LDL Cholesterol: What It Is, How to Read Your Result, and What It Means for Athletes
Table of Contents
Key Takeaways: LDL Cholesterol
- LDL cholesterol is a cause of atherosclerotic cardiovascular disease, not just a marker of it. Risk tracks both how high LDL is and how long the arteries are exposed to it.
- There is no single LDL cholesterol target that fits everyone. Recommended goals depend on your overall cardiovascular risk, and the strictest goal is below 55 mg/dL (1.4 mmol/L) for patients with cardiovascular disease at very high risk.
- You usually don’t need to fast before an LDL cholesterol test. Lp(a) is worth measuring at least once.
- A very high LDL (190 mg/dL or more) is a reason to assess for familial hypercholesterolemia, however fit the person is, although most people at that level do not have it.
- Exercise training lowers LDL only modestly. Fitness is linked to lower cardiovascular mortality, but masters endurance athletes still develop coronary plaque.
- Low-carbohydrate and ketogenic diets can raise LDL substantially in athletes. The studies discussed here did not assess whether that rise affects cardiovascular outcomes.
- Statins cause a small excess of mostly mild muscle symptoms, mainly in the first year; most muscle complaints in statin users are not caused by the statin.
- In my clinical experience, a high LDL cholesterol often comes as a surprise to patients, and dietary change alone is often not enough, so many of my patients end up on a statin.
- When my patients on a statin report muscle symptoms, switching to another statin works for many of them; in my experience, stopping a statin on one’s own often lets cholesterol rise again.
Introduction: LDL Cholesterol
LDL cholesterol is one of the central numbers on a lipid panel, and its link to cardiovascular disease has been tested in large randomized trials. In a meta-analysis of 26 randomized statin trials with about 170,000 participants, each 1.0 mmol/L reduction in LDL-C cut the rate of major vascular events by 22%, and there was no sign of a threshold within the cholesterol range studied.[1]
In my own occupational health practice, cholesterol is checked at almost every periodic health examination and initial examination, so LDL cholesterol is a common test in my work. Many of my patients are already on cholesterol-lowering medication. In my clinical experience, cholesterol is also the result most often outside the reference range in my patient population, usually because LDL cholesterol is elevated.
For athletes, LDL raises its own set of questions. Does a high training volume protect you from a high result? Why did your LDL jump after you cut carbohydrates? Can you train hard on a statin? These questions tend to get answered with either alarm or a shrug, and neither helps.
This article covers what LDL is, why it matters, how to read your result, and what the research shows for people who train, from recreational runners to masters endurance athletes.
What Is LDL Cholesterol?
Cholesterol does not travel freely in the blood. It is packaged into lipoproteins, and low-density lipoprotein (LDL) is the main particle carrying it. The LDL cholesterol value (LDL-C) on a lab report is the amount of cholesterol inside those particles. It is not a count of the particles themselves.
That distinction is why apolipoprotein B (apoB), a protein carried on LDL and related atherogenic particles, is sometimes measured as well. The 2026 ACC/AHA dyslipidemia guideline says apoB testing can be useful to improve risk assessment and guide therapy once LDL-C and non-HDL-C goals are met, particularly in people with elevated triglycerides, diabetes, or an achieved LDL-C below 70 mg/dL.[2]
LDL is a different measure from HDL cholesterol, the so-called “good cholesterol.” For that side of the lipid panel, see HDL Cholesterol in Athletes and Triglycerides in Athletes.
Why It Matters: A Cause, Not Just a Marker
The European Atherosclerosis Society Consensus Panel reviewed genetic studies and separate meta-analyses of more than 200 prospective cohort studies, Mendelian randomization studies and randomized trials. Together these covered more than 2 million participants, over 20 million person-years of follow-up and over 150,000 cardiovascular events.[3] The panel found a consistent, dose-dependent, log-linear relationship between the absolute amount of LDL-C the arteries are exposed to and the risk of atherosclerotic cardiovascular disease (ASCVD), with the effect appearing to grow as exposure lasts longer. It concluded that the evidence unequivocally establishes LDL as a cause of ASCVD, and that lowering LDL should reduce risk in proportion to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the LDL-C reduction matches the reduction in LDL particle number and there are no competing harmful off-target effects.[3]
Duration matters too. In a Mendelian randomization analysis of 312,321 people, having genetically lower LDL-C from birth was associated with a 54.5% lower risk of coronary heart disease for each 1 mmol/L (38.7 mg/dL) lower LDL-C. That was a 3-fold greater risk reduction per unit of LDL-C than seen with statin treatment started later in life.[4]
This is the main reason LDL is relevant to a 25-year-old athlete and not only to a 60-year-old patient. The arteries keep a running total of exposure, and that total starts early.
