LDH in Athletes: What Elevated Lactate Dehydrogenase Really Means in Your Blood Work
Table of Contents
Introduction: Why LDH in Athletes Can Be Difficult to Interpret
Lactate dehydrogenase is an unfamiliar marker for much of the general public, and in my experience, it is also less familiar to many clinicians than enzymes such as creatine kinase, ALT, or AST. In primary care, LDH is not usually one of the first-line blood markers used in everyday assessment, although in specialist care it is by no means an obscure concept.
When I review blood work from athletes, I approach LDH with particular caution. LDH in athletes can be difficult to interpret because exercise, tissue injury, and hemolysis can all influence the result simultaneously. Their values may also differ from those seen in the general population, which makes training context essential before assuming that an elevated result represents disease.
I wrote this article to break down the science of LDH in athletes: what the enzyme does, why athletes may show higher values than the general population, how to distinguish physiological elevation from genuine pathology, and what LDH can tell us about exercise-induced hemolysis — an important and often overlooked process in endurance sports medicine.
What Is LDH and Why Does It Matter for Athletes?
Lactate dehydrogenase is an enzyme that catalyzes the interconversion of pyruvate and lactate — the critical fuel exchange at the heart of anaerobic energy metabolism. It is present in almost all tissues in the body, with high concentrations in muscle, liver, and kidney; red blood cells also contain LDH [1].
LDH in athletes exists as five distinct isoforms — LDH-1 through LDH-5 — each reflecting different tissue origins. LDH-1 is the major cardiac isoenzyme; LDH-2 is prominent in the reticuloendothelial system and red blood cells; LDH-5 is strongly expressed in liver and skeletal muscle [1]. This tissue specificity matters in clinical interpretation. When LDH is elevated in an athlete, the isoenzyme pattern can provide tissue-specific clues — but results must always be interpreted with clinical context and other markers.
A standard LDH blood test reports only total LDH — a single number that collapses all five isoforms into one value. For the general population, this is often sufficient. For athletes, total LDH can be difficult to interpret without clinical context and, in selected cases, isoenzyme or companion-marker testing.
In clinical work, I think of LDH as a general marker of tissue injury rather than a diagnosis in itself. Because LDH is present in almost all cells, its release into the bloodstream usually tells us that cells have been damaged, destroyed, or are leaking their intracellular contents into circulation. On its own, LDH is not specific for any single disease process or organ system. Its value comes from interpreting it alongside other markers, symptoms, and the wider clinical context.
This is why I approach LDH as a clue, not an answer. It may rise in ischemic conditions, such as myocardial ischemia, intestinal ischemia, or infarction affecting the lungs or other internal organs. It can also increase after skeletal muscle stress, in hemolysis involving red blood cells, and in some liver-related conditions such as hepatitis or other forms of hepatocellular injury.
I would also add that LDH can sometimes be used as an indirect marker of disease activity in oncology. This does not mean that LDH diagnoses cancer, and it is far too non-specific to be interpreted that way. However, in certain cancers, LDH may help reflect tumour burden, tissue turnover, or overall disease activity when interpreted together with imaging, symptoms, and other disease-specific markers.
In surgical and emergency settings, LDH can sometimes become part of the broader picture when clinicians are evaluating an acute abdomen or another potentially urgent tissue-injury state. I would not use LDH alone to decide urgency, but it can provide additional information alongside physical examination, imaging, and other laboratory findings. That is exactly why LDH is both useful and easy to overinterpret: it can tell us that tissue injury may be present, but it rarely tells us the full story by itself.
Why LDH in Athletes May Run Higher Than Population Reference Ranges
Elite athletes may have LDH distributions and upper reference limits that differ from general-population reference intervals — and therefore, an isolated LDH elevation should be interpreted in training context before assuming pathology.
A study analyzing 14,010 blood samples from 3,588 elite athletes across 32 sport modalities over nine years found that exercise produces changes in the basal values of biochemical and hematological parameters in athletes compared to the general population, with LDH showing characteristically higher values and a wider distribution of results compared to general population reference intervals [2].
