The effects of exercise on myocarditis have been studied using various animal models, particularly focusing on viral myocarditis, the most common type (Sagar et al., 2012). Many studies utilize the Coxsackievirus B3 (CVB3) myocarditis model (Favere et al., 2024; Gatmaitan et al., 1970; Kiel et al., 1989; Reyes et al., 1981; Ilback et al., 1989; Cabinian et al., 1990). In a recent study, mice underwent 8 weeks of moderate, forced treadmill training prior to receiving a single intraperitoneal injection of CVB3. The researchers observed that exercise influenced the inflammatory response in viral myocarditis (Favere et al., 2024). Specifically, the inflammatory infiltrates exhibited a higher cellular density and increased CD8⁺ T lymphocytes and macrophages (Favere et al., 2024). Both the trained and untrained groups infected with CVB3 developed myocardial fibrosis; however, the trained group showed a greater extent of interstitial fibrosis (Favere et al., 2024). This may explain why there is a tendency for ventricular arrhythmias in the group of infected animals exercising (Favere et al., 2024). A study conducted on mice infected with CVB3 demonstrated that exercising during the acute phase of the infection significantly increased the viral load in cardiac tissue and exacerbated myocardial inflammation and necrosis (Gatmaitan et al., 1970). Half of the mice in this study died during exercise due to congestive heart failure. Conversely, when swimming was introduced 9 days after the onset of the disease, both virulence and lethality only increased moderately (Gatmaitan et al., 1970). This suggests that exercise in the initial phase of infection worsens cardiac inflammation and tissue damage, ultimately deteriorating the overall health condition (Gatmaitan et al., 1970). Another study also used swimming as a method of forced exercise and found heightened virulence in the groups that exercised (Kiel et al., 1989). Specifically, this study revealed significantly increased viral titers on day 6 and day 9. These findings were linked to greater myocardial fibrosis, enlarged hearts, and an overall increase in mortality (Kiel et al., 1989). The CVB3 model is a reliable model for dilated cardiomyopathy, and exercise during the acute phase has also been shown to be the cause of larger atrial thrombi (Reyes et al., 1981). The presence of thrombi was linked to an increased risk of arrhythmias. The exercised group generally exhibited more significant issues related to left ventricular dilation, fibrotic scarring, and calcium deposits (Reyes et al., 1981). Exercise has also been linked to an increase in inflammatory cells, including CD8⁺ T cells, macrophages, and monocytes (Ilback et al., 1989). During myocarditis, maintaining a balanced immune response is crucial. This study demonstrated that exercise disrupts this balance. Specifically, there was an increase in pro-inflammatory cell types, such as CD8⁺ T cells, and M1 macrophages, while regulatory T cells (Treg) and M2 macrophages were slightly reduced (Ilback et al., 1989). Reducing T cell activity decreased the severity of myocarditis, even in physically active mice (Cabinian et al., 1990). Immunosuppression resulted in fewer negative effects on the heart due to exercise (Cabinian et al., 1990). In a different model of myocarditis associated with Chagas disease, it was observed that exercising while undergoing benznidazole treatment had harmful effects (Mendonca et al., 2019). Trained animals that did not receive treatment exhibited higher levels of inflammation and oxidative stress, along with increased pro-inflammatory cytokines such as IL-6 and TNF-α (Mendonca et al., 2019). However, treatment effectively reduced markers of inflammation, oxidative stress, and overall myocardial damage, demonstrating its cardioprotective effects (Mendonca et al., 2019). Notably, combining exercise with treatment diminished these positive outcomes. These findings suggest that exercise may exacerbate inflammation and oxidative stress to a degree that counteracts the benefits of benznidazole treatment (Mendonca et al., 2019). One recent study, using a chronic Chagas cardiomyopathy (CCC) model in hamsters, found that 8 weeks of treadmill aerobic physical training (APT) reduced inflammation and fibrosis. APT was performed at moderate intensity and improved left ventricular remodeling and cardiac dysfunction. Significant differences were observed in the degree of myocardial inflammation, but not in the extent of total fibrosis. Damasceno et al. also reported that the sedentary group exhibited progressively worsening perfusion defects throughout the experiment (Damasceno et al., 2024). Finally, another recent study using the same disease model, but in C57BL/6 mice, showed that 5 weeks of aerobic training reduced fibrosis in both cardiac and skeletal muscle in diseased animals, although the number of infiltrating inflammatory cells remained unchanged. Moreover, trained mice exhibited reduced severity of cardiac arrhythmias and lower expression of pro-inflammatory and pro-fibrotic genes in the heart (Improta-Caria et al., 2025).

Most of these studies, summarized in Table 1, point towards exercise being detrimental to the course of myocarditis. However, it is crucial to emphasize that the intensity of physical training significantly influences whether physical activity creates a more pro-inflammatory environment. Another important limitation is that nearly all existing animal studies on myocarditis have been conducted in male animals. These potential sex-based immune differences should also be taken into account before drawing any general conclusions.

