Exercise is Medicine

published online on 26.06.2026
https://doi.org/10.34045/SEMS/2026/13

Lipid management in Athletes – The Swiss Approach

Einstieg Lipidmanagement

Niederseer David1,2,3, Betschart Hanspeter4, Gähwiler Roman4,5
1 Hochgebirgsklinik Davos, Medizincampus Davos, Herman-Buchard-Strasse 1, 7265 Davos Wolfgang, Schweiz
2 Center of Translational and Experimental Cardiology (CTEC), Department of Cardiology, University Heart Center of Zurich,
University Hospital of Zurich, University of Zurich, Zurich, Switzerland
3 Christine Kühne-Center for Allergy Research and Education (CK-CARE), Medicine Campus Davos, Davos, Switzerland
4 Berit Sportclinic, Vögelinsegg 5, 9042 Speicher, Schweiz
5 ALTIUS Swiss Sportmed Center AG, Habich-Dietschy-Strasse 5a, 4310 Rheinfelden, Schweiz

Abstract

Athletes are generally perceived as having a favourable cardiovascular risk profile; however, dyslipidaemia, familial hypercholesterinaemia (FH), and elevated lipoprotein(a) [Lp(a)] remain clinically relevant even in highly trained individuals. The recently developed Swiss Olympic/Swiss Society of Sports Medicine (SEMS) algorithm provides a structured and sport-specific approach to lipid management in athletes aged ≥18 years, integrating cardiovascular prevention with the practical realities of elite and recreational sports participation.
This article summarizes the principles underlying the Swiss approach, with particular emphasis on non-pharmacological LDL cholesterol reduction, statin-associated muscle symptoms (SAMS), and the emerging role of Lp(a) assessment. Lifestyle interventions—including Mediterranean ­dietary patterns, reduction of saturated fat intake, plant ­sterols, and soluble fibres—may substantially reduce LDL cholesterol and remain first-line strategies in many athletes. However, inherited lipid disorders frequently require pharmacological treatment despite optimal fitness and nutrition.
Although concerns regarding statin-induced muscle symptoms are common in athletes, contemporary evidence suggests that severe performance impairment is uncommon and that individualized treatment strategies improve tolerability. Furthermore, the Swiss Olympic/SEMS algorithm highlights the importance of one-time Lp(a) measurement, as elevated levels confer substantial inherited cardiovascular risk largely independent of lifestyle and are minimally influenced by statin therapy.
The Swiss Olympic / SEMS algorithm represents a pragmatic framework for individualized cardiovascular prevention in athletic populations, balancing evidence-based lipid management with preservation of exercise performance and long-term athlete health.

Introduction

Elite and recreational athletes are commonly perceived as metabolically healthy individuals with a low cardiovascular risk profile. High levels of physical activity are indeed associated with reduced cardiovascular morbidity and mortality; however, athletic performance does not confer immunity against dyslipidaemia, familial hypercholesterinaemia (FH), or elevated lipoprotein(a) [Lp(a)]. In recent years, sports cardiology, vascular medicine and preventive medicine have increasingly recognized that athletes may harbour clinically relevant lipid disorders despite excellent cardiorespiratory fitness and favourable body composition. [1–3]
The Swiss approach to lipid management in athletes, recently implemented through a collaborative initiative between Swiss Olympic and the Swiss Society of Sports Medicine (SEMS), and composed by the authors attempts to reconcile evidence-based cardiovascular prevention with the unique physiological and practical considerations of athletic populations.
A central challenge in sports medicine is balancing long-term cardiovascular prevention against concerns regarding exercise performance, medication-related side effects, and overtreatment in otherwise healthy individuals. This article summarizes the current Swiss strategy, with particular emphasis on non-pharmacological LDL reduction, statin-associated muscle symptoms (SAMS), the role of Lp(a), and the implementation of the Swiss Olympic/SEMS screening algorithm.

