Fig. 2

Pre and post TRE plasma-mediated alteration of mitochondrial respiration in skeletal muscle cells. We utilized the Agilent Seahorse Metabolic Flux system to assess mitochondrial stress (A and B) and metabolic profile (C) by monitoring oxygen consumption rates (OCR) via adoptive transfer of plasma to cultured C2C12 cells. C2C12 cells were incubated with plasma at 1% final concentration for one hour before initiating the mitochondrial stress energy generation protocol. (A) Averaged values representing tracing of the Seahorse protocol. We assessed baseline respiration up until the addition of oligomycin (ATPase inhibitor) followed by FCCP (uncoupler) and finally rotenone/antimycin A (Rot/Ant, complex I and III inhibitors, respectively). (B) Mitochondrial functional parameters were analyzed for all samples. We saw no change in mitochondrial stress parameters. (C) Metabolic profiling revealed a significant increase (p < 0.05) in mitochondrial-derived ATP in post-TRE plasma, suggesting that factors in the post-TRE plasma can potentially increase mitochondrial function. Groups were n = 20.