Skeletal muscle endurance declines with impaired mitochondrial respiration and inadequate supply of acetyl-CoA during muscle fatigue in 5/6 nephrectomized rats

Author:

Fusagawa Hiroyori12ORCID,Sato Tatsuya13ORCID,Yamada Takashi4ORCID,Ashida Yuki4,Kimura Iori4,Naito Azuma4,Tokuda Nao4,Yamauchi Nao4,Ichise Nobutoshi1,Terashima Yoshinori12,Ogon Izaya12,Teramoto Atsushi2,Yamashita Toshihiko2,Tohse Noritsugu1ORCID

Affiliation:

1. Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine, Sapporo, Japan

2. Department of Orthopaedic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan

3. Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan

4. Graduate School of Health Sciences, Sapporo Medical University, Sapporo, Japan

Abstract

Mitochondrial dysfunction is associated with decreased skeletal muscle endurance in chronic kidney disease (CKD), but the muscle physiological phenotype and major changes in intramuscular metabolites during muscle fatigue in CKD-related cachexia remain unclear. By using a 5/6 nephrectomized CKD rat model, the present study revealed that CKD is associated with reduced tetanic force in response to repetitive stimuli in a subacute phase, impaired mitochondrial respiration, and inadequate supply of acetyl-CoA during muscle fatigue.

Funder

Japan Society for the Promotion of Science

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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