If you’ve ever watched a marathon, you’ve probably seen some runners collapse just short of the finish line. Or you’re out on a run and it suddenly seems like you’ve completely run out of energy, despite your brain raring you to go. It’s almost as if the connection between your brain and your body has been severed. This is known as “Hitting The Wall”, or “Bonking” if you’re a cyclist.
Runners from the Dublin Marathon in 2013 – Photo from flickr
It was thought for a while that using up the body’s glucose reserves was the cause of this. Instead, a new study in Cell Metabolism surprisingly shows that “hitting the wall” actually happens when your brain cannot get access to sufficient glucose. While the muscles in our body can use fat or glucose as fuel, the brain can only use the latter.
When we hear the words “Progressive Training”, we often think of a training plan that increases in intensity and difficulty over time, therefore “improving our fitness” as we get used to longer and tougher bouts of exercise. For example, progressive training for marathon runners would involve increasing the total distance run per week over a period of time leading up to a marathon.
Endurance athletes often use GPS watches to track different aspects of their training such as distance, heart rate, cadence etc. – Photo from flickr
In reality, progressive training actually reprograms our muscles to burn less glucose and more fat while in use, thereby preserving it as an energy source for your brain. Research in the study focused on a transcription factor known as PPARδ (pronounced PPAR-delta). PPARδ triggers muscle composition changes in our body and “teaches” our muscles to consume fat as fuel instead of glucose. Progressive training gradually activates PPARδ.
In the first set of experiments in the study, researches at Lausanne Switzerland’s Ecole Polytechnique Federale genetically knocked out PPARδ in the muscles of mice. The mice were then put on treadmills and the effects of the lack of PPARδ were studied. Dr Michael Downes said “”When we did this and then ran those animals on a treadmill, we found that the genes that are normally induced by exercise failed to be induced.”
With this information, they then fed another group of mice a small molecule drug that activated PPARδ. These mice were able to run for a longer time (160 mins vs 270 mins) compared to the mice that had PPARδ deactivated – despite no progressive training to improv their endurance. By activating PPARδ within the mice, they were able to mimic progressive training.
For endurance athletes like myself, this discovery is revolutionary. No matter how experienced, a marathon runner takes requires approximately 16 weeks of progressive training to achieve a new target time. While the research is still in its preliminary stages, a way to combine the effects of both progressive training and PPARδ could take athletic performance to a whole new level.
However, these findings can be exploited by athletes wanting a competitive edge. An entire new can of worms is opened with regards to the ethics of chemically activating PPARδ in competitive athletic events like the Olympics.
Nonetheless, the best promise lies in being able to improve the endurance in people who are unable to naturally activate PPARδ through training. People who are suffering from Duchenne muscular dystrophy and cystic fibrosis to name a few, are often unable to get the exercise they need. This would eventually result in deterioration of their fitness. Chemically activating PPARδ in these people would allow them to enjoy the benefits of being fit without having to go through an intense training regime.
