COVID in Athletes: What the Science Says About Cardiac Risk, Long COVID, and Return to Play
Table of Contents
Key takeaways: COVID in Athletes
- COVID-19 can affect athletes through several mechanisms, including myocarditis, reduced aerobic capacity, prolonged recovery, and long COVID.
- The overall risk of serious cardiac complications appears to be low, particularly in athletes who recover without concerning cardiopulmonary symptoms.
- COVID-related myocarditis is not unique among viral illnesses; other viral infections can also be associated with cardiac involvement and prolonged recovery.
- Symptoms matter more than the test result alone. Chest pain, palpitations, disproportionate breathlessness, syncope, persistent fatigue, and reduced exercise tolerance warrant closer evaluation.
- Long COVID can be difficult to diagnose because its symptoms often overlap with fatigue syndromes, burnout, depression, deconditioning, sleep disruption, and other common clinical conditions.
- Many COVID-19 infections are no longer formally confirmed, meaning that the absence of a documented positive test does not necessarily exclude prior infection.
- Athletes without cardiopulmonary symptoms can often return to training gradually without extensive cardiac testing, while symptomatic athletes may require further assessment.
- In Finland, athletes with suspected COVID-related cardiac involvement are commonly referred for cardiology assessment or specialist evaluation rather than managed entirely in primary care.
- Recovery after COVID-19 should be guided by symptoms, functional capacity, and response to training rather than by an arbitrary timeline alone.
- For most athletes, the goal is not to avoid training unnecessarily but to return progressively while remaining alert to warning signs that may indicate a more complicated recovery.
Introduction: COVID in Athletes
When SARS-CoV-2 swept through the sports world, it raised questions that went far beyond a standard respiratory illness. I remember that shift clearly from clinical practice. At first, COVID-19 was concerning because it was new and, especially early in the pandemic, clearly dangerous for some patients. But over time, the clinical picture became more complicated: thrombotic complications entered the discussion, myocarditis became a concern, and long COVID added another layer of uncertainty.
For athletes and the clinicians who care for them, the questions became very specific. Does COVID-19 damage the heart? How does it affect aerobic capacity? And when — and how safely — can an athlete return to full competition?
The answers matter enormously. Myocarditis is a leading cause of sudden cardiac death (SCD) in athletes [13]. Even a mild post-COVID performance hit can cost an elite athlete their season. And for those who develop long COVID, the consequences can stretch for months, disrupting not only everyday life but also training continuity, competition schedules, and careers that take years to build.
In my view, this is why COVID in athletes should not be discussed only as a short-term infection. The acute illness may often appear milder today than it did in the early pandemic years, but the virus has not disappeared. For an athlete, the key question is not only whether the fever, cough, or sore throat has resolved. It is whether the heart, aerobic capacity, and recovery system are ready for progressive training again.
How Common Are Cardiac Complications From COVID in Athletes?
The cardiac concern was the most urgent early question, and the research gave us reassurance — with important caveats.
A 2022 systematic review published in BMC Sports Science, Medicine and Rehabilitation examined 15 eligible articles comprising a total of 6,229 athletes, of whom 1,023 were elite or professional athletes. The reported prevalence of myocarditis ranged between 0.4% and 15.4%, pericarditis between 0.06% and 2.2%, and pericardial effusion between 0.27% and 58% [1]. The wide ranges reflect differences in screening protocols across studies — more sensitive imaging consistently finds more cases.
The Big Ten COVID-19 Cardiac Registry provided some of the most comprehensive data on COVID-19 cardiac involvement in collegiate athletes. Cardiovascular testing was performed in 1,597 athletes from 13 universities. Thirty-seven athletes (2.3%) were diagnosed with COVID-19 myocarditis; 9 had clinical myocarditis and 28 had subclinical myocarditis [2]. Critically, a CMR-imaging strategy applied regardless of cardiac symptoms led to a 7.4-fold increase in myocarditis detection compared with a symptom-driven screening strategy alone [2]. The implication is significant: screening protocols that rely solely on clinical symptoms may not detect subclinical myocarditis cases visible on CMR — including athletes with elevated troponin levels who remain asymptomatic.
The systematic review concludes that “this study provides a low prevalence of CV complications secondary to COVID-19 infection in short-term follow-up” — but adds that “early recognition and continuous assessment of cardiac abnormality in competitive athletes are imperative to prevent cardiac complications” and that “establishing a stepwise evaluation approach is critical with an emphasis on imaging techniques for proper diagnosis and risk assessment for a safe return to play” [1].
One point that is worth emphasizing is that the possibility of COVID-related myocarditis does not automatically change clinical decision-making in athletes who have recovered without concerning symptoms. In practice, the approach today is broadly similar to the approach used for other respiratory infections. Once symptoms have resolved, a gradual return to training can usually begin, with attention to how the athlete responds as exercise intensity increases.
From a clinical perspective, this reflects an important distinction between relative risk and absolute risk. We know that COVID-19 has been associated with myocarditis and other cardiac complications, which is one reason the topic received so much attention during the pandemic. However, the overall risk appears to be low, particularly in athletes who are asymptomatic and recovering as expected. For that reason, the mere possibility of myocarditis is not, by itself, a reason to subject every athlete to extensive cardiac investigations.
What continues to matter most is the presence of symptoms. When I assess athletes after COVID-19, the symptoms themselves are often what guide further evaluation. Chest pain, unexplained shortness of breath, palpitations, reduced exercise tolerance, or other cardiopulmonary symptoms may warrant additional assessment. In the absence of such findings, management is often centered on a sensible and progressive return to activity rather than routine cardiac testing.
Long COVID in Athletes: Prevalence and Symptom Profile
Long COVID — defined as a condition where symptoms or complications persist beyond 3 months after COVID-19 infection [3] — can also affect athletes. Although most athletes experience mild symptoms, long COVID can also affect athletes.
A retrospective survey of approximately 7,000 collegiate student athletes across 18 United States schools found that about 4% of student athletes who tested positive from spring 2020 to spring 2021 developed Long COVID, defined as new, recurring, or ongoing physical or mental health consequences occurring 4 or more weeks after SARS-CoV-2 infection [4].
A prospective cohort study following three Belgian professional male football teams during the 2020–2021 season found that aerobic performance was compromised even weeks after infection, with significantly higher percentages of maximal heart rate during the Yo-Yo Intermittent Recovery test at a mean of 52.0 ± 11.2 days post-infection, with this effect resolved at a mean of 127.6 ± 33.1 days after positive PCR testing [5]. The most commonly reported long-lasting symptoms in athletes include a persistent cough and lasting fatigue [5].
What does the symptom picture look like? Post-acute sequelae of SARS-CoV-2 (PASC), or long COVID syndrome, is characterized in the general long COVID population by symptoms that include fatigue, palpitations, chest pain, dyspnea, reduced exercise tolerance, and “brain fog.” Additionally, symptoms of orthostatic intolerance and syncope suggest the involvement of the autonomic nervous system [6]. Signs of cardiovascular autonomic dysfunction appear to be common in PASC and are similar to those observed in postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia [6]. While these mechanisms have been established in general long COVID populations, they can be particularly punishing for athletes — an elite competitor who cannot tolerate exercise without palpitations, orthostatic instability, or post-exertional malaise faces a clinical picture that standard cardiac clearance testing may not fully capture.
The inflammatory response is a parallel mechanism: some studies of long COVID patients have reported persistent elevation of interleukin-6 and other cytokines, though the magnitude and consistency of these findings varies across studies [12].
Another practical issue is that many COVID-19 infections are no longer formally confirmed, especially in everyday clinical settings. In Finland, COVID-19 is now often approached much like other viral respiratory infections, and routine testing has largely disappeared from ordinary practice. From a clinical perspective, this matters because the absence of a documented positive test does not always mean the absence of COVID-19.
In my experience, cost and clinical usefulness strongly influence testing decisions. If a test result does not change treatment, isolation advice, work ability assessment, or follow-up, it is often not ordered in routine healthcare. Many people who still want confirmation use home antigen tests, which are typically much cheaper and easier to access than laboratory-based testing. For athletes, that can sometimes be relevant: a self-performed rapid test may help them understand whether a recent respiratory illness could plausibly have been COVID-19, especially if they are trying to interpret delayed recovery or an unexpected drop in performance.
