Practical Implications of Training
Of what practical value is this knowledge of the muscle adaptations to training? First, the fact that the mitochondrial adaptations to training occur only in the trained muscles and only in the muscle fibers that are active during that exercise indicate that training for a particular event or sport must use the correct muscle groups and more specifically the appropriate muscle fibers and the appropriate metabolic pathways in those fibers. For example, the runner who trains exclusively on the flat is untrained for uphill running because different muscle groups are involved in these two activities (Costill et al, 1974). Similarly, the noncompetitive jogger will train a different fiber type than will the middle-distance runner who exercises at a higher intensity and therefore activates both ST and FT muscle fibers.
Second, studies of detraining show that it is not necessary to maintain the same high intensity of training year-round; a reduction in training by as much as two thirds may maintain a decent level of fitness. This becomes important when we consider the concept of peaking.
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Third, the concept of different training intensities producing different training effects allows the tailoring of individual training goals. Sprinters must aim to increase muscle contractility and the rates of glycolysis and creatine kinase reactions, whereas middle-distance runners must adapt the muscles so that they become progressively more resistant to low pH levels. Marathon runners, on the other hand, must shift their lactate tumpoints to higher running speeds; these runners must increase their capacities for fat oxidation so that they can “spare” carbohydrate stores during racing. They must also maximize their abilities to store liver and muscle glycogen before exercise and must increase their capacities to absorb carbohydrate during competition. Ultramarathon runners must, in addition, adapt their muscles so that they are resistant to racing-induced muscle damage.
The Heritability of the Capacity to Adapt to Endurance Training
The concept that the V02max is determined largely by hereditary factors has been described. We now also know that endurance performance during a prolonged exercise test is even more strongly determined by genetic factors (Bouchard et al, 1986), as is the degree to which any individual can adapt to an endurance training program (Bouchard & Lortie, 1984; Hamel et al, 1986; Prud’homme et al, 1984; Simoneau et al, 1986). Thus, 70 to 80% of both endurance performance and the adaptability to training is determined by genetic factors.
Researchers have identified high and low responders to training, with low responders (Lortie et al, 1984; Prud’homme et al, 1984) showing none of the adaptations to training that this post has described. These individuals simply do not and cannot improve with training regardless of their efforts. Attempts to identify genetic markers for high and low adaptors are currently in progress (Bouchard et al, 1989). Interestingly, the extent to which other beneficial changes develop with training, including the reduction in serum cholesterol concentrations, may also be genetically controlled (Despres et al, 1988).
Thus, elite athletes are not only superiorly endowed with those attributes necessary for successsuch as high V02max values, lactate tumpoints that occur at fast running speeds, fast peak treadmill running speeds (Noakes et al, 1990b), and muscles with a higher capacity to generate ATP from oxidative metabolism even when untrained (Park et al, 1988)but they also have genetic gifts that enable all these variables to adapt to the greatest possible extent with training.
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