Key result
Non-invasive ACL injury resulted in a twofold reduction in mitochondrial respiratory control ratio and a 30-100% increase in mitochondria-derived ROS production from days 7 to 56 post-injury.
Why the study?
It was unclear to what extent mitochondrial derangements are involved in long-term quadriceps dysfunction and weakness after ACL injury.
Does non-invasive ACL injury impair quadriceps mitochondrial health, muscle size, and phenotypic composition in a rodent model?
Does non-invasive ACL injury impair quadriceps mitochondrial health, muscle size, and phenotypic composition in a rodent model?
Non-invasive ACL injury in a rodent model leads to long-lasting impairments in quadriceps mitochondrial health, which are associated with dysregulation of muscle size and composition, particularly in males.
Answers are grounded in this paper and cite their sources.
Mitochondrial impairment may underlie quadriceps deficits after ACL injury in rodents; leaves open human translation and therapeutic targeting.
INTRODUCTION: Despite rigorous rehabilitation aimed at restoring muscle health, anterior cruciate ligament (ACL) injury is often hallmarked by significant long-term quadriceps muscle weakness. Derangements in mitochondrial function are a common feature of various atrophying conditions, yet it is unclear to what extent mitochondria are involved in the detrimental sequela of quadriceps dysfunction after ACL injury. Using a preclinical, non-invasive ACL injury rodent model, our objective was to explore the direct effect of an isolated ACL injury on mitochondrial function, muscle atrophy, and muscle phenotypic transitions. METHODS: A total of 40 male and female, Long Evans rats (16-week-old) were exposed to non-invasive ACL injury, while 8 additional rats served as controls. Rats were euthanized at 3, 7, 14, 28, and 56 days after ACL injury, and vastus lateralis muscles were extracted to measure the mitochondrial respiratory control ratio (RCR; state 3 respiration/state 4 respiration), mitochondrial reactive oxygen species (ROS) production, fiber cross sectional area (CSA), and fiber phenotyping. Alterations in mitochondrial function and ROS production were detected using two-way (sex:group) analyses of variance. To determine if mitochondrial characteristics were related to fiber atrophy, individual linear mixed effect models were run by sex. CONCLUSION: Long-lasting impairments in quadriceps mitochondrial health are present after ACL injury and play a key role in the dysregulation of quadriceps muscle size and composition. Our preclinical data indicate that using mitoprotective therapies may be a potential therapeutic strategy to mitigate alterations in muscle size and characteristic after ACL injury.
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Davi et al. (2022) studied Anterior cruciate ligament (ACL) injury (n=48). Non-invasive ACL injury vs. Healthy controls was evaluated on Mitochondrial respiratory control ratio (RCR) (twofold reduction, p=<0.05). Non-invasive ACL injury resulted in a twofold reduction in mitochondrial respiratory control ratio and a 30-100% increase in mitochondria-derived ROS production from days 7 to 56 post-injury.
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