- or sympathetic nervous system was overreacting.

Table 1: Characteristics of study groups at pre and post | Data are means XS± . Pre, pretraining; post, at the end of 8-week training; mid, at the end of 4-week training. Utmost, utmost intensity endurance training; moderate, moderate intensity endurance training; high, high intensity endurance training (Tian. 2014)

The subjects, 72 nonsmoking male students whose characteristics are summarized in Table 1, followed the routine they had been randomized to for 8 weeks. As you can see, there were no statistical significant changes in body composition over the course of the 8-week study. Although, it sould seem that the body fat percentage (I assume BFR is body fat) declined a tad bit more in the high intensity group.

Greater fat loss with HIIT, this wouldn't be a surprise - That's no news for you as a SuppVersity reader. I've repeatedly pointed out that the short intense workouts are more suitable for fat loss; and that not in spite of, but rather because they may burn less body fat during exercise.

If you have no idea what I am talking about, I suggest you take another look at my June 2012 article "Are You Still Burning Calories or Already Losing Fat? Study Shows: 5x15 Min HIIT Reduce Body Fat & Improve Fitness Twice as Effectively as 5x40min of Classic Cardio" (learn more) after you've finished this article.

Where the subjects differed, however, was in their response to the specific aerobic exercise programs they've been assigned to (I will directly quote the results from Tian et al (2014) and briefly comment on each of them):

• Heart rate variability (HRV): No significant changes in HRV parameters were found in all groups at pre and mid. But at post, the moderate intensity group showed more significant increases in RMSSD, PNN50, HF, LF and SDNN (P < 0.05 or 0.01) and much greater reduction in LF/HF than the other two groups (P was 0.033, 0.037 respectively). HFn of the moderate intensity group was significantly higher than that of the utmost intensity group (P = 0.012), while the opposite pattern occurred in LFn and LF/HF of the two groups (P was 0.025, 0.015 respectively).
  
  As you would expect the changes in HRV in the moderate and utmost intensity group reflect increases in parasympathetic and sympathetic nervous system activity, respectively.
• Circadian Changes in Cold Pressor Test (CPT): From pre to post marked differences were not found in SBP and DBP of all groups and their increases. At post HR was much less increased in utmost intensity group during CPT than the other two groups (average P < 0.05).
  
  Next to a high basal heart rate an inhibited increase in heart rate is another characteristic of later stages of sympathetic overtraining.
• Plasma catecholamine (NE & EPI): Norepinephrine (NE) concentration was considerably lower in utmost intensity group than the other two groups (P was 0.001, 0.00 respectively). At post marked inter-group differences were still not found in plasma PEI concentration.
  
  A reduced catecholamine release is a classic characteristic of long(-er) term sympathetic overtraining - a phenomenon, some people may call "adrenal fatique" that occurs after an initial phase of catecholamine overproduction in sympathetic overtraining.

Overall, the results of the study at hand confirm previous research that found associations between classic "moderate intensity" endurance training and parasympathetic dominance (Yamamoto. 2001; Pichot. 2002; Myslivecek. 2002).

For the utmost intensity group, on the other hand, the scientists diagnosed an "over-excited SN [sympathetic nervous system]" (Tian. 2014), which is in contrast to the medium intensity and high intensity group, where the head-up tilt test did not indicate an "impairing effect on autonomic regulation" (Tian. 2014).

What about muscle loss? Oh, yes! I almost forgot that scientists from the University of the Witwatersrand (Oost- huyse. 2014) in South Africa have recently been able to show that 3 h of race- simulated cycling on 4 consecutive days may improve the cyclists' ability to tap into their fat stores as an energy reserve. Unfortuna- tely, it will also lead to a 28-46% greater reliance on endogenous protein catabolism during exercise on day 2-4.

Now, every SuppVersity reader knows that protein catabolism doesn't necessarily translate ot "muscle loss", but for the average 10h of cardio + 20% energy deficit "dieter", it could.

Bottom line: A least in the study at hand, the intense, albeit better short bouts of high intensity exercise in the HIIT-like high intensity group of the study at hand turn out to be the least overtraining prone type of aerobic activity.

Even the classic medium-intensity cardio training appears to be more overtraining-prone, due to the comparatively long duration and the subsequent increase in parasympathetic nervous system activity. If you're looking for a "side-effect free" cardio regimen, 3-5x intervals of 3x400m sprints could be a good way to incorporate cardio training into your exercise routine.

One thing we should keep in mind, though, is that someone who is sympathetically overtraining in the gym with all its negative consequences (see Figure 1) would probably be better of with classic "moderate intensity cardio" to bring up the parasympathetic tone and avoid "weight lifting induced" sympathetic dominance | Comment on Facebook!