LDL Reduction Without Medication: Greater Potential Than Assumed

For many athletes, especially younger individuals with mildly elevated LDL cholesterol levels, lifestyle modification remains the cornerstone of treatment. Notably, even highly trained athletes frequently demonstrate substantial room for improvement regarding nutritional strategies.
Regular endurance exercise alone only modestly lowers LDL cholesterol concentrations, typically by approximately 5–10%. [4] However, dietary interventions can achieve considerably greater effects. A Mediterranean-style dietary pattern rich in unsaturated fats, fibre, legumes, vegetables, whole grains, and omega-3 fatty acids has consistently demonstrated clinically meaningful LDL reductions. [5] Furthermore, reducing saturated fat intake and replacing it with polyunsaturated fats may lower LDL cholesterol by an additional 10–15%. [6]
Plant sterols and soluble fibres represent underutilized but evidence-based interventions in athletic populations. Daily intake of approximately 2g of plant sterols may reduce LDL cholesterol by 7–12%, while soluble fibres such as psyllium or beta-glucans can contribute an additional 5–10% reduction. [7,8] In selected athletes, combined lifestyle measures may therefore achieve LDL reductions approaching 20–30% without pharmacological intervention.
Nevertheless, clinicians must recognize that isolated lifestyle measures are insufficient in many athletes with genetically mediated dyslipidaemia. Particularly in FH, elevated LDL levels primarily reflect impaired hepatic LDL receptor function rather than poor lifestyle habits. [9] In these individuals, delayed pharmacological treatment may expose athletes to decades of cumulative vascular risk despite excellent fitness.
The Swiss approach therefore differentiates carefully between moderate lifestyle-responsive dyslipidaemia and potentially inherited lipid disorders requiring specialist evaluation.
This brief case report aims to illustrate the potential of lifestyle change in a 43-year old male mountain bike coach and former professional athlete who demonstrated elevated cholesterol and Lp(a) levels within a routine sports medical examination (Figure 1).


The patient is an otherwise healthy non-smoker with known elevated cholesterol levels in the family (father). He is still very active after his professional career and exercises 10-15 hours per week (mostly on the bike). The patient has been advised to adapt lifestyle modifications refer to nutrition (mediterranean diet with almost no meat, increase amount of dietary fiber), stress management/sleep and training. Since the athlete was very motivated to avoid statin-medication he has been very disciplined with regard to the implementation of the lifestyle recommendations. The lifestyle changes resulted in a significant improvement of his lipid profile without any additional medication (Figure 2).

Statin-Associated Muscle Symptoms: Real Problem or Overestimated Concern?

Concerns regarding statin-induced muscle symptoms remain obvious barriers to lipid-lowering therapy in athletes. This issue is particularly relevant in elite sport, where even minor reductions in muscle performance or increased perception of fatigue may affect training quality and competition outcomes.
Statin-associated muscle symptoms (SAMS) encompass a spectrum ranging from mild myalgia without creatine ­kinase (CK) elevation to rare cases of rhabdomyolysis, sometimes aggravated by exercise. Athletes appear more susceptible to perceived SAMS, likely due to high training loads, frequent muscle microtrauma, increased symptom awareness, and overlap between exercise-induced soreness and medication effects. [10]
However, contemporary evidence suggests that the true incidence of pharmacologically mediated muscle toxicity is substantially lower than historically assumed. Several blinded trials have demonstrated a significant nocebo component, with symptom rates in placebo groups approaching those observed during statin therapy. [11,12]
Importantly, severe exercise impairment due to statin therapy is uncommon. Most athletes tolerate treatment well, particularly when individualized strategies are applied. Practical approaches include:
• initiating therapy with lower doses of highly potent statins such as atorvastatin and rosuvastatin and avoiding statins with lower potency such as simvastatin,
• selecting hydrophilic statins such as rosuvastatin or pravastatin,
• considering pitavastatin if SAMS occurs in other statins
• considering combinations of statins with ezetimibe to achieve treatment targets with lower doses of statins
• considering alternate-day dosing,
• avoiding unnecessary polypharmacy and drug interactions (also with supplements)
• and carefully evaluating training load before attributing symptoms solely to statins. [13]