Reading Your LDL Cholesterol Result
No single target fits everyone
A lab report may print a single reference limit for LDL cholesterol, but guidelines set goals according to overall cardiovascular risk. For adults aged 30 to 79 without known ASCVD or subclinical atherosclerosis and with LDL-C of 70–189 mg/dL, the 2026 ACC/AHA guideline recommends estimating 10-year risk with the American Heart Association’s PREVENT-ASCVD equations instead of the older Pooled Cohort Equations.[2] In primary prevention, LDL-lowering therapy can be considered when the 10-year PREVENT-ASCVD risk is 3% to <5% and should be considered at 5% to <10%.[2] For patients with established ASCVD who are at very high risk, the guideline recommends a goal of LDL-C below 55 mg/dL (1.4 mmol/L) and non-HDL-C below 85 mg/dL (2.2 mmol/L).[2]
In my practice, family history is an important part of how I assess risk. Many of my patients have a family history of coronary artery disease, stroke or other cerebrovascular or cardiovascular disease, and in my view, a hereditary component like this generally adds to these patients’ own risk. With many patients, I use the FINRISK risk calculator to estimate their statistical risk, and in my experience, many patients find that the result makes their risk easier to understand.
You usually don’t need to fast
A joint consensus statement from the European Atherosclerosis Society and the European Federation of Clinical Chemistry and Laboratory Medicine recommended that non-fasting blood samples be routinely used for the assessment of lipid profiles. After habitual meals, the largest average change in LDL-C within 1 to 6 hours was −0.2 mmol/L (−8 mg/dL), which the authors did not consider clinically significant. Fasting sampling may be considered when non-fasting triglycerides are above 5 mmol/L (440 mg/dL).[5] The same statement reports that apoB and Lp(a) are not affected by fasting status.[5]
In my own occupational health practice, the laboratory we use offers both fasting and non-fasting lipid tests. Even so, I often order a fasting sample, because it conveniently gives a fasting glucose at the same time, along with any other tests that require fasting.
Triglycerides moved the most after a meal, rising on average by up to 0.3 mmol/L (26 mg/dL).[5] If triglycerides are the specific question, the practical details are in Preparing for Blood Test Athletes.
Measure Lp(a) at least once
Lipoprotein(a) is a separate LDL-like particle, and a standard lipid panel does not measure it separately. The 2026 ACC/AHA guideline recommends measuring Lp(a) at least once to identify people at higher risk of ASCVD, and treats a level of 125 nmol/L (50 mg/dL) or more as a risk-enhancing factor.[2]
When the Result Comes Back High
In my experience, a high LDL cholesterol often comes as a surprise to patients. Many of my patients feel they eat quite well, but when we go through their diet in more detail, it often turns out to contain quite a lot of animal fat. Many of my patients are also overweight, which in my experience often goes hand in hand with an elevated cholesterol, especially LDL cholesterol. I have also noticed that many of my patients with elevated cholesterol have a slightly raised ALT, which in my clinical judgement may point to mild fatty liver in many of them.
For a mildly elevated cholesterol, especially LDL cholesterol, my usual approach is a strict dietary change and a recheck after about six months. In our occupational health service, we can also consult dietitians, which in my experience usually gives good results. If the patient is overweight, we often agree that losing weight would be worthwhile, with the aim of improving both LDL and total cholesterol. I also encourage patients to exercise as part of an overall lifestyle change, because in my experience the combined effect of lifestyle habits works best.
In my experience, dietary change alone all too often doesn’t last, doesn’t get done, or doesn’t lower cholesterol enough even when it is made. If cholesterol is still above the reference range despite a careful dietary change, or if the patient simply cannot keep up the diet, I often offer a statin, and with many of my patients we end up starting one. In my experience, a statin is also often started when the starting level is very high. Some of my patients are reluctant to start medication, while others welcome it.
From time to time, my patients ask when they can stop their statin. Often, I have to explain that the statin was started because their cholesterol could not be kept low otherwise, whether for hereditary or lifestyle reasons. Once the statin brings cholesterol down, some of my patients assume that the medication is no longer needed. I usually advise against stopping, because in my experience, unless something else has changed significantly, cholesterol is likely to rise again, especially in patients with a strong genetic component. Some of my patients still stop the statin on their own, for example because they are reluctant to take any medication and feel the problem has been solved now that their cholesterol is lower. In many of these patients, cholesterol rises again, and we later have to restart the medication.
Very High Values: Think Familial Hypercholesterolemia
When LDL is markedly high, a genetic cause is one of the first things to consider. In a meta-analysis of general-population studies covering 10,921,310 subjects, heterozygous familial hypercholesterolemia (FH) had a pooled prevalence of 0.32%, or 1 in 313.[6] Among people with severe hypercholesterolemia, defined as LDL-C of 190 mg/dL or more, the prevalence was 7.2%, or 1 in 14.[6]
In my clinical experience, diet has its limits when the hereditary component is strong. In my practice, there is a group of patients whose cholesterol, and particularly their LDL cholesterol, stays elevated however good their diet is. In some of my patients, I also see familial hypercholesterolemia, where in my experience cholesterol stays especially high largely regardless of diet, because the genetic component is so large.
