New Study Shows: Endurance Training Changes the Nerves That Control the Heart

Regular physical activity may benefit the heart in ways that scientists are only beginning to understand. Beyond improving cardiovascular fitness, new research suggests that moderate endurance training reshapes the nerves that regulate the heart. These findings could ultimately help doctors develop more precise treatments for common heart diseases.

Nerves Controlling the Heart as the Key to New Therapies for Heart Disease

Researchers at the University of Bristol (United Kingdom) have discovered for the first time that regular endurance training alters the nerves controlling the heart differently on the left and right sides of the body. The study, published in Autonomic Neuroscience, revealed a striking left-right difference that could one day lead to better treatment strategies for cardiac arrhythmias, chest pain, angina pectoris, and stress-related “broken heart” syndrome.

Heart rhythm disorders (arrhythmias) occur when the heart’s electrical control system becomes unbalanced and the heartbeat becomes too fast, too slow, or irregular. Some forms may be harmless, while others can increase the risk of serious complications. The autonomic nervous system plays an important role in this process, as it influences the heart’s electrical activity and, when overactive, can contribute to certain arrhythmias.

Angina pectoris refers to chest pain or a feeling of pressure in the chest area that occurs when the heart muscle is temporarily deprived of sufficient oxygen. This is often caused by a narrowing of the coronary arteries due to atherosclerosis. However, there are also forms of angina pectoris in which nervous system control, vascular regulation, or a spasm of the coronary arteries play a role. Those affected often describe the symptoms as tightness, pressure, or a burning sensation behind the breastbone, sometimes radiating to the arm, shoulder, neck, or jaw.

Broken-heart syndrome, medically known as Takotsubo syndrome, is a temporary weakening of the heart muscle that often occurs after severe emotional or physical stress. Triggers can include, for example, a severe loss, an accident, extreme stress, or a sudden traumatic experience. It is believed that an excessive activation of the stress response and a strong release of stress hormones such as adrenaline temporarily impair the heart. The symptoms often resemble those of a heart attack—such as chest pain and shortness of breath—although the coronary arteries are usually not blocked by a clot. In many cases, heart function recovers completely; nevertheless, the condition can be acutely distressing and requires medical monitoring.

Exercise Alters the Nerves that Control the Heart

The study’s lead author, Dr. Augusto Coppi, a lecturer in veterinary anatomy at the University of Bristol, explained: “The discovery points to a previously hidden left-right pattern in the body’s ‘autopilot’ system that supports heart function. “These nerve bundles act like a dimmer switch for the heart, and we have shown that regular, moderate physical activity reconfigures this switch in a side-specific manner. This could explain why some treatments work better on one side than the other and help doctors in the future to tailor therapies more precisely and effectively.”

The project was conducted in collaboration with University College London (UCL) in the United Kingdom, the University of São Paulo (USP), and the Federal University of São Paulo (UNIFESP) in Brazil. Using advanced three-dimensional imaging techniques, known as stereology, the team investigated how exercise alters the nerve bundles that help regulate heart function. After ten weeks of training, the trained rats had about four times as many neurons in the cardiovascular nerve bundle on the right side of their bodies as on the left, compared to untrained animals. At the same time, the size of the neurons on the left side nearly doubled, while those on the right side became slightly smaller. These results suggest that exercise reshapes the heart’s neural network differently on each side.

Potential Benefits for Future Heart Treatments

The study’s findings could, in the long term, open up new possibilities for tailoring heart therapies more specifically to the individual functioning of the nervous system. Of particular interest is the role of the stellate ganglia—two small nerve clusters that are part of the sympathetic nervous system and influence the heart’s activity via nerve fibers. These structures act as a kind of amplifier for stress and strain signals: they can increase heart rate, boost contractile force, and alter the electrical excitability of the heart muscle. In healthy people, these signals are important for the heart to adapt to physical activity or stressful situations. However, excessive or abnormal activation of these nerve pathways can become problematic. Increased sympathetic activity is associated, among other things, with certain cardiac arrhythmias, heightened pain sensitivity in angina pectoris, and the development of stress-induced broken-heart syndrome.

For this reason, the stellate ganglia are already being specifically targeted in certain medical situations. These include, for example, procedures such as nerve blocks, in which signal transmission is temporarily interrupted, or denervation procedures, in which certain nerve fibers are permanently reduced. The goal of these interventions is to curb overactive stress regulation of the heart and prevent dangerous electrical malfunctions. The new study now provides evidence that the two stellate ganglia do not react identically but are altered differently by physical exercise. The researchers speculate that these left-right differences could help tailor treatments more precisely in the future. Instead of treating both sides equally, it might be more effective to specifically target the side that is more heavily involved in a particular condition.

A better understanding of these differences could be particularly helpful in complex clinical conditions where existing therapies do not always work sufficiently well. For example, patients with certain heart rhythm disorders or chest pain that is difficult to treat could benefit from a more individualized selection and placement of nerve treatment. However, the scientists emphasize that this possibility is still a long way off. The current results come from experiments with rats and, for now, show only structural changes in the nerve cells. It is not yet known whether the same adaptations occur in humans, to what extent they influence heart function, or whether they would actually lead to better treatment outcomes.

The next phases of research will therefore investigate whether the observed changes are also associated with measurable functional improvements in the heart. This will include assessments of cardiac output during exercise and at rest, as well as studies using larger animal models and, ultimately, in humans. If this correlation is confirmed, the research could, in the long term, help to further personalize therapies for cardiac arrhythmias, angina pectoris, and broken heart syndrome.

Next Steps in the Research

The researchers are now focusing on determining what functional effects the observed changes in the nerve cells actually have on the heart. So far, the study has shown that regular endurance training alters the structure of the nerve nodes that control the heart. The crucial question, however, is whether these anatomical adaptations also lead to measurable improvements in cardiac regulation. To this end, the scientists plan to investigate how the heart reacts under various conditions—both at rest and during physical exertion. They are particularly interested in whether the stellate ganglia, altered by exercise, improve the heart’s adaptability—for example, through more efficient control of heart rate, more stable electrical excitation of the heart muscle, or a better response to stressful situations.

Another focus is on determining whether the observed left-right pattern also occurs outside the current rat model. Using non-invasive examination methods and biological markers, the researchers aim to investigate whether similar differences between the two sides of the sympathetic nervous system can also be detected in larger animal species and, ultimately, in humans. These studies are particularly important because the results from animal models cannot automatically be applied to humans. The human heart and its nervous system are more complex, and many factors—such as age, fitness level, medical conditions, or genetic differences—can influence the response. Dr. Coppi added: “Understanding these left-right differences could help us tailor treatments for cardiac arrhythmias and angina pectoris to individual patients. Our next step is to investigate how these structural changes affect function and whether similar patterns occur in larger animals and in humans.”

However, if it is confirmed that physical activity alters the nerves that control the heart in humans in a similar way, this could open up new avenues for personalized cardiac medicine. Doctors might be better able to assess which nervous system structures are particularly involved in a patient’s condition and which treatment—such as a targeted nerve block or other neuromodulatory procedures—promises the greatest benefit. The researchers therefore view the results not only as evidence of the positive effects of exercise on the heart, but also as a potential starting point for future therapies. The long-term goal is to better understand the connection between physical exercise, the nervous system, and heart function, and to use this knowledge to develop more personalized treatment strategies for conditions such as cardiac arrhythmias and angina pectoris.