Sunday, December 14, 2014

Phosphatidylserine: Where's the Research?

Seeking the truth?
Do not strive to prove, but to disprove.

From my perspective, the increasing popularity of phosphatidylserine (PS) as an ergogenic aid is entertaining. When a new supplement hits the market with claims of improved performance, increased this, decreased that... The "gurus" want a piece of the action - they jump on the bandwagon; like they've known all along. Now they're giving dosing protocols, touting the supposed benefits of "the next big thing."

PS is not a new supplement - you can find research on PS and exercise dating back to the 80's. It used to be obtained from bovine cortex (cow brains), but after the mad cow disease scare, it has more recently has been extracted from soy (Jager et al., 2007).

If you rely on the gurus' supplement reviews or forums for your nutrition information, you may be on your way to the nearest supplement shop. But before we get carried away, I have a few thoughts and questions about PS:

If PS decreases salivary/plasma cortisol following exercise, what effect does this have on subsequent protein synthesis? Cortisol has been demonized as a catabolic hormone, but it is a normal response to exercise. Perhaps cortisol is not the demon.

No, cortisol's a necessary hormone - it mobilizes glucose, fatty acids and amino acids during times of stress (like exercise). Isn't maintaining plasma glucose important during exercise? And couldn't having free amino acids available for protein synthesis following exercise improve recovery?

Further, if phosphatidylserine decreases the cortisol response to exercise, does this reduce the stimulus for adaptation?

Training induces stress, this stress results in perturbation from the normal homeostatic environment and triggers a response. Whether it's from a hormonal standpoint or substrate availability, perhaps it's physical damage from a mechanical stimulus; it's these deviations from homeostasis that provoke adaptation. If you limit the stress response, do you limit the stimulus of the training?

Take antioxidants for example: Ten years ago, antioxidants were miracle molecules. And because athletes (especially endurance athletes) are exposed to high levels of free radicals, they were advised to take antioxidants like herbal supplements and vitamins A,C,E. 

Well, guess what - reactive oxygen species may stimulate mitochondrial biogenesis (Baar, 2014). And taking in excessive antioxidants may limit the stress response, limiting the stimulus for adaptation (Paulsen et al., 2014).  Is phosphatidylserine supplementation any different?

Similar arguments can be made for or against the use of NSAID's following training (Trappe & Liu, 2013).

Sure, antioxidant supplementation could be, and has been shown to be beneficial in specific circumstances. PS may be the same. But in this arena of uncertainty, one thing is for sure - we need more research. Specifically, we need more training studies - not just looking at the supplement's effects on acute performance or hormonal measures.

Further Reading
Antioxidant supplementation:


Baar, K. (2014). Nutrition and the adaptation to endurance training. Sports Med, 44 Suppl 1, S5-12.

Jager, R., Purpura, M., & Kingsley, M. (2007). Phospholipids and sports performance. J Int Soc Sports Nutr, 4(1), 5.

Paulsen, G., Cumming, K. T., Hamarsland, H., Borsheim, E., Berntsen, S., & Raastad, T. (2014). Can supplementation with vitamin C and E alter physiological adaptations to strength training? BMC Sports Sci Med Rehabil, 6, 28.

Trappe, T. A., & Liu, S. Z. (2013). Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise. J Appl Physiol (1985), 115(6), 909-919.

Thursday, December 11, 2014

Altitude Acclimation: Potential Application for Improved Exercise Economy

The "big three" determinants of endurance exercise performance are VO2max, pH threshold (sustainable pace) & exercise economy. We could also include anaerobic capacity and maximal speed/power as components that could determine the outcome of a sprint finish.

The importance of running economy has been documented many times, and is often regarded as a strong predictor of performance, especially between individuals with similar VO2max values (Saunders et al. 2004; Daniels 1985).

I've written on training for economy in the past. Training strategies such as hill sprints, resistance training, plyometrics or high intensity intervals have all shown improvements in economy.  In two studies, Saunders et al. (2004, 2009)  have also shown improvements in running economy following altitude acclimation. A study by Czuba et al. (2014) produced similar results in elite level biathletes and Latshang et al. in mountaineers (2013).

Potential mechanisms? Stays at altitude are not likely to result in improved power or stiffness of the muscle tendon system...

But, remember those uncoupling proteins? Perhaps altitude exposure down-regulates uncoupling protein gene expression, decreasing # of those uncoupling proteins (Levett et al., 2012). This would help maintain that H+ gradient between the intermembrane space and mitochondrial matrix - ensuring that more H+ is available to "run" ATPase. Or perhaps an increase in economy, measured by O2 consumption, is due to a change in substrate utilization. Utilizing more glucose and fewer fatty acids would decrease O2 cost, but net energy cost may or may not change (Shaw et al., 2014). This change could potentially be detrimental to endurance performance as endogenous CHO stores are limited.

So, really we need more research to evaluate changes in uncoupling proteins and energy cost, independent of O2 uptake.

An inverse relationship between economy and VO2max has been documented (Hunter et al., 2005). But, could altitude exposure provide a pathway to increasing or preserving VO2max while also improving economy?


Czuba, M., Maszczyk, A., Gerasimuk, D., Roczniok, R., Fidos-Czuba, O., Zajac, A., . . . Langfort, J. (2014). The Effects of Hypobaric Hypoxia on Erythropoiesis, Maximal Oxygen Uptake and Energy Cost of Exercise Under Normoxia in Elite Biathletes. J Sports Sci Med, 13(4), 912-920.

Hunter, G. R., Bamman, M. M., Larson-Meyer, D. E., Joanisse, D. R., McCarthy, J. P., Blaudeau, T. E., & Newcomer, B. R. (2005). Inverse relationship between exercise economy and oxidative capacity in muscle. Eur J Appl Physiol, 94(5-6), 558-568.

Latshang, T. D., Turk, A. J., Hess, T., Schoch, O. D., Bosch, M. M., Barthelmes, D., . . . Bloch, K. E. (2013). Acclimatization improves submaximal exercise economy at 5533 m. Scand J Med Sci Sports, 23(4), 458-467.

Levett, D. Z., Radford, E. J., Menassa, D. A., Graber, E. F., Morash, A. J., Hoppeler, H., . . . Murray, A. J. (2012). Acclimatization of skeletal muscle mitochondria to high-altitude hypoxia during an ascent of Everest. FASEB J, 26(4), 1431-1441.

Saunders, P. U., Telford, R. D., Pyne, D. B., Cunningham, R. B., Gore, C. J., Hahn, A. G., & Hawley, J. A. (2004). Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure. J Appl Physiol (1985), 96(3), 931-937.

Saunders, P. U., Telford, R. D., Pyne, D. B., Hahn, A. G., & Gore, C. J. (2009). Improved running economy and increased hemoglobin mass in elite runners after extended moderate altitude exposure. J Sci Med Sport, 12(1), 67-72.

Shaw, A. J., Ingham, S. A., & Folland, J. P. (2014). The valid measurement of running economy in runners. Med Sci Sports Exerc, 46(10), 1968-1973.

