An increase in mitochondrial respiration capacity was observed in patients with statin-induced myalgia and levels of intramuscular coenzyme Q10 concentrations were unrelated to myalgia pain, according to study results published in The Journal of Clinical Endocrinology and Metabolism.
The underlying mechanisms of statin-induced myalgia are not understood, though statin therapy has previously been shown to have associations with impaired mitochondrial plasticity and mitochondrial functions. In addition, production of coenzyme Q10, an end product of the mevalonate pathway, is likely reduced with statin therapy. Low levels of coenzyme Q10 have been associated with myalgia in previous case reports and research, but the association has not been confirmed in larger clinical trials. In this cross-sectional study, researchers examined the relationship between statin-induced myalgia and the impairment of mitochondrial respiration and muscle coenzyme Q10 levels. The researchers analyzed screening interview responses, body composition, maximal oxygen consumption, blood samples, and muscle biopsies of 84 participants.
Participants were categorized into 3 groups: 25 patients taking statin therapy who experienced myalgia, 39 patients taking statin therapy who were not experiencing myalgia, and 20 control participants with untreated high cholesterol. The researchers measured mitochondrial respiration and H2O2 production, intramuscular and plasma coenzyme Q10 concentrations, and levels of citrate synthase, a biomarker for mitochondrial content in skeletal muscle.
Most participant characteristics were comparable across the 3 study groups, with the exception of the untreated control group having higher total cholesterol and low-density lipoprotein levels (P <.001 for both) and the patients with myalgia experiencing higher myalgia pain scores (P <.001). Coenzyme Q10 levels and citrate synthase activity were similar between all 3 groups, while the group with myalgia showed increased intrinsic mitochondrial respiratory capacity.
The investigators suggested future studies measure compliance with statin use among participants, discontinue statin therapy for patients with myalgia to observe if symptoms dissipate, and further examine mechanisms of intrinsic mitochondrial respiration to evaluate the hypothesis that impaired plasticity of the mitochondrial network might be a factor contributing to myalgia.
The researchers concluded that “statin-induced myalgia is coupled to an increased intrinsic mitochondrial respiratory function, while intramuscular [coenzyme Q10] levels are unaltered.”
Dohlmann TL, Morville T, Kuhlman AB, et al. Statin treatment decreases mitochondrial respiration but muscle coenzyme Q10 levels are unaltered: the LIFESTAT study [published online October 8, 2018]. J Clin Endocrinol Metab. doi:10.1210/jc.2018-01185
This article originally appeared on Endocrinology Advisor