Being an athlete does not exclude significant hypercholesterolaemia, and the most important task in sport and exercise medicine (SEM) is to avoid assuming that a fit person with a high cholesterol simply needs more exercise. Training improves the lipid profile modestly, mainly by raising high-density lipoprotein cholesterol and lowering triglycerides, but it has limited effect on low-density lipoprotein cholesterol and none at all on the underlying defect in inherited disorders. A markedly raised cholesterol in a young, lean, highly trained athlete should therefore raise suspicion of familial hypercholesterolaemia (FH) rather than reassurance. This page covers how lipids are assessed and treated under current UK guidance, how inherited hypercholesterolaemia is recognised, and the issue that dominates lipid management in athletes: muscle symptoms on statins, and why creatine kinase is such an unreliable guide in people who train hard.
How Are Lipids Assessed?
A full lipid profile measures total cholesterol, high-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol and triglycerides. A fasting sample is not mandated, although severely raised triglycerides may need repeat assessment under appropriate conditions, and laboratories may not report a calculated low-density lipoprotein cholesterol when triglycerides are high. Non-high-density lipoprotein cholesterol, obtained by subtracting the high-density fraction from the total, has become the working measure in UK practice because it captures all the atherogenic particles and does not depend on fasting.
Cardiovascular risk is then estimated formally, using a validated calculator within its validated population, which in current UK practice means adults roughly between the ages of 25 and 84 without established cardiovascular disease. A risk calculator should not be used at all in several groups where it will underestimate risk: people with established cardiovascular disease, people with type 1 diabetes, people with an estimated glomerular filtration rate below 60 mL/min/1.73 m2 or with albuminuria, and people with familial hypercholesterolaemia or another inherited lipid disorder. Recognising when the calculator does not apply is a more common exam point than the calculation itself. Secondary causes should also be excluded before attributing a raised cholesterol to a primary disorder, including hypothyroidism, poorly controlled diabetes, liver and kidney disease, excess alcohol, and some medicines.
When Should You Suspect Familial Hypercholesterolaemia?
Familial hypercholesterolaemia (FH) is an inherited disorder of low-density lipoprotein clearance that produces lifelong elevation of cholesterol and a markedly increased risk of premature coronary disease. It is considerably more common than most clinicians assume and is substantially underdiagnosed, which matters because it is eminently treatable once identified. Current UK guidance advises suspecting it in an adult with a total cholesterol above 7.5 mmol/L, or with a personal or family history of premature coronary heart disease, defined as an event before the age of 60 in the individual or a first-degree relative.
Features that should raise suspicion of familial hypercholesterolaemia: tendon xanthomata at the Achilles and hand extensor tendons, premature corneal arcus, xanthelasma, and a family history of premature coronary disease. Their absence does not exclude the diagnosis.
Tendon xanthomata, thickening of the Achilles tendon or the extensor tendons of the hands, are the most specific clinical sign and are directly relevant in SEM because they can be mistaken for Achilles tendinopathy in a runner. Corneal arcus appearing before middle age and xanthelasma are supportive but not diagnostic, and non-specific Achilles thickening has many other causes. Importantly, the absence of clinical signs does not exclude the diagnosis. Achilles ultrasound is not recommended as a diagnostic test for familial hypercholesterolaemia; diagnosis rests on clinical examination, lipid values, family history and formal criteria such as the Simon Broome criteria or the Dutch Lipid Clinic Network score, with referral to a specialist service for genetic testing where those criteria are met. Cascade testing of first-degree relatives follows and is one of the highest-yield interventions in preventive cardiology. Treatment uses a high-intensity statin, aiming for a reduction in low-density lipoprotein cholesterol of at least 50% from baseline, and is indicated regardless of any calculated risk score, because the score does not apply.
How Is Hypercholesterolaemia Treated?
Current UK guidance makes atorvastatin the initial choice. For primary prevention the usual starting dose is 20 mg daily, offered when the estimated ten-year cardiovascular risk reaches 10% or more, and it is not withheld simply because the score falls below that threshold if the person has an informed preference or there is reason to think the score underestimates their risk. For secondary prevention in established cardiovascular disease the starting dose is 80 mg daily unless there is a reason to use less. A full lipid profile and liver transaminases are measured 2 to 3 months after starting or changing lipid-lowering treatment, aiming for a reduction in non-high-density lipoprotein cholesterol of more than 40% in primary prevention, while secondary prevention targets a low-density lipoprotein cholesterol of 2.0 mmol/L or less, or a non-high-density lipoprotein cholesterol of 2.6 mmol/L or less.