Current evidence does not support generalized avoidance of statins in athletes. Rather, sports medicine physicians should adopt a nuanced and individualized strategy balancing cardiovascular benefit with individualized treatment targets against tolerability.
Beside statins and ezetimibe, the current pharmacological armamentarium include PCSK9 (proprotein convertase subtilisin/kexin type 9)-Inhibitors, bempedoic acid and inclisiran (a small interfering RNA [siRNA] therapy targeting PCSK9). All these have been shown to have less SAMS than statins and can therefore be either used instead of statins in patients with SAMS or on top of statins in patients that do not meet treatment targets with statins plus ezetimibe alone.
The Swiss perspective is therefore deliberately pragmatic: athletes with clear indications for LDL lowering should not be denied evidence-based therapy purely because of theoretical concerns regarding performance impairment. In 2020 a comprehensive review concluded that there is “limited evidence for statins impairing exercise adaptations or reducing exercise capacity for the majority of the investigated populations” and that “the benefits of engaging in physical activity while on statin medication largely outweigh the risks”. [14]

Lipoprotein(a): The “Hidden” Cardiovascular Risk Marker in Athletes

Among all aspects of lipid management in sports medicine, Lp(a) may represent the most underrecognized issue.
Lp(a) is a genetically determined LDL-like particle associated with accelerated atherosclerosis, calcific aortic valve disease, and increased cardiovascular risk independent of traditional lipid parameters. [15,16] Importantly, Lp(a) concentrations are largely unaffected by training status, diet, or body composition. Consequently, even elite endurance athletes with exemplary lifestyles may exhibit markedly elevated levels.
The Swiss Olympic/SEMS algorithm therefore recommends one-time Lp(a) measurement in all adult athletes undergoing cardiovascular screening. This recommendation reflects growing international consensus that elevated Lp(a) constitutes a major inherited cardiovascular risk factor deserving early identification and is in line with screening recommendations for the general population. [20]
Clinically, Lp(a) values above 180 mg/dL (or >430 nmol/L) are considered particularly concerning because they confer a lifetime cardiovascular risk comparable to heterozygous familial hypercholesterinaemia.
A particularly important educational aspect is the limited influence of statin therapy on Lp(a). While statins effectively reduce LDL cholesterol, they generally do not lower Lp(a) and may even slightly increase concentrations in some individuals. [17] This distinction is frequently misunderstood by both patients and physicians.
Currently, PCSK9 inhibitors represent the most effective clinically available strategy for simultaneous LDL and Lp(a) reduction, lowering Lp(a) by approximately 20–30% in addition to profound LDL reduction. [18,19] Although these therapies are presently reserved for selected high-risk patients due to cost considerations, they may become increasingly relevant in athletic populations with severe inherited dyslipidaemia or markedly elevated Lp(a).
Future RNA-based therapies specifically targeting Lp(a), including antisense oligonucleotides and small interfering RNA approaches, may fundamentally transform preventive cardiology in the coming decade.

The Swiss Olympic/SEMS Algorithm: A Structured Preventive Strategy

The recently proposed Swiss Olympic/SEMS algorithm provides a pragmatic and sport-specific framework for lipid management in athletes aged 18 years and older (Figure 3).
The algorithm should be included into the widely adopted comprehensive sports medical evaluation (“SPU”) including:
• focused family history regarding premature cardiovascular disease,
• resting ECG,
• and (newly implemented) laboratory analysis including a complete lipid profile and one-time Lp(a) measurement.

Particular emphasis is placed on premature cardiovascular events among first-degree relatives, reflecting the strong hereditary component of both FH and elevated Lp(a).
Athletes with clearly pathological findings—including LDL-C ≥4.9 mmol/L—are referred for further evaluation
of possible familial hypercholesterinaemia and specialist ­cardiovascular assessment.
For athletes with LDL-C ≥4.0 mmol/L but below the FH threshold, management depends on age, SCORE2 cardiovascular risk estimation, family history, and Lp(a) levels. Younger athletes (<40 years) generally receive individualized lifestyle counselling and periodic reassessment, whereas athletes ≥40 years undergo more formal risk stratification incorporating SCORE2 categories. This suggestion is essentially what the guidelines on dyslipidemia of the European Society of Cardiology recommend also in the general population. [20]
The algorithm also highlights the particular relevance of markedly elevated Lp(a). Individuals with Lp(a) >180 mg/dL (430 nmol/L) are considered sufficiently high-risk to justify specialist referral independent of LDL levels.
Importantly, the Swiss model intentionally avoids excessive medicalization of low-risk athletes while still identifying individuals with potentially dangerous inherited disorders. This balance reflects a broader philosophy within Swiss sports medicine: prevention should be individualized, evidence-based, and compatible with athletic performance goals.

