Rodrigo Mancilla presented during the NVDO meeting about the slow activation of oxidative metabolism at the onset of exercise and how this is associated with low CRAT protein activity.
Metabolically compromised subjects, such as obese and type 2 diabetic patients, exhibit a strong reliance on oxygen-independent pathways (for example PCr hydrolysis) to resynthesize ATP when exercise starts. This phenomenon seems to be due to deficiency of intramyocellular Acetyl Coa availability, causing a delayed activation of mitochondrial oxidation-derived ATP generation. Here we showed the molecule Acetylcarnitine stored in skeletal muscle might supply additional acetyl coa groups for oxidation when exercise starts, mediated by CrAT protein activity. Specifically, well-trained subjects exhibited a short time reliance on PCr hydrolysis (reflecting an early mitochondrial activation), exhibit a higher CrAT protein activity and greater skeletal muscle acetylcarnitine content compared with obese and type 2 diabetic subjects. In summary, we believe that regular exercise training equip muscle tissue to overcome sudden increases in energy demand. Furthermore, we suggest that acetylcarnitine molecule stored in human skeletal muscle and CrAT protein activity can be potential targets to prevent early muscle fatigue in metabolically compromised individuals.