Key result
Myocardial infarction cuts skeletal muscle mitochondrial ATP synthesis by ~50% in preclinical models.
Why the study?
In heart failure, skeletal muscle shows increased acidification during exercise and impaired recovery, indicating altered bioenergetics and oxidative function that need quantification and relation to cardiovascular function.
Does myocardial infarction impair skeletal muscle bioenergetics during exercise and recovery in Wistar rats?
Population
Wistar rats studied four weeks after myocardial infarction or sham operation
Comparison
Myocardial infarction vs sham operation
Design
Preclinical study using 31P magnetic resonance spectroscopy
Authors
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Skeletal muscle mitochondrial impairment may follow MI without overt failure; leaves open relevance to human exercise limitation.
Does myocardial infarction impair skeletal muscle bioenergetics during exercise and recovery in Wistar rats?
Myocardial infarction in rats leads to a significant reduction in the maximum rate of mitochondrial ATP synthesis in skeletal muscle, explaining the increased anaerobic metabolism during exercise.
Thompson et al. (1995) studied Myocardial infarction. Myocardial infarction vs. Sham operation was evaluated on Maximum rate of mitochondrial ATP synthesis and phosphocreatine recovery. Myocardial infarction in rats led to impaired phosphocreatine recovery, suggesting an approximate halving of the maximum rate of mitochondrial ATP synthesis in skeletal muscle.
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