Wednesday, December 10, 2014

Training for Endurance: Progressive Recruitment

I read an article on VeloNews a while back describing how many cycling races are won and lost in the final hour or minutes of racing. And this is generally true, it often comes down to who can sustain the highest power output in the final push to the finish after three, four, or five+ hours in the saddle. Rationally, it makes sense that being able to delay fatigue and enter that last hour of racing with a greater capacity for work will enable an athlete to finish faster. Many of this spring's one day classics have served prime examples - those that produce the greatest amount of power in the end will prevail. Take this years's Milan-San Remo for example: after 6 hours of riding, the race hits a series of small climbs before a sprint to the line. This year, it was Alexander Kristoff in the final sprint (after nearly 7 hours on the bike) who took the win - out-sprinting the likes of Mark Cavendish and Fabian Cancellara. When asked about the finish, Kristoff acknowledged that a sprint after 300km is not the same as a sprint after 200km and stated that he usually does not "lose much power" late in a race.

A similar story played out in Ponferrada this year where Kwiatkowski launched an attack with 7 km to go and rode away from the field after more than 6 hours of racing. Thanks to Strava, we can take a look at what it took to win the 2014 World Championship. Kwiatkowski averaged 370W for those final 8 minutes of racing - not a particularly impressive figure considering he weighs in at 68 kg. Then again, considering this came after 6:20:00 of racing at an average of 240W, may help to put it into perspective.

My point being, fatigue happens - but some can resist fatigue better than others.

There are many strategies athletes can employ on race day to delay fatigue. For example: drafting decreases the work required from the athlete; proper carbohydrate supplementation decreases reliance on muscle glycogen, preserving it for later in the race; and proper hydration limits or prevents dehydration, maintaining stroke volume and cardiac output. But how might an athlete's training prevent fatigue late in a race?

Enter Progressive Recruitment
I want to address the training component of fatigue resistance in this post with the concepts of  progressive recruitment and the VO2slow component in mind. Progressive recruitment occurs as slower twitching motor units become fatigued or depleted and faster twitching motor units begin to be recruited to maintain force/power output.

With progressive recruitment, your EMG over time with fatigue looks like this:

Eight motor units were recruited for the first contraction.
By the 10th contraction, 12 motor units were recruited to maintain the same force output (Adam and De Luca, 2003).
Typically, when an athlete begins sub-maximal exercise like an easy run or ride, he recruits slower twitching motor units (once a steady state is reached). But as time passes and exercise progresses, even at a constant sustained workrate or pace, the athlete begins to fatigue and faster twitching motor units are recruited to do the work to maintain the workrate. In short, these faster twitching fibers are not as efficient and do not have the same oxidative capacity and fatigue resistance as slower twitching fibers (Jones et al., 2011). This may lead to an increase in O2 uptake at a constant workrate over time.

While progressive recruitment has been linked to the slow component of VO2 (Saunders et al., 2000), the relationship between the two has been questioned and debated many times (Zoladz et al., 2008; Borrani et al., 2009). Some debate whether progressive recruitment occurs, but the phenomena has been documented in many studies (Adam & De Luca, 2005). Also, couldn't reports of increased blood lactate in the final stages of a marathon indicate that faster twitching fibers are being recruited (Billat et al., 2002)?

Training with the Concept of Progressive Recruitment
No ground breaking science here. Essentially, our understanding of progressive recruitment reinforces the practices many endurance athletes and coaches have relied on for decades: hard, fatigue inducing work. There's no way around it. If you want to get better, you have to induce fatigue (hopefully with sport/event specificity in mind) and this is not going to be comfortable. But, knowing that faster twitching motor units are recruited after fatigue has been induced gives us a window to target those motor units specifically.

With progressive recruitment in mind, we can theoretically train to both delay recruitment of the faster twitching motor units and to improve the oxidative capacity of those faster twitching fibers when they are recruited so that they are more efficient and fatigue resistant.

What about time trials?
Time trials are not paced in the same way. They are typically a hard sustained effort from the get go. Or what about those athletes that just want to run a personal best marathon? While these sustained efforts don't necessarily require sprints at the finish to break opponents, the athlete will still recruit faster twitching fibers to get the job done once fatigue sets in. In the last few miles of a marathon, an athlete will recruit faster twitching motor units (Borrani et al., 2001).

There is some evidence indicating that these faster twitching motor units have the ability to become more fatigue resistant and take on characteristics of slower twitching motor units. In a review, Kubukeli et al. (2002) note that several studies have documented shifts in muscle fiber types from the faster type IIb fibers to slower type IIa or type I. While this could, in theory, be helpful - Kubukeli et al. also point out that much of the literature on fiber type conversion has shown inconsistent results. To take a theme from my previous post - what are we training for here? Increased type IIa MHC or increased fatigue resistance/increased power output? Should the goal of training be to convert fiber types or to maximize performance?

I know I want to maximize performance, regardless of fiber type.

Understanding the concept of progressive recruitment helps enforce the need to make those faster twitching motor units fatigue resistant. There are a few different ways this can be done - but the common theme is the recruitment those faster twitching motor units. To recruit those motor units, you have to either demand a lot of force, demand high velocities, or both. As mentioned above, inducing fatigue will also recruit those motor units.

Here are some example training techniques that would recruit faster twitching motor units, potentially increasing fatigue resistance:

  • Lifting - moderate to heavy loads
  • Power training/plyometrics
  • Hill sprints
  • High intensity interval training (induce fatigue and demand high force/velocity)
  • Extensive endurance training (going long)
  • Cumulative fatigue? (doubles, multiple days/weeks of intensified training)

Recruitment and fatiguing of faster twitching motor units will stimulate PGC-1a through glycogen depletion, oxidative stress, ADP/AMP accumulation, calcium release, epinephrine, Lactate/NAD+, etc. PGC-1a promotes mitochondrial and capillary growth - which, in theory, makes muscles more efficient at a given workrate and more oxidative/fatigue resistant. In the simplest sense; chronic recruitment of motor units triggers adaptation, making them more fatigue resistant.

Here, if an athlete performs high intensity work the goal will not be to improve VO2max or to improve lactate/H+ production and clearance, but to make those faster twitching fibers more oxidative (efficient) and fatigue resistant.

Another strategy the athlete could employ would be strength training with the goal of increasing a muscles maximal force. If the athlete can increase the strength of those slower type I fibers, they will operate at a lower percentage of their max during submaximal exercise, potentially extending their ability to complete work before recruiting the less efficient type II fibers. Additionally, through resistance training - recruiting the faster twitching motor units again and again may increase their resistance to fatigue, potentially shifting their characteristics from faster twitching (type IIa) to slower twitching (type IIx). There are many other benefits to resistance training as described by  Ronnestad and Mujika here.

To summarize:
Progressive recruitment occurs when slower twitching muscle fibers become fatigued. This results in faster twitching motor units being recruited to maintain force/power output. These faster twitching motor units are not as efficient or fatigue resistant. There are many paths to improving performance, and some of those paths may involve training to prevent progressive recruitment and/or training to improve the endurance and efficiency of those faster twitching motor units for when they are recruited.

Thursday, August 7, 2014

Are we on a Quest for Mitochondria or a Quest for Maximized Performance?

What I don’t understand is when I see teams and athletes pursuing marginal gains and ignoring the basics and fundamentals of sound training. There is no sense pursuing the last 2% until you have taken care of the first 98%.
-Vern Gambetta
As science advances, we identify transcription factors and map cellular signalling pathways in clinical settings to potentially maximize muscles' oxidative capacities. While mitochondrial biogenesis and angiogenesis are undoubtedly important for improving a muscle fiber's resistance to fatigue, we have to ask - should these be the target or the byproduct of training?

