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?

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