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||P.1 left column: "Mitochondria are key regulators of cellular function and hence their dysfunction is implicated in the pathogenesis of many diseases [refs 1, 2, 3, 4] and the very process of aging itself [refs 5, 6]. For this reason, the study of mitochondrial function has become central to a wide variety of clinical and basic science research. A powerful tool to investigate mitochondrial function was developed more than fifty years ago by Chance and Williams (1956), involving the isolation of mitochondria from skeletal muscle. This method allows the recovery of a relatively pure mitochondrial fraction, through first homogenizing a fresh muscle sample and then purifying the mitochondria through a series of differential centrifugation steps [ref 7]. Notably, this in vitro approach allowed elucidation of the nature of the tricarboxilic cycle (Krebs cycle) in the 1960's [ref 8] and it continues to this day to be used widely to study a variety of aspects of mitochondrial biology in skeletal muscle, including mitochondrial permeability transition pore (mPTP) function [refs 9, 10], respiratory capacity [refs 9, 10, 11], reactive oxygen species (ROS) production [refs 10, 12, 13], mitochondrial protein import and assembly [refs 14, 15] and the mitochondrial genome and proteome [ref 16]. Despite the widespread adoption of this technique, standard isolation methods retrieve a low (generally 20–40% of total) fraction of the total mitochondrial content from muscle [primary sources]. For this reason, isolated mitochondria studies necessitate relatively large amounts of fresh tissue and have been suggested to lead to potential bias because of selective representation of the entire mitochondrial pool [ref 21]." Primary sources 17, 18, 20 investigated humans. Primary source 19 investigated mice.