In other words, is it practical and worthwhile for athletes to manipulate their environments and diets in search of additional stress? What effect might this have on performance? An interesting review has been published recently: Link Here

The review from Baar is focused on using the available molecular knowledge to potentially maximize the activity and number of PGC-1a to stimulate mitochondrial biogenesis and angiogenesis. Essentially, maximizing metabolic stress through manipulation of an athlete's diet. The review notes that prolonged, low intensity training in fasted, glycogen depleted states and calorie restriction may maximally activate PGC-1a, as does training >75% VO2max.

This reminds me of the stories I've heard about cyclists filling their tires with sand or mounting lead filled water bottles on their bikes in an effort to make training harder. But in reality, the athlete could just ride harder and faster without the hassle of these unique "training aids."

I can't help but think dietary manipulation (calorie restriction, glycogen depletion) is much like these training aids. Yes, they will likely make training more difficult - increasing metabolic stress at a given workrate or pace - but could the athlete work harder or go faster without the intervention? How much is a rider's power output going to decline if he trains in a fasted state? How will it affect tomorrow's training? Do you put the athlete at a greater risk of illness? What's more important here - training for mitochondria or training for performance?

As my mentor Dave would say at the end of the day, "mitochondria don't win races, power outputs do."

Looking beyond the molecular aspects of training and beyond anecdotal reports, we have little research on the effects of training in a glycogen depleted state on performance. A few marathoners used periodic low carbohydrate training in preparation for the London marathon, but as this was a case study, there was no control group. And yes, many east African distance runners may voluntarily or unknowingly train in depleted states - but I have yet to see research indicate that their VO2max values are higher than those of runners from other cultures.

The potential of maximizing metabolic stress without added mechanical stress is appealing, particularly for runners, whose training volume may be limited by mechanical stress. And perhaps it can be appropriate as part of a periodized approach, but we should not forget that mechanical stress is also a stimulus for adaptation. More research is needed to address the effects of glycogen depletion/fasted state training on performance - Isn't performance the goal?

Tuesday, August 5, 2014

Endurance Training: Running vs. Cycling

A lot of people ask me, "What's the biggest difference between training for running and training for cycling?"

The simplest answer is that an athlete should have so much more opportunity to suffer on the bike.

If a runner's training not limited by time, motivation, or illness; what is it limited by?
It's fatigue and the ability to recover from previous workouts. If recovery was not a limiting factor, he could go out and run 3+ hours, or complete intervals at 5K race pace day after day without the fear of injury or exhaustion.

What about the cyclist? Yes, fatigue is a real thing for the cyclist; but mechanically, cycling is very different from running. During cycling an athlete experiences very few eccentric muscle contractions.

Meanwhile, the runner is constantly subjecting his quadriceps, hamstrings, hip and plantar flexors to impact forces and eccentric muscle contractions. These eccentric contractions cause muscle damage, in turn causing muscle soreness. Muscle soreness may alter stride mechanics (Tsatalas et al., 2013), decrease economy (Baumann et al., 2014), making running fast more difficult and potentially leaving runners vulnerable to injury.

So, the muscle damage incurred during running puts limits on the volume of work that can safely be completed by the runner.

To demonstrate my point, here's an 8 day block of training aimed at increasing maximal sustainable power output (MSPO), for the cyclist:

Day 1 - 6 x 5:00(5:00) @ 110% MSPO
Day 2 - 5 x 2 x 3:00(90) @ 115-120% MSPO, 8:00 between sets
Day 3 - 5 x 4 x 90(60) @ 120+% MSPO, 6:00 between sets
Day 4 - off
Day 5 - Easy 60-75:00
Day 6 - Easy to Moderate 90:00 - 2 hrs
Day 7 - 6 x 5:00(4:00) @ 110% MSPO
Day 8 - 5 x 2 x 3:00(75) @ 115-120% MSPO, 6:00 between sets

This is nothing outlandish for many cyclists, but outside of Canova's one or two day, "special blocks." Have you ever seen a runner complete a block of training like this? If you have, I'd love to hear about it. The closest thing I can think of is the training of Brenda Martinez from Joe Vigil (HERE). Even that schedule on the bike would not be very daunting.

You'll never see professional runners complete the same amounts of volume as professional cyclists. Cyclists will log 3-6 hours in the saddle a day, even the best marathoners will not equal this volume. And you'll never see a running stage race like that of the grand tours - simply because no runner could survive 3 weeks of 3-6 hours of racing/day - not at the same intensities (I'm not talking about some multiple day charity jog).

So, why then don't we see more block training from runners? The technical answer is eccentric muscle contractions. But simply put, it is the product of common sense and trial and error - the risk of injury is too great.

I will not deny that there could be potential in block training for runners, but with careful manipulation. I think there are components athletes and coaches can transfer across disciplines, but you can't simply mimic cycling training if your a runner and vice versa.

Friday, August 1, 2014

Uncoupling Proteins, Metabolism, Economy

What if I said, overweight people have the potential to be very good endurance athletes. Or you could say; very good endurance athletes are especially susceptible to becoming overweight when they're no longer training for competition.

Well, this is largely rooted in speculation, but for curiosity's sake - stay with me.

The theory is based on mitochondrial efficiency, or how well the electron transport chain can create and maintain a H+ concentration gradient across the inner mitochondrial membrane. This concentration gradient is used to drive ATPsynthase to generate ATP. If you had a leaky membrane and you were losing hydrogen ions, you'd be losing that gradient you worked so hard to create. Like trying to fill a bucket with a hole in the bottom, you'd have to turn up the water (substrate) to get it to fill up.

Uncoupling proteins essentially act as holes in the mitochondrial membrane, allowing protons to pass through them without harnessing their potential energy and this makes the electron transport chain less efficient - requiring more substrate to create "X" amount of ATP.

Depiction of an uncoupling protein releasing H+ from intermembrane space
Now consider the inverse relationship of VO2max and economy (here and here).

Could uncoupling proteins be the culprit? How does training effect mitochondrial efficiency? Could obese people just be really efficient at making ATP? Does it matter?

Further reading:

Monday, July 28, 2014

Concurrent Training: Training Order

I've expressed my opinion several times - separate the two when the goal is either strength or endurance

But if you're into combining them into one workout, recent research (link here) indicates that performing strength training after endurance training results in the more favorable endocrine response than strength before endurance.

Be careful with this information, as no performance measures were taken. While strength training after endurance training resulted in higher serum concentrations of  testosterone and IGFPB-3, it would be irrational to assume that this results in the greatest performance gains - and at what performance measures: strength vs cardiovascular endurance.

At the end of the day, more work completed = more muscle damage and more energy expended.

Monday, June 23, 2014

pH Threshold: More Useful than Lactate

Lets's imagine we have a race or time trial coming up. Maybe it's an 8K run, maybe it's 20K on the bike. But we expect the time trial to last 26-28 minutes.

Now, what will be the physiological governors of our performance?

We could create a long, long list or flow chart of factors that govern exercise performance. But in the simplest sense, it comes down to the maximum sustainable power (work/time) that an athlete can generate for the given race duration. The more power, the faster the time trial (less time) and vice versa.

 So, what governs maximum sustainable power? Here again, a number of factors (VO2max, substrate availability, economy, a central governor?). Assuming these factors are consistent, what about lactate threshold?

For years coaches and physiologists have been proclaiming lactate threshold to be the maximum sustainable pace or power for race distances of ~60:00. Assuming above this threshold, lactate accumulates exponentially and associated hydrogen ions lead to acidosis. But why then can athletes complete shorter races 30-50:00 at paces and powers greater than the lactate threshold?

