Vigorous exercise can increase the risk of motor neurone disease (MND) in people genetically pre-disposed to develop the condition, scientists have found.
The role of physical exercise in the development of motor neurone disease has been controversial and previous studies have not been conclusive.
The University of Sheffield study found exercise is likely to cause motor neurone injury only in patients with a risk-genotype and said people should not stop exercising as a result of the study.
It is thought low levels of oxygen in the body during strenuous exercise could be leading to a process called oxidative stress in the motor neurones - some of the biggest and most oxygen-demanding cells in the body.
This may lead to damage and eventually cause the cells to die in people who have that genetic vulnerability.
Studies have shown that MND has a higher incidence in professional sportspeople, and they are likely to start suffering symptoms from an early age.
Previous research has shown an estimated six-times increased risk of MND in professional footballers, the researchers said.
A number of high profile British sportsmen have shared their experience with MND in recent years, including rugby league’s Rob Burrow, rugby union’s Doddie Weir and footballer Stephen Darby.
Dutch former footballer Fernando Ricksen died aged 43 in 2019 following a battle with motor neurone disease.
MND, or amyotrophic lateral sclerosis (ALS), is a devastating, rapidly progressive and relatively common neurodegenerative disease that affects the motor neurones in the brain and spinal cord that connect the nervous system and muscles to enable movement of the body.
The messages from these nerves gradually stop reaching the muscles, leading them to weaken, stiffen and eventually waste.
MND affects approximately 5,000 people in the UK and the life-time risk of developing the condition is approximately one in 400.
Approximately 10% of MND cases are inherited, but the remaining 90% are caused by complex genetic and environmental interactions which are not well understood.
One of the authors, Dr Johnathan Cooper-Knock said: “We have suspected for some time that exercise was a risk factor for MND, but until now this link was considered controversial.
“This study confirms that, in some people, frequent strenuous exercise leads to an increase in the risk of MND.
“It is important to stress that we know that most people who undertake vigorous exercise do not develop MND.
“Sport has a large number of health benefits and most sportsmen and women do not develop MND.
“The next step is to identify which individuals specifically are at risk of MND if they exercise frequently and intensively; and how much exercise increases that risk.”
Dr Cooper-Knock, who is a senior lecturer in Neurology from the university’s Neuroscience Institute, said: “Complex diseases such as MND are caused by an interaction between genetics and the environment.
“We urgently need to understand this interaction in order to discover pioneering therapies and preventative strategies for this cruel and debilitating disease.”
The Sheffield team say this new research will have a significant impact on the global effort to identify which individuals based on their genetics are at risk of MND.
The aim is to help doctors to be able to offer advice to the families of MND patients about the risks so they can make personal decisions about their exercise habits.
Dr Brian Dickie, director of research development at the Motor Neurone Disease Association, said: “In recent years, understanding of the genetics of MND has advanced, but there has been little progress in identifying the environmental and lifestyle factors that increase the risk of developing the disease.
“This is, in part, because the genetic and the environmental studies tend to be carried out in isolation by different research teams, so each is only working with part of the jigsaw.
“The power of this research from the University of Sheffield comes from bringing these pieces of the puzzle together."
The findings are published in the journal EBioMedicine.