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Up to 80% of CML patients using tyrosine kinase inhibitors (TKIs) reports muscle complaints [1]. These muscle complaints are strongly related to the presence of fatigue and contributes to both diminished disease control [2] and impaired quality of life [3]. Although the mechanism by which TKIs cause muscle complaints is poorly understood, mitochondrial dysfunction has been suggested to play a pivotal role in TKI-induced cardiac muscle toxicity [4, 5]. We assessed whether TKIs disturb skeletal muscle mitochondrial density and function (cellular level), and if this translates into alterations in muscle contractile function (muscle tissue level) and maximal exercise performance (whole-body level). To gain a better insight into TKI-induced muscle complaints, these outcomes were compared between CML patients with and without muscle complaints. Written informed consent was obtained from the participants prior to study enrollment. This study was approved by the Local Committee on Research Involving Human Subjects of the region Arnhem and Nijmegen, the Netherlands and registered at The Netherlands Trial Registry (NTR6373). A total of twenty Ph CP-CML patients on TKI therapy aged ≥ 18 were recruited from the Department of Hematology at the Radboud University Medical Center (Nijmegen, The Netherlands). CML patients were assigned to a group with (CML+MC, N= 10) or without (CML -MC, N= 10) muscle complaints (MC) on the basis of presence, onset and course of muscle cramps, pain, and/or weakness. This was quantified on a Likert scale from 1 (not at all) to 4 (very much) resulting in significant different scores between CML+MC and CML -MC (median 4.0 (interquartile range (IQR) 3.0–4.0) and 2.5 (IQR 2.0–3.0), respectively; P= 0.002). The Brief Fatigue Inventory (BFI) [6] was used to compare the degree of fatigue in CML patients, showing higher fatigue levels in CML+MC when compared to CML -MC (3.58 ± 2.19 and 0.95 ± 1.11, respectively; P= 0.005). Ten control participants were matched on group level for age, gender, BMI and physical activity level, assessed by The Short Questionnaire to Assess HealthEnhancing Physical Activity (SQUASH) [7]. Subjects were ineligible if they had hereditary muscle defects, diabetes mellitus, hypoor hyperthyroidism, severe electrolyte disturbances, or used co-medication known to cause muscle symptoms or have an effect on mitochondrial function (e.g. statins, steroids, and metformin). Furthermore, subjects These authors contributed equally: S. J. C. M. Frambach, N. A. E. Allard and N. M. A. Blijlevens, S. Timmers

Skeletal muscle toxicity associated with tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia