CK-MB in Athletes: Why This “Cardiac Marker” Routinely Rises After Hard Training
Table of Contents
Introduction
In clinical practice, I may occasionally encounter a situation in which cardiac markers need to be tested in an athlete, including CK-MB. The indications are generally the same as in the wider population: concern for a possible cardiac event or myocardial injury. However, CK-MB in athletes can be more complicated to interpret if the athlete has exercised recently, because skeletal muscle can contribute to circulating CK-MB, especially after strenuous exercise — a physiological reality that standard clinical CK-MB thresholds do not fully account for. This is not an everyday clinical scenario, but it is one that clinicians may occasionally have to interpret carefully.
I wrote this article to explain the physiology behind CK-MB elevation in athletes, how I approach the distinction between skeletal and cardiac sources, and why troponin has become the preferred marker when genuine cardiac injury is suspected
For a broader look at how exercise affects related muscle damage markers, make sure to see my article on myoglobin vs creatine kinase.
What CK-MB in Athletes Actually Measures — and Where It Lives
Creatine kinase (CK) is a critical enzyme involved in cellular energy metabolism, catalyzing the reversible transfer of a phosphate group from ATP to creatine [1]. It exists in tissue-specific isoenzymatic forms: CK-MM (muscle), CK-BB (brain), and CK-MB — a hybrid of muscle and brain subunits that has historically served as a key biomarker for detecting myocardial infarction, due to its relative abundance in cardiac muscle [1].
The tissue distribution is worth understanding precisely. The myocardium has 15% CK-MB isoenzyme and 85% CK-MM, while skeletal muscles contain about 1% to 3% of CK-MB [1]. Stated differently at the isoform level: skeletal muscle comprises 98% MM and 2% MB; cardiac muscle comprises 70–80% MM and 20–30% MB [2].
Because cardiac muscle contains a higher proportion of CK-MB than typical skeletal muscle, CK-MB was historically a useful diagnostic marker. The complication in athletes arises because skeletal muscle contains measurable CK-MB, and strenuous exercise can release muscle-derived CK-MB into circulation.
In clinical practice, I still sometimes see CK-MB used as part of a cardiac marker panel, often alongside troponin and other tests, to support diagnostic assessment when there is concern about possible myocardial injury. The challenge in athletes is that CK-MB can sometimes rise without true cardiac pathology, especially after strenuous exercise. This can make the result difficult to interpret if it is viewed in isolation.
For that reason, I place particular emphasis on the clinical history. When I interpret CK-MB in an athlete, I want to know not only whether there are cardiac symptoms such as chest pain, dyspnoea, or palpitations, but also what the athlete has done in the days before the blood test: recent training load, competition, muscle soreness, trauma, and recovery pattern all matter. In this context, the laboratory value is only one part of the clinical picture.
Why CK-MB Is Elevated After Training Even Without Cardiac Damage
The conventional assumption that skeletal muscle contributes negligibly to serum CK-MB collapses under scrutiny in trained athletes. Older reports had indicated that CK–MB was absent from skeletal muscle, but radioimmunoassay enzyme analysis reports levels of CK–MB of 5 to 7% in skeletal muscle — a finding that may account for abnormal levels of CK–MB reported in endurance and contact athletes [3].
The picture becomes even clearer when trained and untrained individuals are compared directly. CK-MB was subsequently shown to lack complete cardiac tissue specificity, especially among athletes in whom skeletal muscle CK-MB concentrations were higher (8.9±1.3% versus 3.3±0.7% in the gastrocnemius muscle of marathoners compared with untrained controls) [4]. This is a substantial difference — the gastrocnemius muscle of a marathon runner contains approximately 2.7-fold higher CK-MB fraction than the same muscle in an untrained individual.
The mechanism is linked to fibre type composition. CS and CK-MB activities were higher in trained groups in both slow-twitch and fast-twitch fibre types, and the ratio for CK-MB increased with a greater degree of endurance training [5]. This suggests that endurance training may be associated with higher CK-MB activity in skeletal muscle, particularly in slow-twitch fibres — a finding consistent with the metabolic demands of sustained aerobic exercise.