FH is relevant to athletes because it is an inherited condition, not a consequence of body composition or fitness. In a lean, highly trained person, a very high LDL may therefore not be explained by lifestyle alone. The EAS panel also found that the effect of LDL on risk appears to increase with longer exposure,[3] which matters in a condition where LDL is high from early life. A fit appearance can delay the question rather than answer it.
LDL Cholesterol in Athletes: What Training Does and Doesn’t Change
Exercise training does lower LDL, but by less than many athletes expect. A 2024 Sports Medicine meta-analysis of 148 randomized trials with 8,673 adult participants found a mean LDL-C reduction of −7.22 mg/dL (95% CI −9.08 to −5.35), or about 0.19 mmol/L.[7] Aerobic and combined training lowered LDL-C significantly, while resistance training on its own did not significantly lower it.[7] The estimated effect varied widely between studies: the 95% prediction interval ran from −23.54 to +9.10 mg/dL, which the authors interpreted as 27.9% of studies showing no beneficial effect.[7] The authors described the changes in the lipid profile as small but favourable, and judged combined training to be the best option.[7]
These were training interventions, so they describe what starting or adding exercise does. They do not show that an already well-trained athlete can keep pushing LDL down by training more. If your LDL is high despite a large training volume, more mileage alone may not be enough to fix it.
LDL particle size and the broader “athletic” lipid pattern are covered in Cholesterol in Athletes: What Your Lipid Panel Is Really Telling You.
Fitness Is Linked to Lower Risk, but It Doesn’t Cancel a High LDL
Higher fitness is linked to better outcomes. In 8,920 men with hypercholesterolemia who were examined at the Cooper Clinic and followed for an average of 17 years, those with high cardiorespiratory fitness had a hazard ratio of 0.55 (95% CI 0.39–0.79) for cardiovascular death compared with men with low fitness, after adjustment for cholesterol and other risk factors.[8] Every man in that cohort had high cholesterol, though, so the study shows that higher fitness was associated with lower cardiovascular mortality within that group. It does not show that fitness makes high cholesterol harmless.
The coronary imaging data in athletes point the same way. Among 152 masters endurance athletes with a low atherosclerotic risk profile and 92 matched controls, 44.3% of male athletes had coronary plaque of any luminal irregularity, compared with 22.2% of sedentary men.[9] Male athletes showed predominantly calcific plaques (72.7%), whereas sedentary men showed predominantly mixed-morphology plaques (61.5%).[9] In a separate study of 284 middle-aged men in competitive or recreational sport, coronary artery calcification was present in 68% of those exercising more than 2,000 MET-minutes per week, compared with 43% of those exercising less than 1,000. Among the men who had plaque, the most active had more calcified-only plaques (38% vs. 16%) and fewer mixed plaques (48% vs. 69%), a composition the authors considered more benign.[10]
These imaging studies do not show that LDL was the cause of the plaque in these athletes. What they do show is that years of endurance training don’t guarantee clean coronary arteries. That makes LDL, a modifiable cause of atherosclerosis,[3] worth taking seriously in masters athletes rather than dismissing because of a good race time. For which tests are worth doing at which age, see Which Blood Tests Do Athletes Actually Need?
In my clinical experience, the athletes I see generally seem to have a lower LDL cholesterol. In my view, being an athlete probably does reduce the risk, but it is not a guarantee against high cholesterol or heart disease. In my experience, these problems are rarer in patients who exercise, but they can still occur. In my patients, diet and genetics seem to play a very large part, and exercise alone often cannot cancel out their effect.
Low-Carb and Ketogenic Diets: Why an Athlete’s LDL Can Jump
One reason an athlete’s LDL can rise markedly is a switch to low-carbohydrate, high-fat eating.
