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:
http://www.ncbi.nlm.nih.gov/pubmed/22928084
http://www.ncbi.nlm.nih.gov/pubmed/22060178
http://www.ncbi.nlm.nih.gov/pubmed/20350594
http://www.gssiweb.org/en/Article/sse-137-endurance-exercise-and-antioxidant-supplementation-sense-or-nonsense---part-1

Phosphatidylserine:
http://www.jissn.com/content/4/1/5
http://www.ncbi.nlm.nih.gov/pubmed/16869708
http://www.ncbi.nlm.nih.gov/pm...MC2503954/
http://www.ncbi.nlm.nih.gov/pubmed/24959196


References
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?

References

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.