This also means that athletes are not usually treated as a separate testing category in standard public healthcare. In most cases, the clinical assessment is still based on symptoms, recovery pattern, and whether there are warning signs such as chest pain, palpitations, disproportionate breathlessness, or unusually prolonged fatigue. A positive test can add context, but it does not replace clinical judgement.
What COVID in Athletes Does to Aerobic Capacity
Beyond cardiac complications, the performance science literature documents a consistent pattern: COVID-19 in athletes reduces aerobic fitness, even in elite competitors, even after mild infection.
A 2025 systematic review and meta-analysis published in Sports (Basel) analyzed 26 studies employing cardiopulmonary exercise testing (CPET) in 2,625 pooled athletes and found that aerobic fitness was reduced in athletes post-COVID-19. Athletes with persistent symptoms had 8 mL/kg/min lower V̇O2max than those without infection (p = 0.04) [7]. For elite endurance athletes, a reduction of this magnitude represents meaningful competitive disadvantage.
The soccer-specific evidence is particularly direct. An observational study of 21 division-1 elite soccer players compared aerobic capacity before and 60 days after COVID-19 recovery. The infected players had significantly lower VO2max values (p < 0.01, d = 0.613, medium effect) and significantly lower VO2 values at respiratory compensation point after recovery [8]. Furthermore, results indicated a significantly lower running time on the treadmill (p < 0.01, d = 0.46) and a significantly lower velocity at VO2max (p < 0.05, d = 0.41) when compared to results obtained before infection [8]. The authors conclude that post-COVID-19 soccer players may not reach full recovery at two months [8].
Recovery timelines also vary between athletes. An IOC Research Centre study (AWARE VIII) prospectively followed 84 athletes with confirmed SARS-CoV-2 infection at a COVID-19 recovery clinic. The total number of acute symptoms was identified as the most significant factor associated with prolonged time to return to full sports performance after infection. The number of systemic symptoms was also strongly associated with delayed return. Females, endurance athletes, and athletes with a history of co-morbidities also experienced a more prolonged return to full performance [9].
Why does this happen? Multiple mechanisms contribute to reduced aerobic capacity after COVID-19, including pulmonary limitations, cardiovascular deconditioning, impaired peripheral oxygen uptake, and autonomic dysfunction affecting heart rate regulation during exercise. Cardiopulmonary exercise testing (CPET) evaluates aerobic and anaerobic delivery limits involving the cardiovascular, musculoskeletal, and pulmonary systems and is a useful tool for assessing exercise capacity in post-COVID athletes [7][14].
The impact of long COVID is not limited to physical performance alone. For athletes, reduced exercise tolerance may be the most visible problem, but the broader clinical picture can involve fatigue, cognitive symptoms, sleep disruption, mood changes, and a loss of confidence in the body’s ability to recover.
In clinical practice, long COVID can be one of the more difficult post-infectious conditions to evaluate. The challenge is not only that symptoms may persist, but that the symptom pattern often overlaps with conditions clinicians already see frequently: fatigue syndromes, burnout, depression, deconditioning, sleep disruption, and stress-related symptoms. In many patients, these factors may also coexist, which makes the clinical picture less clear than a simple “COVID caused this” explanation.
This is one reason I approach long COVID with some caution. A definitive diagnosis is not always straightforward, and in some cases the most honest clinical conclusion is that the patient has persistent symptoms after COVID-19 without one single clearly proven mechanism. Treatment can also be challenging. In practice, care is often rehabilitative and supportive, involving graded physical rehabilitation, physiotherapy, psychological support, and management of specific symptoms rather than one simple curative treatment.
For athletes, this uncertainty can be especially frustrating. The symptoms may be real and functionally limiting, even when standard tests do not provide a neat explanation. That is why long COVID in athletes requires a careful clinical assessment: not dismissing symptoms as “just stress,” but also not assuming that every episode of fatigue or poor performance after infection is automatically long COVID.
Assessing COVID in Athletes Before Return to Training
A rigorous return-to-play approach is no longer optional when managing COVID in athletes. The 2022 American College of Cardiology (ACC) Expert Consensus Statement on COVID-19 cardiovascular sequelae provides a practical framework: regardless of symptomatology, all athletes with prior COVID-19 should implement a graded return-to-play regimen [10].