References:

• Myslivecek, P.R., Brown, C.A. and Wolfe, L.A. (2002) Effects of Physical Conditioning on Cardiac Autonomic Function in Healthy Middle-Aged Women. Canadian Journal of Applied Physiology, 27, 1-18. 
• Oosthuyse, T., & Avidon, I. (2014). Changes in substrate utilisation and protein catabolism during multiday cycling in well-trained cyclists. Journal of Sports Sciences, (ahead-of-print), 1-11.
• Pichot, V., Busso, T., Roche, F., Garet, M., Costes, F., Duverney, D., Lacour, J.R. and Barthélémy, J.C. (2002) Autonomic Adaptations to Intensive and Overload Training Periods: A Laboratory Study. Medicine & Science in Sports & Exercise, 34, 1660-1066. 
• Tian, Kaixin, et al. "Effect of Endurance Training on the Autonomic Nervous System Function of Young Male." International Journal of Clinical Medicine 5.19 (2014): 1189.
• Yamamoto, K., Miyachi, M., Saitoh, T., Yoshioka, A. and Onodera, S. (2001) Effects of Endurance Training on Resting and Post-Exercise Cardiac Autonomic Control. Medicine & Science in Sports & Exercise, 33, 1496-1502. 

HIIT is the Hit! Interval, not Steady State Aerobics is the Way to Go - Even for Patients with Myocardial Infarctions!

Image 1: Right in the starting block is where heart health begins... and on the finish line of a marathon race probably is where heart health ends (if not much earlier)

I think it is unnecessary to pose this question again, but in case you missed the innumerable blogposts, where I asked you whether you would rather like to look like an ultra-endurance runner or like a sprinter - here you go: Whose physique would you rather want to have? The sinewy physique of Haile Gebrsellasie or the muscled physique of Usain Bolt and co? I assume in most cases this question is unnecessary... but what if you are sick, obese or even have a heart failure? Obviously you cannot train like a sprinter, then... can you? Yes, you can - at least within your personal physiological limitations! In view of the results of a recent study from the KG Jebsen Center of Exercise Medicine at the Norwegian University in Trondheim, Norway, aerobic interval training would even be the healthier choice (Moholdt. 2011)!

For their study Trine Moholdt and her colleagues recruited 107 patients who had been hospitalized for myocardial infarction 2-12 weeks before the study and randomly assigned them to usual care rehabilitation or an aerobic interval training performed. In the course of the 12 week study period the exercise protocol was performed thrice a week. Two sessions were supervised, the other one had to be performed at home.

• usual care rehabilitation program - the standard program comprised 60 minutes of aerobic exercises performed to music; the sessions were lead by a physiotherapists, and after a 10-minute warm-up, the patients did aerobic exercises like walking, jogging, lunges and squats for 35 minutes, which were followed by a 5-minute cool-down with stretching and relaxation exercises.
• aerobic interval training - the total session time of the interval training was 38 minutes; it consisted of an 8-minute warm-up, followed by 4x4-minute intervals at 85–95% of the maximum heart rate (monitored by heart rate monitor), with active rest of 3 minutes of walking at 70% of maximum heart in between the intervals; the exercise session was terminated with a 5-minutes cool-down.

In view of the still commonly held believe that interval training could easily become (over-)exerting, quite a few medical practitioners, would probably shake their heads over the "irresponsibility of [their] Norwegian collegues - how dare those idiots put ailing cardiac patients on such an tortorous exercise regimen" ... I think I won't have to continue, you know the whole litany... and if you, just like me cannot stand that anymore, and your own (your father's, mother's, grandpa's or grandma's) doctor is one of those, take the following data, print it and use it to shut him up.

Figure 1: Improvements in VO2Max, peak heart rate, respiratory exchange rate at peak heart rate and heart rate recovery in cardiac patients after 12 weeks on the usual care rehabiliation program or an intense aerobic interval training (data calculated based on Moholdt. 2011)

Obviously, the poor cardiac patients did not only survive the "torture", their hearts even thrived on it. The increase in peak oxygen uptake (VO2Max), the standard measure of aerobic performance, was 2.7x higher in the interval group than in the patients who did the usual 60-minutes reha-sessions (cf. figure 1). For the other parameters the differences were not statistically significant after analysis for initial randomization:

Flow-mediated vasodilatation, both non-normalised and normalised to shear stimulus, increased significantly after exercise training in both groups [...] Quality of life increased significantly after exercise training (between-group differences, not significant)

If we look at the blood parameters, however, we do yet see some interesting differences, even your medical practitioner could not argue away:

Figure 2: Changes in high density lipoprotein and adiponectin in cardiac patients after 12 weeks on the usual care rehabiliation program or an intense aerobic interval training (data calculated based on Moholdt. 2011)

While the changes in triglycerides, CRP, ferritin, haemoglobin, and glucose were - within their respective standard-deviations - identical in both groups, there was a marginal but statistically significant greater improvement in high density lipoprotein (HDL) levels (a statistician would say there was an improvement in the interval group, while there was none / no statistically significant one in the reha-group) in the interval group. While this would indicate a lower risk of future (recurrent) heart disease, the accompanying  increase in adiponectin would suggest that the interval training group either had already or were about to lose more body fat than their endurance trained peers.