If the target is not met, the response is to check adherence and the timing of the dose, reinforce dietary and lifestyle change, and consider increasing the statin dose. Ezetimibe may be added where a statin alone is insufficient or not tolerated. Beyond these, injectable monoclonal antibodies that inhibit proprotein convertase subtilisin/kexin type 9 are available through specialist services for familial hypercholesterolaemia and other high-risk groups, and inclisiran is a distinct option that reduces synthesis of the same protein through a small interfering ribonucleic acid mechanism rather than by antibody binding, so it should not simply be grouped with the antibodies. It is worth reassuring athletes explicitly that statins and ezetimibe are not prohibited substances in sport, since many assume any cardiovascular drug is a problem.
Statin Muscle Symptoms in the Athlete
Statin-associated muscle symptoms (SAMS) is the term for muscle symptoms occurring in someone taking a statin, and it deliberately does not assert that the statin caused them. Symptoms commonly involve symmetrical large muscle groups, but the pattern is variable. The spectrum runs from myalgia with a normal creatine kinase (CK), through myopathy with weakness, to rhabdomyolysis, which is genuinely rare. Randomised n-of-1 trials, in which individual patients cross over between statin and placebo while blinded, have repeatedly shown similar symptom rates on each, indicating that a large share of attributed symptoms reflect a nocebo effect. That finding does not make the symptoms less real or less deserving of attention, and the cardiovascular risk still needs treating.
A creatine kinase result in a trained athlete is interpreted against several factors at once, including recent training, the individual's own rested baseline, symptoms, urine colour, renal function and the magnitude of the rise.
The athlete-specific trap is creatine kinase. Trained athletes commonly run resting values above the standard laboratory reference range, variation between trained individuals is very wide, and hard training, unaccustomed or eccentric loading and competition raise values further for days, so a single result proves very little on its own. Interpretation should weigh the mode and volume of recent exercise, the individual's own rested baseline where known, the presence of symptoms or true weakness, urine colour, renal function, and the magnitude of the rise relative to the upper limit of normal. UK guidance offers useful anchors here: muscle symptoms with a creatine kinase below five times the upper limit of normal generally prompt reassurance and a search for alternative causes, whereas a persistent level at or above five times the upper limit calls for greater caution. Misreading an exercise-induced rise as statin toxicity leads to stopping an effective drug unnecessarily, while genuine rhabdomyolysis with a very high level, muscle pain and dark urine needs urgent attention regardless of the statin.
Practical management of suspected statin-associated muscle symptoms is to review adherence and dose timing, look for interacting medicines, and check thyroid function or vitamin D only where clinically indicated rather than routinely. Depending on symptom severity and the creatine kinase result, the options are to continue treatment, interrupt it temporarily, rechallenge, reduce the dose, use alternate-day dosing or switch statin, agreed through shared decision-making, with ezetimibe added if needed. Statins do not inevitably impair athletic performance, and short-term trials combining exercise with statins have not shown reduced maximal oxygen uptake compared with exercise and placebo, but individual muscle symptoms and training tolerance should still be monitored.
Exam Tips
•Exercise raises high-density lipoprotein cholesterol and lowers triglycerides but has little effect on low-density lipoprotein cholesterol.
•A risk calculator must not be used in familial hypercholesterolaemia, established cardiovascular disease, type 1 diabetes or significant kidney disease.
•Suspect familial hypercholesterolaemia with a total cholesterol above 7.5 mmol/L or premature coronary disease before age 60 in the individual or a first-degree relative.
•Absence of tendon xanthomata does not exclude familial hypercholesterolaemia, and Achilles ultrasound is not a diagnostic test for it.
•Recheck the lipid profile and liver transaminases 2 to 3 months after starting or changing treatment.
•Creatine kinase is unreliable in athletes; weigh recent training, the rested baseline, symptoms and the magnitude of the rise.