Conclusion

Lipid management in athletes requires a distinct clinical perspective integrating preventive cardiology and angiology with exercise physiology and performance medicine. While many athletes can achieve meaningful LDL reduction through lifestyle optimization alone, inherited lipid disorders remain common and clinically relevant even in highly trained populations.
The fear of statin-associated muscle symptoms (SAMS), although understandable, should not preclude evidence-based therapy when cardiovascular risk justifies treatment. Wise treatment choises allow for reaching treatment targets without SAMS. Equally important is the recognition that Lp(a) represents a genetically determined and currently largely non-modifiable risk factor inadequately addressed by traditional lipid management strategies.
The Swiss Olympic/SEMS algorithm offers a pragmatic framework combining systematic screening, individualized risk assessment, and targeted specialist referral. In doing so, it represents an important step toward precision cardiovascular prevention in athletic populations.

Authors

David Niederseer, PD Dr. med.
Leitender Arzt Kardiologie,
Sportkardiologe Hochgebirgsklinik
Davos
david.niederseer@hgk.ch

 

Hanspeter Betschart, Dr. med.
Chefarzt Berit Sportclinic,
Chief Medical Officer
Swiss Olympic
hanspeter.betschart@klinik.ch

 

Roman Gähwiler, Dr. med. Dr. sc. med.
Leitender Arzt,
ALTIUS Swiss Sportmed Center
roman.gaehwiler@hin.ch

 

References
1. Thompson PD, et al. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Arterioscler Thromb Vasc Biol. 2003;23:e42–49.
2. Pelliccia A, et al. ESC Guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J. 2021;42:17–96.
3. Baggish AL, Levine BD. Coronary artery calcification among endurance athletes. Circulation. 2017;136:149–151.
4. Kodama S, et al. Effect of aerobic exercise training on serum levels of high-density lipoprotein cholesterol. Arch Intern Med. 2007;167:999–1008.
5. Estruch R, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368:1279–1290.
6. Mensink RP, et al. Effects of dietary fatty acids on serum lipids. World Health Organization. 2016.
7. Demonty I, et al. Continuous dose-response relationship of the LDL-cholesterol-lowering effect of phytosterol intake. J Nutr. 2009;139:271–284.
8. Whitehead A, et al. Cholesterol-lowering effects of oat β-glucan. Am J Clin Nutr. 2014;100:1413–1421.
9. Nordestgaard BG, et al. Familial hypercholesterolaemia is underdiagnosed and undertreated. Eur Heart J. 2013;34:3478–3490.
10. Thompson PD, et al. Statin-associated side effects. J Am Coll Cardiol. 2016;67:2395–2410.
11. Wood FA, et al. N-of-1 Trial of a Statin, Placebo, or No Treatment to Assess Side Effects. N Engl J Med. 2020;383:2182–2184.
12. Herrett E, et al. Statin treatment and muscle symptoms. Series of randomised, placebo controlled n-of-1 trials. BMJ. 2021; Feb 24:372:n135.
13. Parker BA, et al. Effect of statins on skeletal muscle function. Circulation. 2013;127:96–103.
14. Schweitzer AM, et al. The impact of statins on physical activity and exercise capacity: an overview of the evidence, mechanisms, and recommendations. European Journal of Applied Physiology. 2020; Jun;120(6):1205-1225.
15. Tsimikas S. A test in context: Lipoprotein(a). J Am Coll Cardiol. 2017;69:692–711.
16. Nurmohamed NS, et al. Considerations for routinely testing for high lipoprotein(a). Curr Opin Lipidol. 2023 Aug 1;34(4):174-179.
17. O’Donoghue ML, et al. Lipoprotein(a), PCSK9 inhibition, and cardiovascular risk. Circulation. 2019;139:1483–1492.
18. Bittner VA, et al. Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. J Am Coll Cardiol. 2020;75:133–144.
19. Nissen SE, et al. Antisense inhibition of apolipoprotein(a) in patients with elevated lipoprotein(a). N Engl J Med. 2020;382:244–255.
20. Mach F, et al. 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J. 2025 Nov 7;46(42):4359-4378.

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