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With age, skeletal muscle mitochondria lose their oxidative capacity and their ability to respond to energy demand. These phenomena can lead to a reduction in skeletal muscle oxygen consumption, atrophy, and increased risk of developing age-related diseases such as sarcopenia. Whether age-derived changes in mitochondrial function correspond to structural changes in the mitochondrial reticulum remains unknown. PURPOSE: Investigate age-related changes in mitochondrial morphology and function using primary skeletal muscle cells derived from healthy young and old men. METHODS: Primary skeletal muscle progenitor cells (SkM) derived from the Rectus abdominis muscle of healthy active 18-19-year-old men (SkM Young), and 66-69-year-old men (SkM Old) were obtained from Cook MyoSite Inc. (Pittsburgh, PA). The mitochondrial network was analyzed in live cells using confocal microscopy. Oxygen Consumption Rate (OCR) was measured in intact cells using extracellular flux assays and a Seahorse analyzer (Agilent Technologies

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