Aerobic Exercise Performance and Muscle Strength in Statin Users


Thomas Morville; Tine Lovsø Dohlmann; Anja Birk Kuhlman; Ronni Eg Sahl; Margit Kriegbaum; Steen Larsen; Flemming Dela; Jørn Wulff Helge


Med Sci Sports Exerc. 2019;51(7):1429-1437. 

In This Article

Abstract and Introduction


Introduction: Statins are widely used in both primary and secondary prevention of cardiovascular disease. The treatment increases the risk of muscle pain (myalgia) which can affect muscle function and levels of physical activity. We investigated whether statin-associated myalgia is coupled to impaired aerobic exercise performance including fat oxidation as well as impaired muscle strength.

Methods: A population-based survey (6000 people) was performed to assess the prevalence of statin-associated myalgia in the Danish population. In addition, 64 statin users in primary prevention with myalgia (M; n= 25; 61 ± 1 yr) or without myalgia (NM; n = 37; 63 ± 1 yr) as well as a control group not taking statins (C; n = 20; 60 ± 2 yr) were enrolled in a cross-sectional study where they performed aerobic exercise and muscle strength tests.

Results: The response rate for the survey was 51% and data showed a prevalence of statin-associated myalgia in 19% of responders using statins. The experimental study showed no difference between the groups in aerobic capacity (C, 29 ± 1 mL O2·min−1·kg−1; M, 27 ± 1 mL O2·min−1·kg−1; NM, 28 ± 1 mL O2·min−1·kg−1) or maximal fat oxidation (C, 247 ± 26 mg·min−1; M, 295 ± 24 mg·min−1; NM, 279 ± 17 mg·min−1). Measurements of strength were similar in all three groups including rate of force development (C, 795 ± 56 N·m·s−1; M, 930 ± 93 N·m·s−1; NM, 971 ± 57 N·m·s−1) and leg extension power (C: 2.6 ± 0.2; M: 2.3 ± 0.1; NM: 2.4 ± 0.1 W·kg−1). All results are mean ± SEM.

Conclusion: Statin users in primary prevention experiencing myalgia do not have impaired aerobic exercise performance or muscle strength compared to nonmyalgic statin users or control subjects.


Statins, or HMG-CoA-reductase inhibitors, are the primary choice of medical treatment when aiming to lower blood cholesterol concentrations. These drugs are generally well tolerated and have been shown to reduce cardiovascular morbidity and mortality.[1] Before statin prescription in primary prevention current guidelines encourage change of lifestyle including diet and physical activity (PA) to lower cholesterol concentrations.[2]

The positive effects of lifestyle changes and in particular PA are pleiotropic and include reduction in cardiovascular disease (CVD) in a dose dependent manner.[3] Chronic pain is associated with physical inactivity[4] and muscle pain (myalgia) is the most common adverse effect reported with the use of statins.[5] Although statin use has been associated with lower PA,[6] the question of causality remains unanswered. The complex association can roughly be regarded in two ways: the use of statins may lead to myalgia which in turn, similar to chronic pain, leads to reduced PA. This implies that myalgic statin users become less physically active because of the myalgia and this may explain the observations of decreased leg strength and increased fall risk in older adults taking statins.[7] On the other hand, the reported myalgia may be caused by the combination of statins and PA which implies that those who report myalgia are more physically active than other statin users. In support of this latter view is the reported exacerbation of myalgia with PA[8] especially in athletes.[9]

Although both causative pathways may exist, they both represent problems as discontinuation of statin treatment due to myalgia compromises the proven effective treatment and prevention of CVD.[1] The mechanisms underlying statin-associated myalgia remain unknown, and the prevalence varies greatly depending on the study methodology and choice of patient groups.[10,11] A number of mechanisms leading to statin-associated myalgia have been proposed, including mitochondrial dysfunction, apoptosis, and genetic predisposition.[5,12] Furthermore, statin use has been linked to changes in lipid metabolism,[13–15] and studies have shown that statin-associated myotoxicity may be fiber type-specific.[16]

The multiple causative pathways underlying statin use, myalgia, and PA may explain why previous studies show divergent results. Measurements of aerobic exercise performance and muscle strength have been used to assess the physical capabilities of statin users with some studies reporting lower or decreased aerobic exercise performance or strength with statin use[6,7,14,17] and other studies reporting no differences or changes over time.[18–21] Thus, it remains unclear to what extent statin-associated myalgia is linked to changes in levels of physical capabilities and in particular the direction of causation in regard to these parameters and PA.

In the present study, we have investigated the aerobic performance and strength in statin users experiencing myalgia compared to nonmyalgic statin users and a control group. Specifically, we investigated the aerobic capacity as well as substrate utilization during exercise to assess overall aerobic exercise performance and lipid metabolism during exercise. Measurements of strength range from dynamic contractions assessing leg extension power but also the rate of force development (RFD) in the initial phase of an isometric muscle contraction as the combination allows for a more detailed and qualitative description of muscle force. Furthermore, we have conducted a population-based survey to study the prevalence of muscle and joint symptoms in Danish statin users and the associations between PA and muscle and joint symptoms. Although the experimental study provides insight into the physical capabilities of statin users with or without myalgia, the survey data provide information regarding the associations between statin use, myalgia and PA. The combination of the two types of studies will thus provide a comprehensive description of the complex associations between statin use, myalgia, physical capabilities, and PA.

As stated, the causative pathways allow for several and opposing hypotheses but the working hypothesis of the experimental study is that the experience of myalgia will be associated with impaired performance of both aerobic as well as strength performance.