This finding has practical consequences. Standard laboratory reference ranges are derived from the general population — not from individuals training once or twice daily. A flagged LDH in an athlete should be interpreted in relation to recent training, symptoms, and other laboratory markers rather than judged solely against general-population reference intervals.
Skeletal muscle is one plausible contributor to LDH elevation in athletes, because LDH is abundant in muscle tissue and exercise-related muscle stress can affect serum enzymes. Serum creatine kinase (CK) and LDH give an indication of the degree of metabolic adaptation to physical training of skeletal muscles, and both increase considerably after intensive exercise [3]. For a detailed breakdown of how CK behaves alongside LDH in this context, see the dedicated article on creatine kinase elevated in athletes. When myoglobin is also elevated, skeletal muscle injury becomes an important clinical consideration — this is covered in the article on myoglobin vs creatine kinase.
In clinical work, I think of LDH as a general marker of tissue injury rather than a diagnosis in itself. Because LDH is present in almost all cells, its release into the bloodstream usually tells us that cells have been damaged, destroyed, or are leaking their intracellular contents into circulation. On its own, LDH is not specific for any single disease process or organ system. Its value comes from interpreting it alongside other markers, symptoms, and the wider clinical context.
This is why I approach LDH as a clue, not an answer. It may rise in ischemic conditions, such as myocardial ischemia, intestinal ischemia, or infarction affecting the lungs or other internal organs. It can also increase after skeletal muscle stress, in hemolysis involving red blood cells, and in some liver-related conditions such as hepatitis or other forms of hepatocellular injury.
I would also add that LDH can sometimes be used as an indirect marker of disease activity in oncology. This does not mean that LDH diagnoses cancer, and it is far too non-specific to be interpreted that way. However, in certain cancers, LDH may help reflect tumour burden, tissue turnover, or overall disease activity when interpreted together with imaging, symptoms, and other disease-specific markers.
In surgical and emergency settings, LDH can sometimes become part of the broader picture when clinicians are evaluating an acute abdomen or another potentially urgent tissue-injury state. I would not use LDH alone to decide urgency, but it can provide additional information alongside physical examination, imaging, and other laboratory findings. That is exactly why LDH is both useful and easy to overinterpret: it can tell us that tissue injury may be present, but it rarely tells us the full story by itself.
The Isoenzyme Story: How LDH in Athletes Differs by Training Type
One of the most clinically interesting aspects of LDH in athletes is that its isoenzyme profile may diverge significantly based on training type — a distinction that total LDH alone cannot reveal.
Muscle biopsy and enzyme studies suggest that LDH isoenzyme profiles may differ between endurance- and strength-oriented athletes: endurance athletes have been reported to show lower total LDH with a prevalence of LDH1–2 isoenzyme activity, while strength athletes tend toward higher total LDH and LDH5 predominance [3]. These differences are thought to relate to different metabolic demands and biochemical adaptation associated with different training types.
Longitudinal marathon training data are consistent with training-related shifts in LDH isoenzyme distribution: in a 30-week marathon training programme in 38 sedentary middle-aged men (aged 35–50 years), LDH1 and LDH2 isoenzyme activity increased by 2.5% and 4% of total LDH respectively, while LDH3 and LDH5 decreased by 3.9% and 2.4% respectively over 30 weeks [4].
The practical implication: a well-trained endurance athlete with mildly elevated total LDH but a predominantly LDH1–2 profile may be showing metabolic adaptation to training. This pattern is compatible with endurance training adaptation, but cardiac, hepatic, and hemolytic causes must still be interpreted using symptoms, other biomarkers, and clinical context. This is particularly important when LDH1 elevation triggers concern about cardiac injury — a topic covered in detail in the article on CK-MB in athletes.
In everyday clinical practice, LDH isoenzymes are usually not the main focus. They are scientifically interesting and can provide tissue-specific information in selected situations, but for most clinicians, LDH is used as a total value rather than separated into subtypes. This is because LDH remains a non-specific diagnostic marker, even when the isoenzyme pattern is available.