- Cross-sectional data: Among 20 elite male ultra-endurance runners, those who had followed a low-carbohydrate diet for more than 6 months had LDL-C that was 83% higher when measured directly than in runners on a high-carbohydrate diet.[11]
- Randomized crossover trial: In 7 highly trained, recreational male distance runners, calculated LDL-C was 108 ± 17 mg/dL during six weeks on a low-carbohydrate, high-fat diet, compared with 74 ± 13 mg/dL during six weeks on a high-carbohydrate, low-fat diet (p = 0.001). Triglycerides were lower during the high-fat diet.[12]
- Short-term trial: In 6 trained cyclists and triathletes, fasting LDL-C was 102.8 mg/dL after 14 days on a ketogenic diet, compared with 79.5 mg/dL on their habitual diet and 84.0 mg/dL on a high-carbohydrate diet. The LDL-C differences were not statistically significant in this small sample, but the rise in total cholesterol was.[13]
These diets changed more than carbohydrate intake: in the crossover trial, fat provided 69% of energy during the low-carbohydrate, high-fat diet and 28% during the high-carbohydrate, low-fat diet,[12] so the studies cannot separate carbohydrate restriction from the difference in fat intake. None of these studies followed athletes long enough to show whether a diet-driven LDL rise affects cardiovascular outcomes. The authors of the ultra-runner study suggested that an expanded circulating cholesterol pool might serve a functional purpose in fat-adapted athletes.[11] That is a hypothesis, not a finding. Without outcome data in athletes, a reasonable clinical reading is that a large, persistent rise deserves the same evaluation as it would in anyone else, in the context of overall cardiovascular risk, with apoB as an option in selected cases.
In my practice, some patients still follow a ketogenic diet, although in my experience it was much more common earlier. As I recall, around 20 years ago the Atkins diet was in fashion, and my impression is that it was seen as an easy way to lose weight. My patients did lose weight on a ketogenic diet, but those of my patients who follow a ketogenic or paleo diet often have fairly high cholesterol values, which naturally concerns me as their doctor.
Statins and Training: What About Muscle Symptoms?
For anyone who trains, the obvious worry about statins is muscle side effects. Large-scale evidence comes from an individual participant data meta-analysis of 19 double-blind, placebo-controlled trials with 123,940 participants. Muscle pain or weakness was reported by 27.1% of people on a statin and 26.6% on placebo, a rate ratio of 1.03 (95% CI 1.01–1.06).[14] During the first year, statins produced a 7% relative increase in muscle pain or weakness, an absolute excess of 11 events per 1,000 person-years; after the first year there was no significant excess in first reports of these symptoms.[14] The authors concluded that statins cause a small excess of mostly mild muscle pain and that more than 90% of muscle symptom reports in statin users were not due to the statin.[14]
These trials were not done in athletes, so they don’t answer every performance question. For someone who trains hard, two practical points follow. Muscle aches are common even without a statin, as the 26.6% rate on placebo shows,[14] so recent training load is one relevant factor to consider before attributing symptoms to the drug. And because creatine kinase rises after hard exercise, any CK test on a statin should be timed and interpreted with recent training in mind, as discussed in Creatine Kinase Elevated in Athletes.
In my practice, patients on a statin often report muscle or joint pain. I usually tell patients that if this happens, we can switch to another statin, and in my clinical experience, switching works for many of my patients. With some of my patients, the statin has had to be changed more than once before a suitable one is found. If cholesterol is still elevated, I may add ezetimibe, and in some of my patients who tolerate no statin, ezetimibe is used on its own, although in my experience this is less common.
Conclusion: LDL Cholesterol
LDL cholesterol is a cause of atherosclerotic disease, and its effect builds up with both level and time. In statin trials, each 1.0 mmol/L reduction cut major vascular events by 22%,[1] and genetically lower LDL-C from birth was associated with a larger reduction in coronary heart disease risk per unit than statin treatment started later in life.[4] For athletes, the research gives a balanced message. Fitness is associated with lower cardiovascular mortality, but training lowers LDL only modestly, masters endurance athletes still develop plaque, and low-carbohydrate, high-fat diets can push it up substantially.
My own practice points the same way. In my clinical experience, cholesterol is the result most often outside the reference range in my patient population, and the athletes I see generally seem to have lower LDL values, but they are not immune: in my patients, diet and genetics often matter more than exercise alone can offset.
In practice, that means knowing your LDL cholesterol and your overall risk, measuring Lp(a) once, taking very high values seriously whatever your fitness, and considering a repeat lipid test after a major diet change. Good training habits and a well-understood LDL result work best together.
Bibliography
[1] https://doi.org/10.1016/S0140-6736%2810%2961350-5
[2] https://doi.org/10.1161/CIR.0000000000001423
[3] https://doi.org/10.1093/eurheartj/ehx144
[4] https://doi.org/10.1016/j.jacc.2012.09.017
[5] https://doi.org/10.1373/clinchem.2016.258897
[6] https://doi.org/10.1016/j.jacc.2020.03.057
[7] https://doi.org/10.1007/s40279-024-02115-z
[8] https://doi.org/10.3390/jcm11175211
[9] https://doi.org/10.1161/CIRCULATIONAHA.116.026964
[10] https://doi.org/10.1161/CIRCULATIONAHA.117.027834
[11] https://doi.org/10.1136/bmjsem-2018-000429
[12] https://doi.org/10.3390/nu14061135