Powers and paces above lactate threshold do not always induce acidosis.
We now know that the old perceptions of lactic acid are not correct. Instead of being a culprit of acidosis, lactate production consumes protons, preventing or delaying acidosis and enables high intensity exercise (Morris & Shafer, 2010; Robergs, 2011).

Lactate production consuming a proton and regenerating NAD+
But while lactate production can prevent or delay H+ accumulation, we've always known that acidosis occurs at high intensities and decreases in pH can limit performance. So, if lactate isn't a contributor to acidosis, what is?

ATP hydrolysis generates hydrogen ions, as do a number of mechanisms involved in glycolysis. These protons created in glycolysis can be consumed by pyruvate kinase and lactate dehydrogenase (lactate production). But during intense exercise the pathways for proton buffering and consumption can be overwhelmed because of an very high demand for ATP. At this point, ATP hydrolysis exceeds the rate of ATP resynthesis, the athlete cannot create enough lactate to consume all of the H+ released so H+ accumulation (acidosis) occurs.

What implication does this biochemistry have on training for athletes?

and start training above pH threshold

Research from Morris and Shafer (2010) has demonstrated that acidosis, or a decrease in blood pH, does not occur at lactate threshold. Instead, acidosis occurs at a greater workrate. Table 1 below demonstrates that while lactate threshold occured at 219W, blood pH did not change until 261W was reached. Logically then, the athlete should be able to maintain a workrate just below pH threshold for the duration of a time trial. And that's exactly what Morris and Shafer found.
(Morris & Shafer, 2010)

Increase pH Threshold to Increase Sustainable Power 

Since pH threshold is a reliable indicator of sustainable power or pace, an athlete should not train to improve his lactate threshold, but he should train to improve his pH threshold. By training at intensities above the pH threshold, one can increase his pH threshold by training the muscle fibers' ability to create lactate, transport lactate/H+, and buffer H+ (Juel, 2008; Juel and Halestrap, 1999; Pilegaard et al., 1999). As Morris and Shafer (2010) note, the most effective way to improve physiological capacity is to train at an intensity that exceeds current capacity. One way to do this is to separate bouts of training above your current capacity with periods of recovery. This is nothing profound; it's just high intensity interval training. But, the key being - train at intensities above the pH threshold. Do not underestimate your sustainable pace or power.

Of course, pH threshold as a function of pace or power can also be increased through extensive endurance training. By increasing mitochondrial density, these mitochondria consume H+ while performing oxidative phosphorylation. Shifting the curve further to the right. I would never advocate that an "endurance athlete" forgo endurance training all together. Rather, endurance athletes should incorporate high intensity training into their schedules.

What about performances that are not limited by acidosis, like the marathon?

The marathon may not be limited by acidosis. Instead, it is often an issue of economy, substrate availability, or mechanical breakdown. An athlete should be able to maintain a pace just under his pH threshold as long as he can maintain adequate glycogen stores or blood glucose, but what we often see is that marathons are run just below lactate threshold. Here, the athlete is more efficient with glycogen and glucose. High intensity intervals can increase VO2max and pH threshold. I've written on the value of high intensity intervals for the marathon runner in the past, and I stand by that philosophy.

If you recall from Billat (2002), as elite marathon runners completed high intensity intervals in a "pre-competitive" phase, they were able to decrease their all out 1000m run times. I believe all that was happening here was the athletes were improving their pH threshold and subsequently, maximal sustainable pace. If we could take a group of elite runners, say sub-2:08 marathoners and have them run an all out 800, 1500, and 5000m, I suspect that the finishing places would correlate well with marathon performances. Meaning, between a group of similar abilities (< 2:08 marathon), pH threshold would be a reliable indicator of marathon performance. I do not believe, however, that all 800m, 1500m, or 5000m times can be correlated to marathon performance because you will have people with different fiber type compositions and body types.

Can pH threshold be determined outside of the laboratory?

No, not exactly. But, from what I've seen and what Dave Morris has shared with me, pH threshold occurs roughly around 30:00 power or a pace that sustainable for 30:00-40:00. For some this may be 10K race pace. 

Sample pH Threshold test involving treadmill running at 1% gradient.
pH threshold is indicated by the arrow, occurring at 10 mph or 6:00/mile pace.
For this athlete, the 10K race pace would fit well. The athlete's 10K best is 36:48. The determined pH threshold on the treadmill was 6:00/mile or 37:17 for 10K. So, even if you do not have access to a lab and the equipment to do pH threshold analyses, you can approximate pH threshold pace or power if you have data from a 10K race or a 30:00-40:00 time trial.

Take that pace or power and design interval workouts, modulating work to recovery intervals so that the athlete can sustain paces or powers greater than his current pH threshold and create large amounts of lactate. This will improve the athlete's ability to create lactate to buffer H+ and transport that lactate and H+ in and out of muscle fibers - increasing maximal sustainable pace or power.

Practical application: Workouts

Increasing pH threshold requires an increased ability to create lactate. Remember that H+ inhibits glycolysis, so to be able to continue to run glycolysis and create lactate, we must clear H+ from the cytosol; this is where monocarboxylate transporters (MCTs) come in. These transporters on the muscle cell membranes transport H+ and lactate in and out of cells. MCT concentrations are effected by training, particularly high intensity training where low pH values are seen (Juel, 2006).

Therefore, workouts need to be completed at power outputs or paces greater than the athletes current pH threshold. There is no formula for calculating the optimal work to recovery times or total volume, but in general, the work and recovery needs to be manipulated so that the athlete can achieve powers/paces greater than pH threshold. For example, if an athletes pH threshold is 300W, 10:00 intervals at 300W or even 310W may not provide an adequate stimulus for MCT transcription. But, if the athlete can break the workout into 3 sets of 3 x 3:00 with 3:00 recoveries between reps; maybe then the athlete can complete the intervals at 350 or 360W, induce acidosis and trigger MCT transcription. But MCT transcription is not the only adaptation that could come from intervals of this length at these intensities; VO2max may also improve. Together these adaptations increase maximum sustainable pace.

So then, why can't athletes maintain paces or powers below pH threshold, but above lactate threshold for longer durations (1-2+ hours)? Well, it turns out using glycolysis and faster twitching muscle fibers is not the most efficient way to oxidize glucose and glycogen for ATP resynthesis. So, glycogen and blood glucose availability becomes an issue later in the race. Further, muscle damage, decreased economy of movement and/or the slow component may play a role.


Billat, V., Demarle, A., Paiva, M., & Koralsztein, J. P. (2002). Effect of training on the physiological factors of performance in elite marathon runners (males and females). Int J Sports Med, 23(5), 336-341.
Juel, C. (2006). Training-induced changes in membrane transport proteins of human skeletal muscle. Eur J Appl Physiol, 96(6), 627-635.
Juel, C. (2008). Regulation of pH in human skeletal muscle: adaptations to physical activity. Acta Physiol (Oxf), 193(1), 17-24.
Juel, C., & Halestrap, A. P. (1999). Lactate transport in skeletal muscle — role and regulation of the monocarboxylate transporter. J Physiol, 517(3), 633-642.
Morris, D. M., & Shafer, R. S. (2010). Comparison of power outputs during time trialing and power outputs eliciting metabolic variables in cycle ergometry. Int J Sport Nutr Exerc Metab, 20(2), 115-121.
Pilegaard, H., Domino, K., Noland, T., Juel, C., Hellsten, Y., Halestrap, A. P., & Bangsbo, J. (1999). Effect of high-intensity exercise training on lactate/H+ transport capacity in human skeletal muscle. American Journal of Physiology - Endocrinology And Metabolism, 276(2), E255-E261.
Robergs, R. A. (2011). Nothing ‘evil' and no ‘conundrum' about muscle lactate production. Experimental Physiology, 96(10), 1097-1098.

