The ‘train low, race high’ theory is not particularly new but still remains somewhat controversial as to whether it really delivers.
Basically this theory says that because humans evolved in an environment where carbohydrate was not freely available, our ancestors made use of so-called ‘thrifty’ genes. These genes would have enabled our forebears to hunt, run and survive without muscles crammed full of carbohydrate (glycogen), by improving fat metabolism.
Fast forward to the 21st century and lo and behold, modern man still has these thrifty genes. The thinking therefore is that by training with low muscle glycogen, we can enhance the activity of these genes and maximise fat burning for energy, prolonging endurance. Combine this with a high-carbohydrate intake leading up to a race, and you have the best of both worlds.
That’s the theory. The problem is that while studies on low-glycogen training have shown that fat burning is indeed enhanced, there’s disagreement as to whether it leads to actual performance gains in a race situation. But now a new Swedish study provides some further evidence that a little bit of low-glycogen training might be worthwhile after all.
In the study, the scientists set out to try and discover the effects of low-glycogen training on the synthesis of mitochondria in exercising muscles. You can think of mitochondria as the ‘aerobic energy factories’ in your muscle cells.
The more mitochondria per unit volume of muscle, the better that muscle will be at using oxygen to produce energy – exactly what’s required for excellent endurance.
To do this, ten highly trained cyclists exercised for 60 minutes at approximately 64 % of their maximum aerobic capacity (VO2max) with either low stores of muscle glycogen (around 166mmol per kilo of dry muscle) or normal stores (around 478mmol per kilo of dry muscle).
To ensure either ‘low’ or ‘high’ glycogen stores for the test, the cyclists’ levels of muscle glycogen were manipulated beforehand using either exercise (to deplete glycogen) or a high-carbohydrate diet (to raise glycogen).
Samples of the cyclists’ muscles were taken before and after the test and were analysed for a number of molecular markers that indicate mitochondria are being synthesised in the muscle. The higher the levels of these markers, the greater the rate of synthesis of mitochondria.
In a nutshell
Firstly, the levels of an important molecular marker known as PPAR (that is always raised following aerobic type training) was enhanced to a greater extent when exercise was performed with low-glycogen training compared with normal-glycogen training; when the cyclists trained with normal glycogen levels, PPAR was raised 2.5-fold.
However, when they trained with low glycogen stores, PPAR was raised 8.1-fold. Two other key markers of mitochondria synthesis were also measured – the rather exotic sounding ‘cytochrome-c oxidase subunit I’ and ‘pyruvate dehydrogenase kinase isozyme 4 mRNA’. Neither of these were raised after normal-glycogen training but both were increased after low-glycogen training, by (1.3-fold and 114-fold respectively)!
Up to now, the rationale for low-glycogen training has been mainly to help prolong endurance by enhancing fat oxidation in the muscles.
However, this study shows that training with low glycogen levels amplifies the expression of the major genetic markers for mitochondrial synthesis, which in turn could help boost the overall capacity of muscles to use oxygen and produce energy.
In plain English, it indicates that some low-glycogen training could not only improve how long you can pedal for, it could also improve how fast you can sustain that pace.
Two caveats however; firstly we’ll need to wait for more research to roll in before we can confidently recommend this mode of training. Secondly, all cyclists should be very aware that low-glycogen training is potentially quite stressful so should only be carried out on a very limited basis and with careful monitoring.
Eur J Appl Physiol. 2012 Oct 2. [Epub ahead of print]