Exercise will not slow ageing process, says Loughborough scientist
Physical activity will not slow down the ageing process, according to a Loughborough University scientist.
The discovery by Professor Jamie Timmons and fellow scientists not only challenges the long held belief that keeping active will automatically hold back the hands of time but highlights a new perspective on the ageing process in humans.
Jamie Timmons, professor of Systems Biology in the School of Sport, Exercise and Health Sciences, says they now have evidence that turns many of the assumptions about ageing on their head.
He says the research shows that ‘a simple link between muscle ageing and lack of exercise is not plausible.’
He added: “When it comes to tackling ageing, the UK Centre for Ageing Research experts are advising the government that muscle ageing is caused by factors such as inactivity.
“However, when we look at the changes in human muscle with age, in both people from the UK and the USA, we do not observe physical activity altering the age-related biological changes.
“So, for some people exercise might produce good functional effects while for other people it will not stop the loss of muscle as they are unable to effectively grow muscle tissue. In short, a simple link between muscle ageing and lack of exercise is not plausible.”
Professor Timmons and his team have collaborated with teams led by Dr Philip Atherton at the Royal Derby Hospital and the Karolinska Institutet in Stockholm.
The lead post-doc on the project, Dr Bethan Phillips, a former Loughborough graduate now based at the Royal Derby Hospital, said this was ‘definitely an important finding’ and she hopes it will help her continue her work on ageing and exercise.
Professor Timmons says he is excited by the findings and hopes a drug can now be found to slow down the ageing process in people who suffer from rapid ageing.
He said: “It’s been a great team effort. While the concept that we age at different rates is something that people are familiar with, the fact that we have discovered a reliable set of genes that associates with that process is something new.
“What we are now trying to do is build on the discovery. Ideally, we could identify a drug that slows down the rate of the ageing process for use in people who suffer rapid ageing, especially in those people who are unable to build muscle tissue with exercise training.
“There have been attempts to find genes which control ageing in humans using classic genetics (DNA sequence analysis) but they have failed to find much.
“We take a different approach, measuring the variation in the products being made from the genetic code. In this way we are able to capture the relevant features more easily and with far less cost.”
The discovery of a reproducible human muscle age fingerprint means that drug screening efforts now have a valid benchmark to aim for rather than abstract theory.
Many theories of ageing are currently being pursued, such as ‘inflammation’ and ‘oxidative stress or free radicals’, and these have been based on studying people with a pre-existing disease or carrying out genetic manipulation studies.
Professor Timmons said: “While it is significant that we can rule out many of these old ideas, what’s really important is that progress is made to build on our new observation and that will take more investment.
“If, in 10 years’ time, we are sitting here with a new drug that slows down ageing in people who suffer rapid decline in muscle function then it will be time well spent.
“Or, if our ageing ‘fingerprint’ helps prioritise hospital transplantation or managing health risks, then it can also make an important impact.”
Professor Timmons expects a mixed reaction to the findings.
He said: “The ageing research science community will have a polarised view on the findings. If our data challenges the usefulness of their pre-clinical models they will, of course, be sceptical.
“I would think the biotech world will also say ‘this is interesting, this could be useful to follow up”.
Professor Timmons first started investigating muscle ageing while working for Pfizer, the world’s largest pharmaceutical company, 12 years ago.
He says since then he has had to ‘beg, borrow and innovate’ through a series of small grants to generate the raw gene-chip data required to make progress.
The award of a £1m grant by the UK Research Medical Council in 2012 has made life a bit easier.
He said: “It means I now have a post-doc entirely dedicated to modelling the vast amount of human clinical data we have. However, there is still a great need to increase the funding of translational medicine studies as we are drowning in good quality human data but I see very little appetite for this in the UK.”
Professor Timmons believes, based on his experience in the pharmaceutical industry, that it is also vital to work with humans, rather than say flies, worms or mice to understand the human ageing process.
He said: “Industry has spent £400 billion on a model for finding cures for human disease over the past two decades, one that has largely failed, and it is important that we learn lessons from that rather than repeat the same mistakes with public money.”
Article entitled “Molecular Networks of Human Muscle Adaptation to Exercise and Age” will be published in PLOS Genetics on 21/3/2013. The paper will be available online at: http://www.plosgenetics.org/article/metrics/info%3Adoi%2F10.1371%2Fjournal.pgen.1003389