Friday, April 25, 2014

The "Lactate Paradox"

Lower peak lactate levels at high altitudes

Oxidative phosphyorlation is a consumer of NADH + H+. But at altitude or under hypoxic conditions, an individual's ability to utilize oxidative phosphorylation is negatively affected by the decreased availibility of O2. Consequently, NADH + H+ accumulates and acidosis occurs. H+ accumulation inhibits glycolysis. Inhibition of glycolysis = decreased pyruvate and lactate production.

Further, at altitude respiration rate increases at rest. This increases blood pH. This increase in pH at rest causes bicarbonate to be excreted from the kidneys. Loss of bicarbonate reduces the athlete's ability to buffer H+. H+ accumulation ---> acidosis ---> inhibition of glycolysis ---> decreased lactate production.

Again, could supplementation with beta-alanine limit acidosis, offset the lactate paradox, and maintain work capacity at altitude?

Saturday, March 29, 2014

Quick Read: Muscle Damage and Running Economy

Interesting research concerning running economy and muscle damage from researchers (and runners) at Georgia State:

Last year, a colleague and I tried to collect some pilot data assessing ankle jerk/patellar reflexes and running economy following a brutal eccentric workout (drop jumps and leg press). The reflex results were unclear and a broken treadmill threw a wrench into our running economy analysis...

What implication(s) could this have for athletes?
It would be wise to avoid muscle damage (downhill running, eccentric resistance training) in the 2-3 days before major competitions. Could cross training that elicits less muscle damage than running (cycling, elliptical, swimming) in the days immediately prior to a race increase running economy?

Of course, if you have a race coming up that has a substantial amount of downhill, you may be able to attenuate some of the muscle damage that would be attained during the race by consistently training on downhills. The repeated bout effect would make you more resistant to muscle damage.

Tuesday, March 25, 2014

Snake Oil

I was at Rite Aid yesterday picking up a few items and I happened to walk down the "Sports Nutrition" aisle. One product in particular caught my eye, in part, due to its outrageous price tag.

Alphatest from Muscletech is supposedly a "Super-Concentrated Performance and Testosterone Stimulant." The bottle makes the claims, "Anabolic, Anti-Catabolic, Performance." Well first off, if something is anabolic, by nature, it has to be "anti-catabolic." These supplements always make me wonder... Who comes up with this stuff? It's like they have a list of 10 key words that they have to choose from to put on the bottle.

For demonstration purposes only, I took photos of the product (shown below). I certainly do not endorse MuscleTech, and I cannot acknowledge any conflicts of interest.

Looking past the ridiculous name, claims, and price tag; what do we actually have in Alphatest? Here again, we have to look beyond the bombastic rhetoric like, "Testosterone Stimulant Complex" and "Testosterone to Cortisol Ratio Performance Matrix," to unearth proprietary blends of herbs and minerals. So the question then is; Do these ingredients increase testosterone levels in healthy individuals? If the supplement meets this criteria, there should also be several follow up questions like; Is it safe? Is it legal? Is it ethical? Is it worth the price? Will the product increase free testosterone? Will an increase in free testosterone lead to improved performance?

So, let's take a closer look at these ingredients and decipher whether or not this could be an effective supplement.

Zinc gluconate
Saw Palmetto
Astaxanthin - via haematococcus pluvialis (algae)
Ginko Biloba
Boron citrate

When considering a supplement, the first place I go is the Australian Institute of Sport's website. Here they have a list of supplements, classifying them as effective, undecided, ineffective or dangerous/illegal.

Not surprisingly, none of the ingredients make the Group A or Group B classification. Ginseng and Rhodiola are included in Group C. Supplements in this group, "have not been proven to provide a worthwhile enhancement of sports performance. Although we can't categorically state that they don't 'work', current scientific evidence shows that either the likelihood of benefits is very small or that any benefits that occur are too small to be useful." Because the supplement claims to be a testosterone booster, it is classified as a Group D supplement. Group D supplements, are "banned or are at high risk of being contaminated with substances that could lead to a positive drug test."

In summary, we have a mix of ingredients that have not been definitively proven to improve sports performance and the supplement as a whole may be at a high risk of being contaminated.

Turning to the Research
Mytosterone is the blend of saw palmetto and astaxanthin. A quick Google search will turn up a study from the Journal of the International Society of Sports Nutrition (Angwafor & Anderson, 2008). And at first glance, it appears that the proprietary blend of Mytosterone could decrease conversion of testosterone to estradiol by inhibiting aromatase, subsequently increasing serum testosterone. But look who funded the research - Triarco Industries (Mytosterone manufacturer). Further, where did the research take place? It was completed at the University of Yaounde, Cameroon. A PubMed search for the first author will turn up one other article, but it is unrelated to endocrinology or sports performance.

My quick thoughts: Triarco needed some data to support their new product, Mytosterone. They outsourced the research to whoever they could manipulate in Cameroon. And what do you know, it works! We could also look at the subject pool (37-70 year olds, average of 59 years) and the reality that there was no control group, but then we would have to assume that the data is legitimate...

An excerpt from Kreider (1999):
"The rationale for this [boron supplementation] was primarily based on an initial report that boron supplementation (3 mg/day) significantly increased b-estradiol and testosterone levels in postmenopausal women consuming a diet low in boron. However, subsequent studies that have investigated the effects of 7 weeks of boron supplementation (2.5 mg/day) during resistance training on testosterone levels, body composition and strength have reported no ergogenic value."
Prasad et al. (1996) found weak correlations between cellular zinc concentrations and serum testosterone levels. And zinc supplementation only augmented testosterone following a zinc-restricted diet in young adult males. Koehler et al. (2009) found that zinc supplementation, in the form of the supplement ZMA, did not significantly effect serum testosterone levels in subjects who consume a zinc-sufficient diet.

One study (Zhang et al., 2009) examined the effect of a Rhodiola and Ginko supplement on serum testosterone and cortisol. This study found that 7-weeks of supplementation significantly decreased serum cortisol concentrations. Sounds great, but upon further examination - the study was funded by Integrated Chinese Medicine Holdings Ltd., which has a patent on the supplement in question. A review from Walker and Robergs (2006) concludes, "Studies conducted in Western Europe and in North America have indicated that Rhodiola rosea may possess substantial antioxidant properties but have produced mixed results when attempting to demonstrate an ergogenic effect during exercise in humans." Note that the product in question contains Rhodiola crenulata, not rosea and  there is even less research on the crenulata species.

See above. Further, Markowitz et al. (2005) found that two weeks of Ginko biloba supplementation had no effect on serum cortisol or testosterone concentrations.

In Summary:
First off, a preliminary screening of the supplement via the AIS database should deter you from purchasing any sort of "testosterone booster." If that doesn't do it, I hope a further investigation of the research on the supplement's ingredients does. Don't believe everything that you read.