As described in the introduction, following a diagnosis of myocarditis, current guidelines recommend a period of physical activity restriction for all individuals, regardless of age or athletic status (Pelliccia et al., 2019). This is due to the heightened risk of arrhythmias, heart failure, or sudden cardiac death that can occur with exercise during active inflammation. Typically, moderate to high-intensity physical activity, including recreational exercise and competitive sports, should be avoided for at least 3–6 months. During this time, the focus is on cardiac recovery and careful monitoring. Before returning to physical activity, a comprehensive evaluation is required. This includes assessment of symptoms, cardiac biomarkers (such as troponin and inflammatory markers), and cardiac function through echocardiography (Bryde et al., 2023). Additional testing, like 24-h Holter monitoring and exercise stress testing, helps identify any residual electrical or functional abnormalities (Bryde et al., 2023). Cardiac Magnetic Resonance Imaging is commonly used to detect prolonged myocardial inflammation or fibrosis; the presence of late gadolinium enhancement (LGE) may indicate a higher risk and warrant further caution (Bryde et al., 2023). LGE relies on the use of a gadolinium-based contrast agent, which distributes in the extracellular space. In damaged myocardial tissue, the extracellular volume is increased, allowing more gadolinium to accumulate and wash out more slowly compared to normal myocardium. Areas of damage or scarring appear hyperintense in MRI (Aquaro et al., 2023). Once the heart has returned to normal function, inflammation has resolved, and there are no concerning findings on imaging or rhythm monitoring, a gradual and supervised return to physical activity can be considered. This approach applies broadly, from sedentary individuals to elite athletes and across all age groups, to ensure safety and prevent long-term complications (Hurwitz and Issa, 2020; Terry et al., 2024; Maisch, 2015; Van Name et al., 2024). It remains unclear whether this approach is fully scientifically justified. For example, Halle et al. recommended that athletes with uncomplicated myocarditis can resume physical activity as early as 1 month after the acute phase (Halle et al., 2021). Depending on the clinical appearance of the patient, a few studies recommend performing the investigation earlier and starting with moderate activity before 3 months post-inflammation (Schmidt et al., 2022). Overall, these studies provide insight into how individualized decisions should be made, especially in complex or borderline cases, and underscore the importance of a cautious, evidence-based approach to resuming exercise after myocarditis.

Sport is recognized as a crucial protective factor against many lifestyle diseases. Sedentary behaviour combined with the consumption of high-calorie foods can lead to increased fat levels and various lifestyle diseases, such as respiratory and cardiovascular diseases (Silveira et al., 2022). On the other hand, some studies indicate that high-intensity exercise may increase the risk of contracting infections due to a temporary suppression of the immune system. This phenomenon might be explained by a reduction in natural killer (NK) cells and neutrophils that is observed after intense workouts (Dick and Diehl, 2014). Additionally, the downregulation of lymphocyte proliferation, monocyte toll-like receptors, and other important immune functions could also contribute to this risk (Gleeson, 1985). Furthermore, excessive endurance training can elevate levels of adrenaline, cortisol, prolactin, and growth hormone, as well as ROS due to a higher electron flow in the mitochondria, which may harm cellular immunity (Dick and Diehl, 2014; Harris, 2011; Nieman and Wentz, 2019; Chevion et al., 2003). Athletes may experience increased susceptibility to infections after events like marathons, and this is influenced by multiple factors. It is not solely determined by how exercise affects the immune system (Simpson et al., 2020). Therefore, accurately distinguishing the specific impact of exercise and its effects on immunity can be quite challenging. Current research distinguishes between moderate and high-intensity interval training (HIIT), highlighting their different effects on the immune system and their varying suitability for specific applications and goals. Regarding the vascular system, HIIT is significantly more time-efficient than moderate-intensity training in enhancing vascular function (Ramos et al., 2015). Additionally, the positive effects of HIIT have been observed in breast cancer survivors, contributing to improvements in cardiovascular fitness, cardiac regulation, and the sympathetic nervous system (Toohey et al., 2020). HIIT is often praised for its efficiency in achieving similar improvements in aerobic capacity (VO_2peak) and reducing systemic inflammation markers (Bartlett et al., 2017). However, it is important to note that high-intensity exercise can also contribute to increased inflammatory responses, especially concerning upper respiratory tract infections (URTIs) (Terry et al., 2024).

How does physical training, in general, impact the immune system? Table 2 summarizes several studies exploring the effects of different types of training on the human body. Although there are exceptions, most studies in the literature differentiate between moderate- and high-intensity training.