Unfortunately, the body composition of the patients was not tracked in the study, so this leaves us with the "surprising" benefits of intense interval training for the hearts of patients with prior myocardial infarction as the main result of a study some medical practitioners would probably not even have dared conducting.

Exercise: Does It Really Make You Hungry? The More You Train, The Less Hungry You Are. Still, 30 Min of Cardio Are More Productive Than 60 Min to Get in Shape

Start early and don't stop before you drop. If physical activity is a part of your life from the womb to the grave, you won't have to worry about whether cardio makes you hungry.

Friends of the SuppVersity will recognize this question as a recurring motif: "Does exercise really make you hungry?" An in case you are, you will also know that you have to blame Gary Taubes who seems in all honesty to believe that you would be able to cheat diabesity by simply leaving out the "bad calories" (=carbohydrates) for previous SuppVersity articles such as "HIT the Cravings, Eat Less and Improve Your Health", "Every Dog Has It's Day - Dr. Oz Was Right, Exercise Does NOT Just Make You Hungry" or Facebook News like this.

In the end, Gary is also to blame for today's SuppVersity news, or at least the fact that I jumped right at the results of a recent study from the University of Copenhagen (Rosenkilde. 2013)

So does it make you hungry, or what?

In the Danish capitol, Mads Rosenkilde, Michala Holm Reichkendler, Pernille Auerbach, Signe Toräng, Anne Sofie Gram, Thorkil Ploug, Jens Juul Holst, Anders Sjödin, and Bente Stallknecht conducted what I consider to be a very important study - a study that may not be changing the way we deal with the diabesity epidemic, but one that will hopefully shut those people up, who just tell the lazy ones what they want to hear: "Pah, don't bother about working out: It will just make you hungry!"

Taubes lectures Dr. Oz on "bad calories" = carbs and the perils of exercise

Interestingly, the reasearchers started out with an observation Gary Taubes made as well: "Weight loss induced by endurance exercise is often disappointing." They even come to the same conclusion as Gary did, but realize that their assumption that it may be an "increase in energy intake mediated through greater appetite" (Rosenkilde. 2013) which could explain the failure of previous weight loss trials with a focus on endurance exercise is just that: an assumption - not a given truth and thus from a scientific perspective a hypothesis that requires experimental verifi- or falsification.

When the Rosenkilde et al. recruited 64 sedentary, overweight, healthy young men for their study, they wanted to (ab-)use them to elucidate whether endurance exercise would exert any direct or indirect effects on fasting, postprandial and post-exercise appetite regulation that could precipitate their subjects to overeat and thus confirm Gary's (sorry, Mr. Taubes, I know you are not alone with this message, but you are the one people are listening to)

"Some LISS for MORE" - Do you remember?

SuppVersity Highly Suggested Read: "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 full post) - another Rosenkilde study from 2012. And a study in which the Danish researchers were able to show that a HIGH dose of endurance exercise does not produce suprerior fat loss results, even when the energy intake was controlled for and overeating not an issue!

To this ends, the Danes randomized the young men to three groups: A sedentary control group (CON), a moderate dose endurance exercise group (~30min/day; MOD) and a high dose endurance exercise group (~60min/day; HIGH). Now as SuppVersisty veteran you should by now be able to make a prediction about the outcome of the study. Anyone?

I guess you must have forgotten one of my personal favorites, then: "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 full article) - an article in which I describe (among other things) the results of a previous study by Rosenkilde that demonstrated quite clearly that a HIGH dose exercise regimen is not more effective than a MEDIUM dose exercise regimen, even if the calorie intake of the subjects was standardized.

The study period in the study at hand were 12 weeks. For the total amount of hours the subjects were running, cycling or whatever other endurance activity they chose was 12x7x30min or 12x7x60min. The exercise had to be performed at identical intensities 66% of the VO2max in all groups and with 66±1% (MOD) and 67±1% (HIGH) all subjects met this criterial.

On a per exercise session basis, the subjects in the HIGH did thus expend more almost twice as much energy as their medium dose counterparts (HIGH: 649±10 kcal vs. MOD: 338±8 kcal; p < 0.001). According to the Taubes'ian logic this must necessarily lead to an increase in appetite and, since there was no dietary prescription as in the 2012 study, a corresponding increase in energy intake.

