Performance in marathon running is influenced by a variety of factors, most of which are of a physiological nature. Accordingly, the marathon runner must rely to a large extent on a high aerobic capacity. But great variations in maximal oxygen uptake (VO2 max) have been observed among runners with a similar performance capacity, indicating complementary factors are of importance for performance. The oxygen cost of running or the running economy (expressed, e.g. as VO2 15 at 15 km/h) as well as the fractional utilisation of VO2 max at marathon race pace (%VO2 Ma X VO2 max-1) [where Ma = mean marathon velocity] are additional factors which are known to affect the performance capacity. Together VO2 max, VO2 15 and %VO2 Ma X VO2 max-1 can almost entirely explain the variation in marathon performance. To a similar degree, these variables have also been found to explain the variations in the 'anaerobic threshold'. This factor, which is closely related to the metabolic response to increasing exercise intensities, is the single variable that has the highest predictive power for marathon performance. But a major limiting factor to marathon performance is probably the choice of fuels for the exercising muscles, which factor is related to the %VO2 Ma X VO2 max-1. Present indications are that marathon runners, compared with normal individuals, have a higher turnover rate in fat metabolism at given high exercise intensities expressed both in absolute (m/sec) and relative (%VO2 max) terms. The selection of fat for oxidation by the muscles is important since the stores of the most efficient fuel, the carbohydrates, are limited. The large amount of endurance training done by marathon runners is probably responsible for similar metabolic adaptations, which contribute to a delayed onset of fatigue and raise the VO2 Ma X VO2max-1. There is probably an upper limit in training kilometrage above which there are no improvements in the fractional utilisation of VO2 max at the marathon race pace. The influence of training on VO2 max and, to some extent, on the running economy appears, however, to be limited by genetic factors.

CJ. Aerobic exercise capacity at sea level and at altitude in Kenyan boys, junior and senior runners compared with Scandinavian runners.

Eight well-trained middle and long distance male runners added to their regular training program a weekly 20-min treadmill run at a velocity calculated to elicit a blood lactate concentration of 4 mmol X 1-1. VO2 max, the running velocity eliciting 4 mmol X 1-1 blood lactate (VOBLA), and the activities of citrate synthase (CS), phosphofructokinase (PFK), lactate dehydrogenase (LDH) and LDH isozymes in the M. vastus lateralis were determined before and after 14 weeks of this training. Significant increases were observed in VOBLA and the relative fraction of heart-specific LDH, while the activity of PFK and the ratio of PFK/CS decreased after training. The change in VOBLA was negatively correlated to the mean rate of blood lactate accumulation during the last 15 min of the treadmill training runs, and positively correlated to the percentage of slow twitch fibers in the M. vastus lateralis. The data support the hypothesis that a steady state training intensity which approximates VOBLA will increase VOBLA, and will result in measureable local metabolic adaptations in the active skeletal muscles of well-trained runners without a significant change in maximal aerobic power. Muscle fiber type composition may be an indicator of the "trainability" of the musculature.

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