Abstract
The maintenance of functional independence is the top priority of patients with chronic kidney disease (CKD). Defects in mitochondrial energetics may compromise physical performance and independence. We investigated associations of the presence and severity of kidney disease with in vivo muscle energetics and the association of muscle energetics with physical performance. We performed measures of in vivo leg and hand muscle mitochondrial capacity (ATPmax) and resting ATP turnover (ATPflux) using 31phosphorus magnetic resonance spectroscopy and oxygen uptake (O2 uptake) by optical spectroscopy in 77 people (53 participants with CKD and 24 controls). We measured physical performance using the 6-minute walk test. Participants with CKD had a median estimated glomerular filtration rate (eGFR) of 33 ml/min per 1.73 m2. Participants with CKD had a -0.19 mM/s lower leg ATPmax compared with controls but no difference in hand ATPmax. Resting O2 uptake was higher in CKD compared with controls, despite no difference in ATPflux. ATPmax correlated with eGFR and serum bicarbonate among participants with GFR <60. ATPmax of the hand and leg correlated with 6-minute walking distance. The presence and severity of CKD associate with muscle mitochondrial capacity. Dysfunction of muscle mitochondrial energetics may contribute to reduced physical performance in CKD.
Highlights
The maintenance of functional independence is the top health priority reported by patients living with chronic kidney disease (CKD) [1]
Our findings demonstrate that the presence and severity of CKD is associated with decreased in vivo muscle mitochondrial oxidative capacity (ATPmax) in the tibialis anterior muscle, which is involved with mobility tasks
Measurements of mitochondrial energetics by 31phosphorus magnetic resonance spectroscopy (31P MRS) were directly linked with physical performance on a 6-minute walk test, indicating functional relevance and suggesting a link between mitochondrial function and skeletal muscle impairment in CKD
Summary
The maintenance of functional independence is the top health priority reported by patients living with chronic kidney disease (CKD) [1]. Skeletal muscle impairment, which manifests as muscle loss or weakness (sarcopenia), is the final common pathway of multiple adverse metabolic processes that arise from kidney disease, including malnutrition-inflammation and oxidative stress. Greater insights into the mechanisms underlying skeletal muscle impairment in CKD are needed to motivate new therapeutic directions for preserving muscle function critical to independent living. Lipidomic studies show that reduced kidney function is associated with disruption of mitochondrial fatty acid oxidation [5].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