In specialist settings, LDH isoenzyme fractionation may sometimes provide additional information, particularly when the clinical question is narrow and the result can be interpreted alongside other investigations. However, for the everyday clinician reviewing routine blood work, the practical question is usually not which LDH subtype is elevated, but why the total LDH is elevated in the first place — and whether the clinical context suggests exercise, hemolysis, tissue injury, ischemia, liver involvement, or another process.
LDH in Athletes as a Hemolysis Marker
Of all the reasons LDH may rise in athletes, exercise-induced hemolysis is not usually the most clinically dangerous explanation, but it can be an important part of the interpretation. In runners and endurance athletes especially, hemolysis may help explain a mild or transient LDH elevation when the rest of the clinical picture is reassuring.
Exercise-induced hemolysis can be conventionally defined as rupture and destruction of erythrocytes during physical exercise [5]. When red blood cells lyse, they release their intracellular contents into the circulation. LDH, AST, unconjugated bilirubin, and potassium may support the diagnosis of hemolytic processes, although these markers have lower specificity than free hemoglobin and haptoglobin [5]. The behavior of potassium during and after exercise is explored further in the article on potassium in athletes.
A substantial degree of exercise-induced hemolysis is commonplace after short-, medium-, long- and ultra-long distance running, as reflected by significant decrease of serum or plasma haptoglobin and significant increase of plasma concentration of free hemoglobin [5].
This paraphysiological intravascular hemolysis is typically mild — average variations of hemolysis biomarkers are usually comprised between 1.2- and 1.8-fold — almost self-limiting, completely resolving within 24–48 hours, with severity depending on athlete population, analytical technique used for detecting intravascular hemolysis, as well as on number, frequency and intensity of ground contacts, but not on running technique [5].
Repeated forceful ground contacts are one proposed contributor to exercise-induced hemolysis in runners [5]. Erythrocyte lifespan in runners is approximately 40% shorter than in sedentary controls [5]. Exercise-induced hemolysis is detectable in post-exercise biomarker changes, including decreased haptoglobin and increased free hemoglobin, and the full clinical picture of footstrike hemolysis — including its effect on ferritin, haptoglobin, and reticulocyte count — is explored in depth in the article on footstrike hemolysis in distance runners.
Exercise-induced hemolysis may be relevant when evaluating iron status in runners, but ferritin and iron depletion require separate assessment and supporting evidence. The relationship between iron loss and ferritin dynamics is explored further in the article on serum iron vs ferritin, and the downstream effect on hemoglobin levels is covered in the article on hemoglobin levels in runners.
Exercise-induced hemolysis rarely appears to cause clinical danger or clinically significant anemia in athletes, except perhaps in unusual individual cases. In my clinical thinking, I see it more often as a possible explanatory factor than as a primary diagnosis. The degree of hemolysis caused by exercise is usually small enough for the body to compensate effectively, which is why it often becomes relevant only when we are trying to understand a mild or transient LDH elevation.
I would not use exercise-induced hemolysis as the only explanation for an elevated LDH before looking at the broader clinical picture. When I assess this kind of result, I want to know the timing of recent exercise, the athlete’s symptoms, hemoglobin, haptoglobin, bilirubin, CK, liver enzymes, and whether the abnormality persists or normalizes. If the athlete is well, the LDH elevation is mild, and the test was taken soon after hard training or racing, exercise-related hemolysis becomes a plausible part of the explanation.
In practice, I rarely see LDH elevation from exercise-induced hemolysis lead to major clinical intervention by itself. More often, it is a retrospective interpretation: the blood test shows a mild LDH rise, the athlete has a clear recent training or race history, and the rest of the clinical picture is reassuring. The important point is not to ignore the result, but also not to overreact to a small, contextually understandable LDH elevation.
LDH in Athletes During Ultra-Endurance Events: When Numbers Get Extreme
LDH elevations can be substantial after ultramarathon events, and the magnitude depends on distance, terrain, duration, athlete factors, and sampling time. Ultra-distance runners may show LDH values that require careful interpretation in context.
