Abstract
A unique evolutionary feature of skeletal muscle is the co‐existence within the same organs of fast (glycolytic, Type II) and slow (oxidative, Type I) muscle fibers. These fiber‐types have specific contractile properties that generate unique intracellular conditions, to which bioenergetics and mitochondrial function must be tailored. However, the extent to which mitochondrial function differs between fast and slow muscle fibers has not clearly been established. Here, we present extensive data supporting the existence of distinct functional phenotypes in mitochondria from slow and fast fibers, including differences in energy substrate preferences, regulation of oxidative phosphorylation, dynamics of reactive oxygen species release, handling of Ca2+ and regulation of cell death via the mitochondrial permeability transition pore (mPTP). The potential physiological implications on muscle function, and the putative mechanisms responsible for establishing and maintaining distinct mitochondrial phenotype across fiber types are also discussed.
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