Aitor Galdos Caja

The substrates metabolised during exercise reflect the intensity and duration of activity and the requirement for ATP re-synthesis. Typically, low-intensity exercise (<30% of maximum work capacity) relies most heavily on fat metabolism from plasma fatty acids and IMTG, moderate-intensity exercise (60–80% of maximum work capacity) relies upon the full range of available substrates including glucose, glycogen, plasma fatty acids and IMTG, whereas higherintensity exercise (85–90% of maximum work capacity) relies more heavily on muscle glycogen stores to meet ATP re-synthesis demands .


Following an endurance training period the overall effect on substrate selection is a shift towards greater reliance on fat metabolism at the same absolute submaximal exercise workload compared with before training. Early studies in the 1970s revealed that these changes in metabolism were at least partly related to an upregulation of mitochondrial biogenesis that increased the size and number of mitochondria. As a result, the maximal activities of key marker enzymes such as β-HAD, CS, CPT I and cytochrome c were observed to increase in trained skeletal muscle. Nowadays, this greater reliance on fat oxidation during submaximal exercise is known to be driven not only by increased mitochondrial biogenesis but also by several other factors including: increased total work capacity; increased storage, mobilisation, transport and oxidation of IMTGs; reduced sympathetic activation; and changes in other hormonal responses to exercise. The hormonal changes include blunted reduction in plasma insulin and blunted rise in plasma glucagon concentration during an exercise period.


After training there are also reductions in the factors influencing rates of reactions in glycolysis/glycogenolysis that lead to a reduced stimulus for activation of these metabolic pathways