Symptom screening before any return to training should actively probe for:
- Chest pain or pressure at rest or with exertion
- Palpitations or awareness of irregular heartbeat
- Dyspnea disproportionate to exertion level
- Dizziness or presyncope on standing or during exercise
- Profound fatigue or post-exertional malaise — symptoms that worsen in the 24–48 hours following physical activity
- Cognitive changes (“brain fog”), poor concentration, or memory problems
Athletes without cardiopulmonary symptoms after COVID in athletes can gradually return to play without undergoing a battery of cardiac testing [10]. Athletes with new or recurrent cardiopulmonary symptoms warrant cardiac evaluation before clearance — the ACC recommends triad testing consisting of a 12-lead ECG, cardiac troponin (preferably high sensitivity), and echocardiography, with CMR imaging reserved for cases with concerning findings or ongoing symptoms [10].
In Finland, this level of cardiac evaluation is generally no longer a routine primary care assessment. In practice, if an athlete has chest pain, palpitations, disproportionate breathlessness, syncope, or other symptoms raising concern for cardiac involvement, I would usually consider cardiology assessment or referral to specialist care rather than trying to manage the entire evaluation as an ordinary respiratory infection follow-up.
From a practical clinical perspective, COVID-19 is now managed much more like other viral respiratory infections than it was during the early stages of the pandemic. The level of uncertainty that initially surrounded the virus has largely diminished, and in most cases there is no longer a need for the same degree of precaution that characterized the first years of COVID-19.
It is also important to remember that myocarditis and other post-infectious complications are not unique to COVID-19. Clinicians have long recognized that a variety of viral illnesses can occasionally be followed by cardiac involvement or prolonged recovery. COVID-19 brought these issues into sharper focus, but the underlying clinical principle is broader than any single virus. In my experience, this is an important point because it helps place COVID-related risks into a more balanced context. The possibility of myocarditis deserves respect, but it should be viewed as part of the wider spectrum of post-viral complications rather than as a phenomenon exclusive to COVID-19.
Conclusion: COVID in Athletes
COVID in athletes is no longer surrounded by the same uncertainty that defined the early pandemic, but it still deserves careful clinical judgement. For most athletes who recover without cardiopulmonary symptoms, the practical approach is usually a gradual, symptom-guided return to training rather than routine cardiac testing. At the same time, COVID-19 can still be associated with myocarditis, prolonged recovery, reduced aerobic capacity, and long COVID, and these issues matter more in athletes because small physiological changes can have large performance consequences.
In my view, the most useful way to approach COVID in athletes is to avoid both extremes. It should not be treated as a uniquely dangerous infection that automatically requires extensive investigations in every recovered athlete. But it should also not be dismissed as irrelevant once the acute respiratory symptoms have settled. The key is to look at the recovery pattern: chest pain, palpitations, disproportionate breathlessness, syncope, persistent fatigue, post-exertional worsening, or an unexplained drop in performance should change the clinical threshold for further assessment.
Ultimately, safe return to sport after COVID-19 is less about the name of the virus and more about how the athlete recovers from it. A positive test can add context, but symptoms, function, training response, and clinical judgement remain central. For athletes, coaches, and clinicians, the goal is not unnecessary caution, but a balanced return to training that respects both cardiac safety and the realities of athletic performance.
References
[1] https://doi.org/10.1186/s13102-022-00464-8
[2] https://doi.org/10.1001/jamacardio.2021.2065
[3] https://doi.org/10.1080/00913847.2024.2321629
[4] https://doi.org/10.1186/s12879-023-08801-z
[5] https://doi.org/10.1080/07853890.2023.2198776
[6] https://doi.org/10.3390/jcdd8110156
[7] https://doi.org/10.3390/sports13020040
[8] https://doi.org/10.1038/s41598-022-16031-7
[9] https://doi.org/10.1016/j.jshs.2023.10.005
[10] https://doi.org/10.1016/j.jacc.2022.02.003
[12] https://doi.org/10.1186/s40249-023-01086-z
[13] https://doi.org/10.1016/j.csm.2022.02.007
[14] https://www.ahajournals.org/doi/10.1161/CIR.0000000000001348