The exercise-induced muscle disruption that drives elevated myoglobin in athletes also contributes to CK-MB release, since exercise-induced skeletal muscle disruption can release several muscle-derived proteins and enzymes simultaneously.
For this reason, I do not rely on CK-MB alone when assessing possible cardiac pathology. In a patient with suspected cardiac involvement, troponins are always central to the evaluation. CK-MB can provide context, but it should not be interpreted in isolation, especially in athletes who have recently trained or competed.
In general, troponin is the more reliable marker for suspected myocardial injury, but even troponin is not completely straightforward in athletes. Exercise itself can also cause transient troponin elevations, which is why timing, symptoms, ECG findings, and serial measurements all matter. I discuss this in more detail in my article on troponin after marathon.
How Intense Exercise Specifically Drives CK-MB Elevation
Rhabdomyolysis, intense exercise, and trauma result in transient elevation of CK and CK-MB; CK-MB is present in skeletal muscles as well, albeit in lesser concentrations [1]. The effect is described across exercise modalities, including endurance events, resistance training, and contact sports.
In marathon running specifically, serum creatine kinase MB (CK-MB) may be elevated in asymptomatic marathon runners after competition from exertional rhabdomyolysis of skeletal muscle altered by training, limiting its utility for evaluating acute cardiac injury in such athletes [6]. This is a clinically important point: in an asymptomatic athlete with recent strenuous training, isolated CK-MB elevation may not by itself indicate acute cardiac injury, and a skeletal muscle contribution should be strongly considered.
The temporal pattern is instructive. Total serum CK activity is markedly elevated for 24 h after the exercise bout and, when patients rest, it gradually returns to basal levels [7]. If CK-MB is measured within 12–24 hours of major exercise, a skeletal muscle contribution should be strongly considered, especially in a fully asymptomatic athlete.
In one resistance-exercise study in healthy young women, CK-MB increases were transient — returning to baseline within 48 hours — and were interpreted as not indicating persistent cardiac damage [8]. The distinction between this kind of reversible enzyme leakage and pathological myocardial necrosis is a central theme in CK-MB interpretation for athletes.
However, CK-MB kinetics are too slow and too nonspecific to safely rule out cardiac events on their own. A lack of CK-MB elevation, or a delayed rise, does not exclude a cardiac condition. The same principle applies, to a lesser extent, to troponin: a normal troponin result may reduce the likelihood of myocardial injury depending on timing and clinical context, but it does not automatically make the patient “cardiac safe” if symptoms, ECG findings, or overall clinical suspicion remain concerning.
The problem is that these markers do not always rise or fall quickly enough to serve as the sole basis for urgent primary decision-making. In acute clinical care, where decisions often need to be made without delay, the assessment has to be led by the cardiac differential first. True myocardial infarction and myocarditis need to be considered and ruled out appropriately before attributing CK-MB elevation to exercise.
In that sense, exercise-related CK-MB elevation is often more of a retrospective interpretive point than the primary clinical decision-maker. Once serious cardiac pathology has been assessed and excluded, it may be reasonable to consider whether the CK-MB elevation was related to recent training or competition.
Why Troponin Replaced CK-MB as the Gold Standard
The limitations of CK-MB in athletes reflect a broader clinical evolution. CK-MB was subsequently shown to lack complete cardiac tissue specificity, especially among athletes in whom skeletal muscle CK-MB concentrations were higher (8.9±1.3% versus 3.3±0.7% in the gastrocnemius muscle of marathoners compared with untrained controls), and released in response to exercise-induced muscle injury. Accordingly, cTn replaced CK-MB as the gold-standard marker for myocardial injury following the Redefinition of Myocardial Infarction in 2000 [4].