Angwafor, F., 3rd, & Anderson, M. L. (2008). An open label, dose response study to determine the effect of a dietary supplement on dihydrotestosterone, testosterone and estradiol levels in healthy males. J Int Soc Sports Nutr, 5, 12.
Koehler, K., Parr, M. K., Geyer, H., Mester, J., & Schanzer, W. (2009). Serum testosterone and urinary excretion of steroid hormone metabolites after administration of a high-dose zinc supplement. Eur J Clin Nutr, 63(1), 65-70.
Kreider, R. B. (1999). Dietary supplements and the promotion of muscle growth with resistance exercise. / Complements nutritionnels et augmentation de la masse musculaire grace a la musculation. Sports Medicine, 27(2), 97-110.
Markowitz, J. S., DeVane, C. L., Lewis, J. G., Chavin, K. D., Wang, J. S., & Donovan, J. L. (2005). Effect of Ginkgo biloba extract on plasma steroid concentrations in healthy volunteers: a pilot study. Pharmacotherapy, 25(10), 1337-1340.
Prasad, A. S., Mantzoros, C. S., Beck, F. W., Hess, J. W., & Brewer, G. J. (1996). Zinc status and serum testosterone levels of healthy adults. Nutrition, 12(5), 344-348.
Walker, T. B., & Robergs, R. A. (2006). Does Rhodiola Rosea Possess Ergogenic Properties? International Journal of Sport Nutrition & Exercise Metabolism, 16(3), 305-315.
Zhang, Z. J., Tong, Y., Zou, J., Chen, P. J., & Yu, D. H. (2009). Dietary supplement with a combination of Rhodiola crenulata and Ginkgo biloba enhances the endurance performance in healthy volunteers. Chin J Integr Med, 15(3), 177-183. 

Wednesday, March 5, 2014

Run Training for the Multisport Athlete or Injury Prone Runner: Theory and Application

We've seen crossover fitness gains from cycling transfer to improved or maintained running performance in the past (White et al., 2003; Millet et al., 2003; Ruby et al., 1996; Etxebarria et al., 2013). So, I want to propose a method of training to maximize running performance for runners or multisport athletes who, for whatever reason, cannot handle high volumes of running.

Most physiologists will agree that running performance is determined by the following three or four physiological factors: VO2max, lactate threshold, anaerobic capacity, and running economy (RE) (Midgley et al., 2007). Of course, psychology, motivation, and a central/peripheral governor may also play a role, but I want to focus solely on the trainable physiological factors.

The Scenario: 
An athlete is returning from a tibial stress fracture sustained during a high-mileage "base phase" in the month of December. This is the athlete's third tibial stress fracture in four years that can be attributed to running. Upon diagnosis, the athlete completed two weeks of aqua jogging, then progressed back on to the bike with moderate volumes and low-moderate intensities for the next 3-4 weeks. His competitive season will begin in May.

First Impressions:
For no apparent reason, this athlete is prone to tibial stress fractures. High-mileage programs may not be appropriate for the athlete.

Program Considerations, moving forward:
Could/should the athlete replace some of his running volume or workouts with cycling? What might the athlete gain? What will the athlete miss out on?

Fitness gains from cycling:
As noted in the first paragraph, athletes can improve cardiovascular function as VO2max. There is mixed information as to whether training lactate threshold and anaerobic capacity on the bike transfers to running. It is likely that cycling will not attribute to additional stress on the tibia (no impact forces, little eccentric muscle action).

Areas not addressed by cycling:
Perhaps the biggest hole in using cycling training for improving running performance is that the kinematics of cycling are so dissimilar to running. Running relies heavily on stored elastic energy and the use of the stretch shorten cycle (SSC). Being able to utilize the SSC effectively reduces the energy cost of movement, increasing economy. Remember, economy is one of those variables that dictates running performance. Unfortunately for our athlete, cycling will not utilize the SSC to the same extent of running. Further, recruitment patterns and posture are also different. I would speculate that if you had elite level cyclists run on a treadmill, while their VO2max values would be impressive, their RE may very well be similar to untrained individuals.

Plugging the Hole:
So, how can we improve RE with a minimal amount of running? If you've read any other posts on this blog, you probably know that I am very interested in hill sprints. Sprint and distance running coaches like Lydiard, Daniels, and Canova have been using hill sprints for decades, claiming they improve power and economy. While these claims are still up for debate, we have seen some research emerging on the topic (Barnes et al., 2013). Further, we can reason our way through using hill sprints for improved power and economy (Figure 1). We've also seen that plyometric and strength training can improve RE, likely through the same mechanisms, leading to improved stored elastic energy (Saunders et al., 2006; Ronnestad & Mujika, 2013).

Figure 1. Rationale for hill sprints improving running economy.
Training Implementation: 
Operating on the information we have -  the runner can maintain aerobic capacity through cycling. The primary component of fitness to address will be RE, and potentially lactate threshold.

Training Running Economy:
Given the particular scenario, consider the following training methods to create a program that will enhance RE with a minimal amount of running volume:
  1. Hill sprints, fast uphill strides, high intensity or sprint intervals (Barnes et al., 2013; Midgley et al. 2007)
  2. Plyometrics - drop jumps, skips for height, broad jumps, uphill bounding/jumping (Saunders et al., 2006)
  3. Strength training - see previous post here
  4. Explosive strength/power training - jump squats, cleans, I also consider hill sprints to be power training (Paavolainen et al., 1999)   
  5. Altitude training, heat acclimation (Saunders et al., 2004)
  6. Beetroot supplementation? Possibly, though research is generally not as effective for highly trained athletes
Practical application:
Outside of the weightroom, the athlete can incorporate fast running and plyometrics into his/her training routine. In this way, cycling can help maintain aerobic capacity and lactate threshold while the run training is focused on improving RE. Below are a few suggested workouts.
  • 20:00 easy-moderate run with 10 x 10-12s maximal effort hill sprints + 60-90:00 moderate cycling
  • plyometrics with uphill jumps and bounding + 60-90:00 cycling with 20x30(30) intervals
  • 6-8 x 400m run @ >3000m pace + 30-60:00 easy-moderate cycling
Any one of these workouts could be completed as one bout, divided into two sessions in one day, or separated by days (run on one day, ride the next). That will likely depend on the individual athlete's goals, abilities, preferences, and injury concerns.


Barnes, K. R., Hopkins, W. G., McGuigan, M. R., & Kilding, A. E. (2013). Effects of Different Uphill Interval-Training Programs on Running Economy and Performance. Int J Sports Physiol Perform.
Etxebarria, N., Anson, J. M., Pyne, D. B., & Ferguson, R. A. (2013). High-intensity cycle interval training improves cycling and running performance in triathletes. Eur J Sport Sci.
Gregor, R. J., Komi, P. V., & Järvinen, M. (1987). Achilles Tendon Forces During Cycling. Int J Sports Med, 08(S 1), S9-S14.
Midgley, A. W., McNaughton, L. R., & Jones, A. M. (2007). Training to enhance the physiological determinants of long-distance running performance: can valid recommendations be given to runners and coaches based on current scientific knowledge? Sports Med, 37(10), 857-880.
Millet, G. P., Candau, R. B., Barbier, B., Busso, T., Rouillon, J. D., & Chatard, J. C. (2002). Modelling the transfers of training effects on performance in elite triathletes. Int J Sports Med, 23(1), 55-63.
Paavolainen, L., Hakkinen, K., Hamalainen, I., Nummela, A., & Rusko, H. (1999). Explosive-strength training improves 5-km running time by improving running economy and muscle power. J Appl Physiol (1985), 86(5), 1527-1533.
Ronnestad, B. R., & Mujika, I. (2013). Optimizing strength training for running and cycling endurance performance: A review. Scand J Med Sci Sports.
Ruby, B., Robergs, R., Leadbetter, G., Mermier, C., Chick, T., & Stark, D. (1996). Cross-training between cycling and running in untrained females. J Sports Med Phys Fitness, 36(4), 246-254.
Saunders, P. U., Pyne, D. B., Telford, R. D., & Hawley, J. A. (2004). Factors affecting running economy in trained distance runners. Sports Med, 34(7), 465-485.
Saunders, P. U., Telford, R. D., Pyne, D. B., Peltola, E. M., Cunningham, R. B., Gore, C. J., & Hawley, J. A. (2006). Short-term plyometric training improves running economy in highly trained middle and long distance runners. J Strength Cond Res, 20(4), 947-954.
White, L. J., Dressendorfer, R. H., Muller, S. M., & Ferguson, M. A. (2003). Effectiveness of cycle cross-training between competitive seasons in female distance runners. J Strength Cond Res, 17(2), 319-323.

