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Objective: Maximal mitochondrial complex I-, II-, I+II- linked respiration (OXPHOS) and concen-tration of Q10 were measured in skeletal muscle from statin users with myalgia (S+MY, n=14), without myalgia (S-MY, n=31) and healthy controls (n=15). Background: The statins are used for treatment of hypercholesterolemia. Statins inhibit the meva-lonate pathway and there by effectively lowering the concentration of cholesterol in the blood. The statins is however also associated with the development of muscle ache and pain (myalgia). The mechanism behind this statin induced myalgia is unclear, but one theory involves a reduced level of Q10, an essential co-enzyme in the mitochondrial electron transport chain and a reduced OXPHOS capacity in the mitochondria. Method: The mitochondiral OXPHOS capacity for complex I, II and I+II were measured in permeabilized muscle fibres with high resolution resporomtetri by OROBOROS Oxygraph-2k. The concentration of Q10 was measured intramuscularly with high-performance liquid chromatography (HPLC). Results: Mitochondrial complex II-linked respiration was significant lower in S+MY and S-MY compared to the control group (p > 0,005). There were no difference in the respiratory capacity in the I, II and I+II complex between the S+MY and S-MY group. There was no significant difference in the Q10 concentration intramuscular between the three groups, though there was a tendency towards a lower concentration in the two groups treated with statins compared to the control group (p = 0,092). Conclusion: These findings may suggest that mitochondrial respiratory function is altered with statin therapy due to the lower complex II capacity in the two statin groups compared to the control group. The overall results showed no significant difference between the groups in either the Q10 concentration, or the mitochondrial respiratory. The statin induced myalgia is therefore not due to the mitochondria respiratory function or the concentration of Q10 int