From “Hypothesis: Significance of Skeletal Muscle Oxidative Enzyme Enhancement With Endurance Training” by P.D. Gollnick and B. Saltin, 1982, Clinical Physiologist, 2, p. 4. Copyright 1982 by Blackwell Scientific Publications.
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Capacity of each mitochondrion to produce ATP at any substrate concentration is greatly enhanced. Thus at any rate of energy production (exercise intensity) each mitochondrion will be able to work at a higher (ATP)/(ADP)(Pi) ratio and will therefore be less dependent on carbohydrate metabolism for energy.
This means that after training, fat can provide more energy at higher exercise intensities than it can before training, with less need to activate carbohydrate metabolism. So the rate of lactate production is reduced after training; this explains, in part, the shift in the lactate tumpoint with training (Exercises 3.13). Dudley et al. (1987) have shown that the muscle (ATP)/(ADP)(Pi) ratio is indeed higher during exercise in trained than in untrained muscle.
Finally, because the capacities of the shuttles that transfer protons from cytoplasm to mitochondria are increased through submaximal training, there will be a lesser accumulation of protons during exercise. Thus, the escape mechanism for proton transfer onto pyruvate to produce lactate (see Exercises 3.2) is reduced, causing a further shift of the lactate tumpoint to a higher running speed or percent V02max.
In addition, evidence now indicates that the abilities of tissues such as the heart, kidney, liver, and inactive and active skeletal muscles to utilize any lactate produced by the active muscles during exercise are also increased through submaximal training (Donovan & Brooks, 1983). These authors consider this adaptation the most important explanation for the reduced rate of blood lactate accumulation during exercisea proposal that is in line with more recent findings (MacRae et al, 1991).