COMMENT
It is known that traumatic muscle injury damages mitochondria, which may cause them to leak their contents into the cytoplasm and subsequently trigger calcium accumulation, cell death, endoplasmic reticulum stress, and the release of reactive oxygen species (ROS). The latter reduces mitochondrial quality and increases the number of unhealthy mitochondria present in the cell, which may delay post-injury muscle regeneration. Although this knowledge has informed studies demonstrating the beneficial effects of mitochondrial transplant therapy (MTT) on ischaemia-damaged myocardium, its effects on injured skeletal muscle remain undefined.
The aim of this article was to examine the effects of MTT on skeletal muscle function after neuromuscular injury. The latter was induced using BaCl2, which causes widespread muscle proteolysis via myofibre Ca2+ overload and hyper-contractions.
KEY LEARNINGS
Although MTT one day post-injury was not found to induce systemic inflammation nor modify muscle repair over the first week, it did significantly improve gastrocnemius muscle fibre regeneration and restoration of force during the second week following BaCl2 injury. Restoration via MTT was fibre-type specific: repair was preferentially enhanced in type IIB fibres, which globally improved muscle function.
