TO THE EDITOR: To study relationships between muscle mitochondrial function, fatty acid oxidation, intramyocellular lipid (IMCL), and insulin resistance (IR), Laurent et al.(21a) measured Pi/ATP exchange by 31P magnetic resonance saturation (MRS) transfer (ST) in resting rat muscle and found that it decreased transiently by high dietary fat (HF) intake. Following precedent, they identified Pi/ATP exchange with mitochondrial ATP synthesis, noting that “actual rates obtained... in rats at rest are in excellent agreement with recent human data,” and took the decrease as evidence of mitochondrial dysfunction (21a). I would like to make two points about absolute rates and pathophysiological logic.