Note: The the subjects’ adherence to the exercise regimen was excellent, with MOD having only a marginally better compliance to the prescribed amount of exercise than HIGH (MOD: 99±1% vs. HIGH: 96±1%; difference p = 0.047, i.e. non-significant).

So much about "I have not time to go to the gym!"

"Based on each subject’s VO2 max, resting and maximal heart rates (HR) and body weight, the duration of each exercise session was individually prescribed and extensively monitored via requent personal consultations with scientific staff (at least twice weekly).

The exercise prescription was based on each subject’s individual relationship between heart rate and VO2as determined by indirect calorimetry during an exercise test in the laboratory at baseline and was calibrated after the 2 nd , 6 th and 10 th intervention week based on changes in VO2max, heart rate and body weight. Compliance was verified using HR monitors (RS400, Polar Electro OY; Kempele, Finland) that stored information about the subjects’ exercise EE, intensity and duration." (Rosenkilde. 2013)

Both at baseline and at follow-up, the scientists measured the subjective appetite ratings. In addition, plasma ghrelin, glucagon, insulin, peptide YY3-36 (one of the major satiety hormones), glucose, free fatty acids and glycerol were measured during fasting and in response to a breakfast meal and an acute bout of exercise.

Figure 1: Effects on glucagon (goes up, when glucose goes down), ghrelin (hunger hormone), PYY (satiety hormone), and satiety (during breakfast condition), plus effects on body weight and composition (Rosenkilde. 2013).

As you can see in figure 1, the subjects' ad libitum lunch energy intake, which was evaluated three hours after the breakfast meal, did not differ between the endurance exercise groups. Similarly,...

[...d]espite different amounts of endurance exercise, the subjects lost similar amounts of fat mass (MOD: 4.2±0.5 kg; HIGH: 3.7±0.5 kg). Fasting and postprandial insulin decreased ~20% in both exercise groups (P<0.03 vs. CON). [And the a]ppetite measurements were not up-regulated in the fasting and postprandial states." (Rosenkilde. 2013)

So, a high dose of exercise didn't make the subjects hungry. Rather than that, the exact opposite was the case: Fasting and postprandial ratings of fullness and postprandial PYY (one of the major satiety hormones) increased in the HIGH (P<0.001 vs. CON) group to a significantly greater extent than in the supposedly less hungry MEDIUM group and reached a level that "signifies a significant satiety effect" (Rosenklide. 2013) in response to doing 60min of endurance exercise.

---

Outliers, over-eaters and general trends: Despite the fact that exercise training may have reduced the hunger and food intake for the majority of the trainees, there were 3 outliers who increased their energy intake almost 4-fold. Accoring to Rosenkilde et al., "[t]hese subjects did not display any adverse subjective appetite ratings immediately before the meal, nor was their satisfaction with the meal apparently different." Personally, I suspect that these subjects may have had blood sugar issues and were borderline hypoglycemic after the exercise. Since that happens quite easily when you cut carbs, but don't eat enough fat (and or too much protein), I guess some of you may this ravenousness very well, right?

When these subjects were excluded from the statistical analysis, the scientists observed a definite tendency towards a decrease in energy intake in the MOD as compared with CON at follow-up (-115 kcal, CI: -244:13; P = 0.08).

Bottom line: Although we should keep in mind that the overall changes in body composition may not reflect the superiority of the HIGH dose exercise regimen on the appetite ratings, hormonal markers of satiety and perceived fullness of the subjects, the results of the study at hand clearly refute the standard hypothesis of increased appetite as the main reason for the failure of endurance exercise based weight loss interventions.

In view of the previously cited results of the 2012 trial by the Rosenkilde et al., it is however not advisable to waste a whole hour of your precious time on endurance exercise everyday. While it is unquestionably possible (I know many people who do it), it's (a) tiring + boring, and most importantly, (b) stressing to jog or bike 60min every day (the stress is probably also the reason for the deterioration of the body fat levels in the 2012 study referenced previously).

In the real world, doing cardio for 60min every day will also reduce the amount of time you have to (1) do your (imho) obligatory resistance training sessions and to (2) shop and prepare whole foods meals. At least for the real busy-bodies it will also (3) steal half an hour (compared to doing less cardio) of your life-time you could better spend sleeping (for both general health and weight loss reasons). Nevertheless, it is not a reason to "overeat" for the average dieter and my personal observations tell me: Those who make it to the gym for their cardio sessions everyday have not the least problem to starve themselves; and the study at hand suggests this may (partly) be because of, not despite doing all that "cardio"!

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.