Wednesday, February 12, 2014

Marathon Training Specificity: At What Cost?

Marathon training... it can quickly become a complex beast. Chose your running website of choice or do a quick search for training plans and you'll end up with all sorts of ideas and theories (including this one). I would venture to say that the common theme between the marathon training plans you'll find is higher volumes and relatively lower intensities when compared to a 5K or 10K program.

But have you ever stopped to ask, "Why?" Why should an athlete need 20+ mile long runs and 80+ mile weeks? Why should an athlete complete 10 mile tempo runs instead of repeat 400s?

Well, I like to ask questions...

A couple of weeks ago, after helping give a class presentation on the dominance of East-African runners, one of my classmates made the comment that we, as "sports-scientists", tend to over-analyze things. She argued that instead of trying to figure out what makes some athletes better than others, we should just go back to the basics and focus on what we can do. I really struggled (and am still struggling) with my classmate's comment - it didn't so much address the topic of sports performance as much as it raised a philosophical dilemma: why do we question things?

Whether you realize it or not; it is making observations, formulating hypotheses and testing those hypotheses that drives innovation and enables change and progress. I would argue that this scientific method of sorts has led sports performances to where they are today. Certainly, we could stand idly by and keep doing whatever we've been doing, but where is the opportunity for progress there? In my eyes, it is not acceptable to fail to make observations and hypotheses because of your own laziness. We question because we seek answers. If you're not asking questions, you're at a stalemate.

Now, back the topic of marathon training... Certainly, there will be some degree of specialization or training focus. But too often, people put the marathon on a pedestal; viewing it as a special event, unlike any other, believing it takes special and specific preparation. Coaches and athletes often make the remarks "marathoners should put more emphasis on mileage and less on 'speed' or intensity to [somehow] develop their aerobic engine (what the hell is an 'aerobic engine' anyway?)." So these athletes often neglect training at high-intensities in favor of more low-intensity "aerobic" volume; completing 22-26 mile long runs, tempo-runs and marathon pace running in place of high intensity intervals or fartlek.

If this sounds familiar, I think it's time to reassess and ask, "what adaptation(s) will an athlete get from the different approaches, high-intensity vs. high-volume?" And "do high intensity intervals have a place in marathon training?"

To demonstrate, let's take two radically different workouts using a race specific approach - one for the marathon runner and one for the 5000m runner. Both of these workouts might be utilized late in a training cycle for the respective athlete. The marathoner's workout is 25km at marathon race pace (3:28/km), whereas the 5000m runner's workout is 5 x 1000km (60' r) just faster than current 5000m race pace (2:50-2:55/km). To speculate what adaptations the athletes may get from the workouts, we can look to past research, but we can also think about the physiological demands of the different workouts.

25km @ marathon race pace - steady state VO2 @ ~70-80% VO2max, no lactate/H+ accumulation, recruitment of slower twitching/fatigue resistant fibers, glycogen depletion possible (87-88:00 of work)

5 x 1km(60s) @ 5000m race pace - 90-100% VO2max, greater reliance on anaerobic energy sources: high lactate/H+ accumulation, recruitment of faster twitching fibers, glycogen depletion possible (Jenkins et al., 1993; Abernethy et al., 1990; Gollnick et al., 1974)

In the end we have ~90:00 of steady state running or 20:00 of intermittent high-intensity intervals. So the question to ask is: which workout results in the greatest fitness gains, independent of "race specificity?"

We have a lot of research on the efficacy of high intensity intervals now. And the data is compelling (Jeul et al., 2010; Ronnestad at al., 2014; Laursen, 2010; Kubukeli, Noakes, & Dennis, 2002; Lindsay et al., 1996; Abernethy et al., 1990; Londeree, 1997; Sharp et al., 1986; Billat et al., 2002).

I can't summarize all of the findings of the research and reviews here. The studies cited above do not even begin to scratch the surface of the literature on high intensity and sprint intervals, but if you could read just two, I strongly urge you to look through the articles from Laursen (2010) and Billat (2002). A full text version of the article from Laursen can be found here.

Laursen points to the value of both, low-intensity-high-volume and high-intensity-low-volume training, noting that adaptations can come from either; through distinctly different pathways. Mitochondrial biogenesis may be promoted with high-intensity or sprint intervals by activation of the AMPK signalling pathway, while low-intensity-high-volume promotes biogenesis through activation of the calcium-calmodulin pathway. Certainly, the proliferation of mitochondria is not the only event that occurs with training, but it has been recognized as an important adaptation for endurance athletes (Costill, Fink, & Pollock, 1976). Other components of fitness are lactate threshold and running economy - both of which have been improved with high intensity and/or sprint intervals (Kubukeli et al., 2002; Gunnarsson et al, 2012; Barnes et al., 2013, Midgley et al.,2007; Denadai et al., 2006)

Billat (2002) found that an 8 week "pre-competetive phase" of training, including high-intensity interval training at velocities faster than 10,000m race pace, improved VO2peak and subsequently decreased O2 fractional utilization at marathon pace. This means that the runners could maintain the same pace and run at a lower percentage of their VO2max potentially decreasing reliance on glycolysis (and glucose) for ATP production. Interestingly, high-intensity interval training also decreased the runners' time over an all-out 1000m. Could 1000m time and marathon performance be correlated? But that could mean that maximal sustainable velocity/pH threshold and marathon performance are correlated... Oh, my! We've really opened a can of worms now! What implications could this have for 3:28 1500m man, Mo Farah?

These findings prompt the question, why not go after adaptation by employing both strategies (high and low intensity training)? This is nothing profound, coaches and athletes have been utilizing "polarized" approaches to training, like the one described in the article from Billat (2002), for decades. The key point being, marathon runners should not neglect high-intensity or sprint intervals.

Below is an example of a polarized approach to marathon training that utilizes high and low-intensity training. Obviously, low-intensity "easy" runs would be performed on non-workout days. And of course, any of these interval workouts could be replaced with a fartlek of similar time and effort.

Full screen training plan in a new tab: here

Just like that, we have a polarized marathon training plan that encompasses high-intensity intervals and low-intensity "endurance" runs. Just as Juel et al (2010) found, by focusing on high-intensity intervals early in the training block, the athlete develops the ability to buffer H+ ions, improve blood flow and extend time to exhaustion - potentially improving an athletes ability to work at higher workrates/velocities. This may enable the athlete to complete the longer intervals in the subsequent block of training at faster paces, increasing the training stimulus which could lead to greater race performances. All the athlete is working towards is increasing his maximal sustainable pace and this is done by increasing "fitness" (lactate threshold, VO2max and running economy). I will admit, my current training philosophy is strongly influenced by my interactions with physiologist and coach, David Morris. His book can be found here.