Cardiac troponins have largely supplanted CK-MB in routine clinical practice and are now the preferred biomarkers for myocardial injury — when cardiac injury is suspected, evaluation should rely on clinical assessment, ECG, and serial cardiac troponin testing [1].
That said, troponin elevation post-exercise is itself a complex topic. In adolescent adventure race athletes, most cardiac biomarker concentrations returned to baseline by 24–48 h post-exercise, although CK-MB remained elevated after the longer 2-day race, with this response characterised as a standard exercise intensity-dependent response rather than pathological response [9]. The temporal distinction between exercise-related and pathological elevations is clinically useful: a review of the cTn kinetics literature demonstrates a pattern of elevation and peak within the first 4 h after exercise dropping within 24 h; in contrast myocardial necrosis demonstrates a later cTn peak with a slower downslope occurring over several days [10].
As I mentioned earlier, cardiac troponin has become the gold standard biomarker when assessing suspected myocardial injury. In my clinical thinking, this makes sense because cardiac troponin assays are far more specific to cardiac muscle than CK-MB, which can also come from skeletal muscle. That distinction matters especially in athletes, where recent training or competition can complicate the interpretation of CK-MB.
At the same time, I do not treat troponin as a perfect marker in isolation. Exercise itself can cause transient troponin elevations in some athletes, typically with an early peak and decline within about 24 hours [10]. For that reason, I still interpret troponin alongside symptoms, ECG findings, timing, serial measurements, and the wider clinical picture. Even so, troponin’s cardiac specificity, sensitivity, and clinical kinetics usually make it a more useful tool than CK-MB when I am considering a true cardiac event.
I still see CK-MB measured in some clinical settings, particularly in cardiac patients who are being followed on a cardiology ward. In that context, I see CK-MB as a supportive marker rather than a diagnostic anchor. If CK-MB and troponin are both elevated in a patient whose symptoms, ECG, and overall presentation suggest cardiac pathology, CK-MB may add confidence to the broader assessment. But CK-MB alone does not confirm myocardial injury, and a normal CK-MB does not exclude it. For me, it is one piece of context — never the deciding factor on its own.
Conclusion
CK-MB in athletes is a good example of why laboratory results should never be interpreted outside the clinical context. CK-MB was historically useful as a cardiac marker, but it is not completely cardiac-specific. In athletes, recent strenuous exercise, competition, skeletal muscle stress, and training-related muscle adaptation can all make CK-MB harder to interpret than it may first appear.
For me, the most important clinical point is that CK-MB should not be used as the deciding factor when myocardial injury is suspected. A raised CK-MB in an athlete may reflect skeletal muscle release, but that possibility should usually be considered only after serious cardiac causes, such as myocardial infarction and myocarditis, have been assessed appropriately. In acute care, the priority is not to explain the number retrospectively, but to make sure that clinically important cardiac pathology is not missed.
This is why troponin, ECG findings, symptoms, timing, and serial assessment remain central. Troponin is more cardiac-specific and clinically useful than CK-MB, although even troponin can rise transiently after strenuous exercise in some athletes. CK-MB can still provide supportive context in selected situations, but it should never be interpreted in isolation.
Ultimately, CK-MB elevation after hard training is often more of an interpretive challenge than a diagnosis. The safest approach is to combine the laboratory result with the athlete’s recent training history, symptoms, examination findings, ECG, troponin results, and overall clinical picture. When interpreted this way, CK-MB can be understood without causing unnecessary alarm — while still keeping patient safety first.
References
[1] https://www.ncbi.nlm.nih.gov/books/NBK557591/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC3263635/
[3] https://www.ncbi.nlm.nih.gov/books/NBK352/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC8663527/
[5] https://pubmed.ncbi.nlm.nih.gov/4043049/
[6] https://pubmed.ncbi.nlm.nih.gov/9397299/
[7] https://pubmed.ncbi.nlm.nih.gov/17569697/
[8] https://brieflands.com/journals/jkums/articles/84103