Moderate intensity exercise refers to physical activity that causes a noticeable increase in heart rate and breathing. It typically corresponds to 40%–59% of an individual’s maximal oxygen uptake (VO₂max), which is the maximum rate at which an individual can take in, transport, and use oxygen during intense exercise; or 50%–70% of maximum heart rate (HRmax), performed for at least 150 min per week, typically spread across at least 3–5 days (Harris, 2011; Garber et al., 2011). Constant moderate activity is associated with fewer community-acquired infections and strengthens the body’s first line of defence (Chastin et al., 2021). Regular moderate-intensity exercise boosts immune function, enhances the body’s antioxidant defences, and reduces oxidative stress. This leads to more efficient energy production and a lower risk of developing inflammatory diseases (Scheffer and Latini, 2020). It also tends to increase serum and salivary IgA concentrations, which may partly explain its protective effect, as these immunoglobulins are key components of the first line of defence (Dick and Diehl, 2014; Harris, 2011; Nieman and Wentz, 2019; Nieman et al., 1998). Higher levels of IgA are associated with improved mucosal immunity, which plays a critical role in protecting against respiratory infections. The immune system may also benefit from reduced levels of stress hormones (e.g., adrenaline, cortisol, and growth hormone) and decreased circulating ROS (Maisch, 2015; Nieman and Wentz, 2019; Bartlett et al., 2017). Furthermore, increases in lymphocyte, neutrophil, and NK cell counts have been observed following moderate exercise (Dick and Diehl, 2014; Harris, 2011; Nieman and Wentz, 2019; Dixit et al., 2023; Meyer-Lindemann et al., 2023). These cellular changes are supported by improved trafficking of immune cells between the bloodstream and peripheral lymphoid tissues, leading to a more effective immune response (Simpson et al., 2020; Meyer-Lindemann et al., 2023).

Interestingly, in the context of ongoing inflammation, moderate-intensity exercise appears to reduce excessive immune activation (Scheffer et al., 2019). One possible explanation is the muscle-derived release of IL-6 during exercise. IL-6 acts as both a pro- and anti-inflammatory cytokine; in the later, chronic phase of inflammation, its anti-inflammatory effects tend to dominate (Hunter and Jones, 2015). This may be due, in part, to its ability to suppress TNF-α (Dick and Diehl, 2014; Petersen and Pedersen, 1985). Moderate exercise has also been shown to benefit cardiac patients, for example, by improving cardiovascular fitness (Maisch, 2015). In cardiorespiratory diseases, there is evidence that moderate training exerts anti-inflammatory effects, which are essential for resolving persistent inflammation (Dixit et al., 2023). Similarly, in cancer patients, a reduction in pro-inflammatory markers has been observed with this type of physical activity (Khosravi et al., 2019).

High-intensity training, defined as exercise performed at 70%–80% of maximum heart rate for 5–60 min, and prolonged exercise sessions (typically exceeding 60 min), tend to exert negative effects on the immune system, particularly in the short term (Dick and Diehl, 2014; Harris, 2011; Friman and Ilback, 1998). Such activity decreases T-cell proliferation, thereby increasing susceptibility to viral infections and leading to general immunosuppression (Dick and Diehl, 2014). In addition, this type of training elevates stress levels. Stress hormones such as adrenaline and cortisol are significantly increased during strenuous exercise (Dick and Diehl, 2014; Harris, 2011). Some studies also report an increase in ROS during high-intensity training (Supruniuk et al., 2023). For instance, ROS are generated in the mitochondria of muscle cells during and after exercise (Chevion et al., 2003). Other sources include the activation of neutrophils, migrating into the muscle to repair activity-induced damage, and flow-induced ROS production in the endothelium (Chevion et al., 2003). Ultimately, caution must be taken not to exceed safe intensity levels. Excessive training can lead to myocardial fibrosis due to repeated micro-injuries, thereby increasing the risk of sudden cardiac death (SCD) (van de Schoor et al., 2016). This risk is particularly elevated in the presence of acute myocarditis. During training sessions of very high intensity, such as marathon running, even severe organ damage can occur, affecting the liver, intestines, and kidneys. Increased blood flow to the working muscles may lead to hypoperfusion of internal organs, potentially resulting in organ damage and triggering systemic inflammatory responses (Suzuki et al., 2020). However, strenuous exercise is not solely associated with negative effects on the immune system. Recent research indicates that HIIT can lead to significant improvements in cardiovascular fitness, metabolic health, and exercise capacity. Notably, these benefits are often achieved with a lower total exercise volume compared to moderate-intensity training (Soylu et al., 2021; Atakan et al., 2021). Interestingly, in a study examining the effects of high-intensity training in patients with hypertrophic cardiomyopathy, where participants were assigned to either moderate- or high-intensity training, no significant differences were observed between the groups in terms of fitness gains and cardiovascular response (MacNamara et al., 2023).

We can conclude that not all forms of exercise are the same. Different training intensities may be appropriate for different objectives and populations.