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Mitochondrial dysfunction leads to a loss of energy production, fatty acid accumulation, excess reactive oxygen species(ROS) generation, membrane instability, and a shift to glucose metabolism [1,2]

This work shows that injured skeletal muscle recruits inflammatory monocytes that subsequently convert to anti-inflammatory macrophages that stimulate myogenic differentiation and muscle growth

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No evidence of effect modifications was observed for any subgroups, although the evidence was stronger for participants with high cardiovascular risk

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