Abstract des Autors

Interest in rises in oxygen consumption (VO2) with increasing exercise intensity largely originate from the work of Hill and colleagues in the 1920s. Their studies led to a belief that cardiac output and VO2 'plateau' at increasing work rates and that muscle hypoxia leads to fatigue. Hence, it was assumed that the primary benefit of exercise training is to increase muscle oxidative capacity and that the greatest benefit of training would occur at work rates around the 'anaerobic threshold'. In this paper, we question whether working muscles become hypoxic at high work rates. Rather than being a threshold response to hypoxia, we propose that plasma lactate accumulation and curvilinear rises in ventilation at high work rates are both independent consequences of the acceleration of carbohydrate metabolism with increasing exercise intensity. Evidence is also presented to suggest that athletic performances are not exclusively related to muscle oxidative capacity. Once an athlete has adapted to prolonged, 'aerobic' training, intervals of 'anaerobic', high-intensity exercise further improve performance without additional increases in muscle mitochondrial density or alterations in metabolism. Until the mechanisms underlying the latter improvements in performance are understood, it is difficult to advise athletes on how best to prepare for competition. Verf.-Referat