Hours of training might not be necessary to build endurance in sport; a new study suggests a drug could kick-start the process that leads to more efficient energy use in muscles.
After giving the molecular drug to mice, a team of scientists from the US, Australia and Switzerland found the mice could run on a treadmill about 70% longer – up to 270 minutes from 160 minutes – without any extra training.
While there is potential for this effect to be exploited by athletes, the researcher write of their findings, published in the journal Cell Metabolism, it could also assist people unable to exercise due to health problems, such as the elderly or those suffering from conditions such as cystic fibrosis.
“Many people can’t exercise to get the health benefits and, for them, this could be incredible,” says David James, a cell biologist at the University of Sydney who was not involved in the study.
So how does it work?
When we exercise, our muscles burn both fat and glucose. Glucose is the brain’s only source of energy, and when muscles use up all the glucose the result is hypoglycaemia (low blood sugar).
Exercising more frequently trains muscles to preferentially burn fat as the body stores only limited supplies of glucose. Training activates a protein, called PPAR, which in turn activates the molecular pathway that boosts endurance and causes the muscles to favour burning fat for energy.
Led by Weiwei Fan from the Salk Institute of Biological Studies, in California, the scientists first removed PPAR in the mice. When this was done, the genes usually switched on by exercise failed to do so. This indicated that increasing endurance is dependent on the presence of PPAR.
The team then gave the mice the molecular drug designed to activate the protein, essentially replicating the effect of training and pushing back hypoglycaemia.
The discovery, the researchers suggest, may extend the amount of time before an athlete “hits the wall” – the experience of sudden exhaustion that long-distance runners and cyclists encounter when their brains can no longer access glucose.
But James says while the research is important, this suggestion is a bit “nebulous”; while administering the molecular drug has been able to extend the running time on a treadmill for the mice, the results don’t prove it is because of something going on in the brain.
“They haven’t really proven exactly how this drug is doing it,” he says. “But it is doing it, which is the cool part.”
Anthea Batsakis is a freelance journalist in Melbourne, Australia.
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