Why some endurance athletes experience a heart rhythm disturbance called heart block has been identified by researchers using animal models.
The University of Manchester-led study found that long-term exercise in retired racehorses – the best available model of the athlete’s heart – and in mice, triggered molecular changes in a part of the heart known as the atrioventricular (or AV) node.
Despite well-recognised cardiovascular benefits, sustained endurance exercise in athletes, footballers and other sportspeople can lead to the development of abnormal heart rhythms – known as cardiac arrhythmias, including heart block.
While heart block is benign for most people, it can be a precursor to more serious heart problems.
The findings are published days after Denmark midfielder Christian Eriksen was discharged from hospital following a successful operation to fit a defibrillator implant.
The 29-year-old had to be resuscitated on the pitch after suffering a cardiac arrest on June 12 during the first half of his side’s 1-0 Euro 2020 defeat to Finland.
Details of any underlying condition, or what caused the cardiac arrest have not been released, and it is unclear if there is any link between the findings and Eriksen’s condition.
The scientists from Manchester, Montpellier and Copenhagen are the first to research the physiology of the notoriously hard-to-study AV node in athletes.
The heart’s AV node is part of its electrical conduction system controlled by the autonomic nervous system and electrically connects the atria and ventricles.
Published in the journal Circulation Research, and funded by the British Heart Foundation (BHF), the study found that long-term training in both horses and mice caused a reduction in key proteins – known as ion channels – that control AV node conduction.
Researchers investigated mice that followed a programme which modelled long-term exercise training to build their fitness.
The animals were used to explore mechanisms underlying heart block in detail using approaches that would not be possible in racehorses.
Training-induced heart block and underlying ion channel changes were reversible when the exercise was stopped or when mice were given a compound known as an anti-microRNA.
Lead author Dr Alicia D’Souza, a BHF Intermediate Fellow from The University of Manchester, said: “It’s well known that athletes are predisposed to heart block which in itself is often benign.
“But clinical research suggests that this may be ‘a canary in a coalmine’ – it can flag up the risk of abnormal heart rhythms which may for example necessitate the implantation of a pacemaker in some individuals.
“For the first time our research highlights fundamental adaptations taking place.
“Because we found similar effects on both mice and racehorses, it’s fair to assume this mechanism is present in humans too.
“It must be stressed that exercise is good for you – and its benefits far outweigh the risks.”
First author Dr Pietro Mesirca, a researcher from the Institute of Functional Genomics in Montpellier, said: “Understanding the physiology of the athlete’s heart is incredibly helpful.
“It could help us develop new interventions for heart block as well as help doctors more effectively monitor heart rhythm disturbances in top-flight professional athletes.”