So, instead of viewing the marathon as a "special" race that requires specific preparation, view it as an opportunity to increase the athlete's fitness that in turn, enables him/her to sustain a faster pace, no matter what the distance. Given the past research, as well as anecdotal evidence (here and here), I think it's pretty clear that fitness gains will come from high-intensity intervals and those fitness gains enable athletes to maintain greater velocities over any race distance. High intensity intervals may not be "specific" to marathon pace or race demands, but that seems to be a good thing.

Abernethy, P. J., Thayer, R., & Taylor, A. W. (1990). Acute and chronic responses of skeletal muscle to endurance and sprint exercise. A review. Sports Med, 10(6), 365-389.
Barnes, K. R., Hopkins, W. G., McGuigan, M. R., & Kilding, A. E. (2013). Effects of Different Uphill Interval-Training Programs on Running Economy and Performance. Int J Sports Physiol Perform.
Billat, V., Demarle, A., Paiva, M., & Koralsztein, J. P. (2002). Effect of training on the physiological factors of performance in elite marathon runners (males and females). Int J Sports Med, 23(5), 336-341. doi: 10.1055/s-2002-33265
Costill, D. L., Fink, W. J., & Pollock, M. L. (1976). Muscle fiber composition and enzyme activities of elite distance runners. Med Sci Sports, 8(2), 96-100.
Denadai, B. S., Ortiz, M. J., Greco, C. C., & de Mello, M. T. (2006). Interval training at 95% and 100% of the velocity at VO2 max: effects on aerobic physiological indexes and running performance. Appl Physiol Nutr Metab, 31(6), 737-743.
Gunnarsson, T. P., Christensen, P. M., Holse, K., Christiansen, D., & Bangsbo, J. (2012). Effect of additional speed endurance training on performance and muscle adaptations. Med Sci Sports Exerc, 44(10), 1942-1948.
Jenkins, D. G., Palmer, J., & Spillman, D. (1993). The influence of dietary carbohydrate on performance of supramaximal intermittent exercise. Eur J Appl Physiol Occup Physiol, 67(4), 309-314.
Juel, C., Klarskov, C., Nielsen, J. J., Krustrup, P., Mohr, M., & Bangsbo, J. (2004). Effect of high-intensity intermittent training on lactate and H+ release from human skeletal muscle. Am J Physiol Endocrinol Metab, 286(2), E245-251.
Kubukeli, Z. N., Noakes, T. D., & Dennis, S. C. (2002). Training techniques to improve endurance exercise performances. Sports Med, 32(8), 489-509.
Laursen, P. B. (2010). Training for intense exercise performance: high-intensity or high-volume training? Scand J Med Sci Sports, 20 Suppl 2, 1-10.
Lindsay, F. H., Hawley, J. A., Myburgh, K. H., Schomer, H. H., Noakes, T. D., & Dennis, S. C. (1996). Improved athletic performance in highly trained cyclists after interval training. Med Sci Sports Exerc, 28(11), 1427-1434.
Londeree, B. R. (1997). Effect of training on lactate/ventilatory thresholds: a meta-analysis. Med Sci Sports Exerc, 29(6), 837-843.
Midgley, A. W., McNaughton, L. R., & Jones, A. M. (2007). Training to enhance the physiological determinants of long-distance running performance: can valid recommendations be given to runners and coaches based on current scientific knowledge? Sports Med, 37(10), 857-880.
Ronnestad, B. R., Hansen, J., Vegge, G., Tonnessen, E., & Slettalokken, G. (2014). Short intervals induce superior training adaptations compared with long intervals in cyclists - An effort-matched approach. Scand J Med Sci Sports.

Sharp, R. L., Costill, D. L., Fink, W. J., & King, D. S. (1986). Effects of eight weeks of bicycle ergometer sprint training on human muscle buffer capacity. Int J Sports Med, 7(1), 13-17.

Tuesday, February 4, 2014

Beta-Alanine - Past and Future

Around 2009, I discovered the supplement beta-alanine and at that time I was intrigued by something that could potentially improve H+ buffering capacity and exercise performance. In the summer of 2011, I went to a symposium at the ACSM's annual meeting that discussed (as well as promoted PowerBar's) beta-alanine supplementation for performance enhancement.

Below is a presentation I gave later that summer as an intern at Carmichael Training Systems. Since 2011, we've had more literature published and I'll try to discuss a few of those below the posted presentation as well as provide some food for thought and suggestions for future research.

In short - beta-alanine supplementation has consistently shown that it increases carnosine in skeletal muscle and carnosine is understood to be an effective intracellular buffer. What's not clear is if that leads to increases in performance - but there is potential.

Since the time of this presentation, we've had much more literature published on beta-alanine's effects on performance.

A new study (link here) has demonstrated that supplementation failed to improve 1-hr cycling time trial performance. At first look, this may dissuade endurance athletes from supplementing - but one should also ask the question, "Why didn't it work?" Could it be that H+ accumulation is not a limiting factor in 1-hr performances? Certainly. Perhaps the limiting factor was glycogen availability. Therefore, H+ buffering would have no effect on 1-hr performance. Further, what would happen if all the athletes undertook high-intensity-interval training? Would the supplementation group make greater gains in training that would translate to greater performance improvements?

To demonstrate beta-alanine's effects on high intensity interval performance, take a look at this study and beta-alanine's effect on 800m run performance. The 800m run is a unique event that requires both high aerobic and anaerobic contributions to ATP production. The authors note that others have demonstrated exercise performances lasting 60–240s are more likely to show improvement following beta-alanine supplementation because of the high [HLa-] seen (12–14 mmol/L). And indeed, high levels of HLa- were demonstrated in the current study (~9–12 mmol/L).

A review from Hobson et al. (2012) states, "From the data available to date, it can be concluded that b-alanine supplementation elicits a significant ergogenic effect on high-intensity exercise, particularly in exercise capacity tests and measures, and where the exercise lasts between 1 and 4 min."

There are two things I would like to see addressed with beta-alanine supplementation:  its effect on monocarboxylate transporters but also, performance at altitude

We know that when training or racing at altitude, athletes may rely more glycolysis for ATP production. This may result in greater accumulations of lactate and H+ (Engelen et al. 1996) at submaximal work rates and the work rate at VO2max will be reduced. So, could beta-alanine prevent H+ accumulation and declines in power at altitude? Perhaps there is potential there.


Chung, W., Baguet, A., Bex, T., Bishop, D. J., & Derave, W. (2014). Doubling of Muscle Carnosine Concentration Does Not Improve Laboratory 1-h Cycling Time Trial Performance. Int J Sport Nutr Exerc Metab.

Ducker, K. J., Dawson, B., & Wallman, K. E. (2013). Effect of Beta-Alanine Supplementation on 800-m Running Performance. International Journal of Sport Nutrition & Exercise Metabolism, 23(6), 554-561. 

Engelen, M., Porszasz, J., Riley, M., Wasserman, K., Maehara, K., & Barstow, T. J. (1996). Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise. Journal of Applied Physiology, 81(6), 2500-2508. 

Hobson, R. M., Saunders, B., Ball, G., Harris, R. C., & Sale, C. (2012). Effects of beta-alanine supplementation on exercise performance: a meta-analysis. Amino Acids, 43(1), 25-37.