In a study of six male ultra-runners completing a 217-km mountain ultramarathon, serum LDH (baseline 371 ± 66 U/L) increased significantly throughout the race (P < 0.001), with a large effect size magnitude of muscle damage, rising approximately 1.8-fold by 84 km [6]. CK, LDH, and AST rose as part of the muscle-damage biomarker response reported in that study, alongside other inflammatory and renal-risk findings.
Among non-elite runners completing a 67-km mountain ultramarathon, LDH increased by +87% from pre- to post-race, and values of LDH +56% remained elevated at recovery [7]. The authors concluded that CK and LDH levels and leucocytosis may be considered to be relatively harmless “side-effects” of prolonged running in this group of male subjects, while noting that acute kidney injury risk in certain circumstances is clinically relevant [7].
For the clinician reviewing post-race blood work, context about what is normal for various distances is essential. The full picture of expected LDH in athletes after marathon and ultramarathon racing — including which markers normalize first and when to order repeat testing — is covered in the article on post-marathon blood work. It is also worth noting that extreme muscle damage from ultra-endurance exercise can secondarily raise creatinine, complicating renal function interpretation — a distinction explored in the article on creatinine in athletes.
In ultramarathon runners, I am usually more immediately concerned about CK, myoglobin, potassium, renal function, and the athlete’s symptoms than LDH itself. LDH is often included in a broader blood panel, but when I am worried about a serious exercise-related complication, my first priority is to consider and exclude rhabdomyolysis.
If an athlete feels well and has no concerning symptoms, I do not think there is necessarily a strong reason to measure LDH simply because they have completed an endurance event. The fact that LDH can rise after ultra-endurance exercise is useful to understand, but in many cases I see it more as a physiological observation than a stand-alone diagnostic finding.
In practice, I want the clinical picture to lead the interpretation, not the laboratory value alone. In most ultramarathon contexts, elevated LDH reflects the broader biochemical stress of prolonged exercise. However, if the athlete has symptoms, very high CK, myoglobin elevation, electrolyte abnormalities, renal impairment, or dark urine, then I start thinking much more seriously about rhabdomyolysis. In that situation, LDH may support the overall assessment of tissue injury, but I would not use it as the primary diagnostic tool.
Conclusion: Interpreting LDH in Athleteas Requires Context
LDH in athletes should never be interpreted as a diagnosis by itself. It is a non-specific marker that can rise for many different reasons: skeletal muscle stress, hemolysis, liver involvement, ischemia, malignancy-related disease activity, or other forms of tissue injury. In athletes, recent training and competition add another layer of complexity, because LDH may be mildly or even substantially elevated after strenuous exercise without necessarily indicating a dangerous condition.
In my clinical thinking, the most important point is that the athlete should still be assessed like any other patient. Symptoms, timing, physical findings, training history, and companion markers such as CK, myoglobin, haptoglobin, bilirubin, potassium, renal function, and liver enzymes matter far more than LDH alone. A recent ultramarathon, hard strength session, or endurance race may help explain part of the LDH elevation, but it should not be used as a shortcut to dismiss pathology before the broader clinical picture has been considered.
The practical message is simple: LDH is a clue, not an answer. In a well athlete with a mild, transient elevation after heavy exercise, LDH may simply reflect the biochemical stress of training, muscle turnover, or exercise-related hemolysis. In an athlete with symptoms, persistent elevation, very high CK, myoglobinuria, electrolyte abnormalities, renal impairment, chest pain, abdominal symptoms, or other concerning findings, LDH becomes part of a wider diagnostic assessment rather than a reassurance marker.
For most athletes, LDH does not need to be measured simply because they train hard. When it is measured, it should be interpreted carefully, not reflexively against a general-population reference range and not automatically blamed on exercise. The value of LDH is not that it gives a final answer, but that it can help complete the picture when combined with the athlete’s history, symptoms, and the rest of the blood work.
References
- https://www.ncbi.nlm.nih.gov/books/NBK557536/
- https://doi.org/10.3390/ijerph19053059
- https://pmc.ncbi.nlm.nih.gov/articles/PMC2492050/
- https://pmc.ncbi.nlm.nih.gov/articles/PMC1478243/
- https://doi.org/10.21037/atm.2019.05.41
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6186806/
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6843057/
